Showing posts with label diabetes. Show all posts
Showing posts with label diabetes. Show all posts

Sunday, August 5, 2018

Hepatitis C-Diabetes associated w-advanced fibrosis and progression in HCV non-genotype 3 patients

In case you missed it

Dig Liver Dis. 2018 Jul 17. pii: S1590-8658(18)30814-4. doi: 10.1016/j.dld.2018.07.003. 
[Epub ahead of print]

Diabetes is associated with advanced fibrosis and fibrosis progression in non-genotype 3 chronic hepatitis C patients.

Researchers investigated if diabetes is associated with progression from the non-cirrhotic liver to cirrhosis in non-genotype 3 chronic hepatitis C (CHC) patients. In the study 976 non-genotype 3 patients with HCV were studied, out of the 976 participants, 684 did not have cirrhosis. According to ultrasound findings, 60 patients developed cirrhosis during the follow-up period. In non-genotype 3 CHC patients, diabetes was correlated with progression from the non-cirrhotic liver to cirrhosis.

Diabetes is a risk factor of fibrosis progression in chronic hepatitis C (CHC). However, only one longitudinal study exploring whether diabetes is associated with progression from non-cirrhotic liver to cirrhosis in CHC patients has been conducted.

We investigated whether diabetes is associated with progression from non-cirrhotic liver to cirrhosis in non-genotype 3 CHC patients.

A cohort consisting of 976 non-genotype 3 patients histologically proven to have CHC was studied. After excluding patients with biopsy-proven or ultrasound-identified cirrhosis, there were 684 patients without cirrhosis. All 684 patients underwent hepatocellular carcinoma surveillance using ultrasound every 6 months, with a median duration of follow-up evaluation of 102.4 months. During the follow-up period, 60 patients developed cirrhosis according to ultrasound findings.

For the subgroup of 684 patients without cirrhosis, Kaplan-Meier survival analyses showed no significantly different cumulative incidences of cirrhosis (log-rank test; P = 0.71) among the patients with diabetes as compared to those without. However, after making adjustments for age, gender, fibrosis, steatosis, sustained virological response status, and obesity using Cox's proportional hazard model, diabetes was found to be an independent predictor for cirrhosis (HR = 1.9; 95% CI = 1.05-3.43, P = 0.03).

Diabetes is associated with progression from non-cirrhotic liver to cirrhosis in non-genotype 3 CHC patients.

Diabetes; Genotype 3; Hepatitis C virus; Liver cirrhosis; Ultrasound
PMID: 30076015 DOI: 10.1016/j.dld.2018.07.003 
Full text article requires payment 

Tuesday, July 17, 2018

Protective liquid enables oral insulin delivery in rats

July 17, 2018
Protective liquid enables oral insulin delivery in rats
—by Sharon Reynolds

More than 30 million people in the United States live with diabetes, a disease in which the body has trouble managing and using blood glucose, the sugar that serves as the body’s fuel. Tens of millions more live with prediabetes, a condition where blood glucose levels are higher than normal, but not high enough to be considered diabetes. When blood sugar isn’t controlled for long periods of time, it can cause a range of health problems, including nerve damage and heart or kidney disease.

People with diabetes must actively monitor and control their blood sugar levels. Many need injections of insulin, a hormone that helps the body process glucose, several times a day to keep their blood sugar levels under control. But it can be difficult and painful to keep up with insulin injections. An oral form of insulin would drastically ease the difficulty of maintaining healthy blood sugar levels.

Insulin runs into many obstacles when taken by mouth. First, acid in the stomach can degrade it. Second, any insulin that reaches the small intestine from the stomach can be chopped up by the enzymes that help break down food. Finally, insulin needs to be absorbed into the bloodstream through the cells that line the small intestine.

A research team led by Dr. Samir Mitragotri of Harvard University has been exploring the uses of an ionic liquid called CAGE. Ionic liquids contain both positively and negatively charged molecules. CAGE is made from two non-toxic compounds, choline and geranate. In previous work, the team showed that CAGE could be used to deliver antibiotics and insulin through the skin of rats.

In their latest study, the team tested whether CAGE could protect insulin from degradation by the digestive system and help it through the intestinal lining. The research was funded in part by NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Results were published in the Proceedings of the National Academy of Sciences on July 10, 2018.

The researchers first tested whether their insulin-CAGE solution was stable. The structure and function of insulin remained intact in CAGE for 2 months at room temperature and at least 4 months when refrigerated.

When injected directly into the small intestines of non-diabetic rats, the solution quickly lowered blood sugar levels by up to 65%. Insulin-CAGE delivered through the small intestine lasted longer in the bloodstream than insulin injected under the skin.

The researchers next packaged insulin-CAGE into enterically coated capsules. Enteric coatings are resistant to stomach acid but dissolve when they reach the small intestine. When given by mouth to rats, the capsules caused a slow and steady drop in blood sugar, by about half over 10 hours. This drop was smoother and longer lasting than that caused by injection. Samples taken from the intestinal walls after administration showed no damage caused by the insulin-CAGE solution.

“Once ingested, insulin must navigate a challenging obstacle course before it can effectively be absorbed into the bloodstream,” Mitragotri says. “Our approach is like a Swiss Army knife, where one pill has tools for addressing each of the obstacles that are encountered.”

The researchers are now planning studies with diabetic animals to gauge the long-term safety and effectiveness of oral insulin-CAGE. They hope to eventually test the approach in a human clinical trial.

References: Ionic liquids for oral insulin delivery. Banerjee A, Ibsen K, Brown T, Chen R, Agatemor C, Mitragotri S. Proc Natl Acad Sci U S A. 2018 Jul 10;115(28):7296-7301. doi: 10.1073/pnas.1722338115. Epub 2018 Jun 25. PMID: 29941553.

Funding: NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); the National Science Foundation; Harvard University; and the Natural Sciences and Engineering Research Council of Canada.

Thursday, May 24, 2018

Blood test may predict who is most at risk for diabetes

Blood test may predict who is most at risk for diabetes 
Lisa Rapaport
(Reuters Health) - Adding a test normally used for diabetes monitoring to employee wellness exams could identify people who don’t have the disease but are at high risk of developing it, a recent study suggests. Researchers examined data from two different types of blood sugar test for more than 34,000 participants in a U.S. employee wellness program who didn’t have diabetes. At the start of the study, they all also had fasting blood sugar in a healthy range.

Diabetes Care, online April 26, 2018
Dov Shiffman, Carmen H. Tong, Charles M. Rowland, James J. Devlin, James B. Meigs and Michael J. McPhaul
Diabetes Care 2018 Apr; dc172500.

Recommended reading
HCV-Infected Patients With Diabetes Improve With Direct-Acting Antiviral Therapy: Presented at AACE

Wednesday, May 23, 2018

HCV-Infected Patients With Diabetes Improve With Direct-Acting Antiviral Therapy: Presented at AACE

FirstWord Pharma

HCV-Infected Patients With Diabetes Improve With Direct-Acting Antiviral Therapy: Presented at AACE
By Michael Bassett
BOSTON -- May 22, 2018 -- Treatment of hepatitis C virus (HCV)-infected patients who have diabetes with direct-acting antiviral therapy results in significant and durable improvement in their diabetes, according to study presented here at the American Association of Clinical Endocrinologists 27th Annual Scientific & Clinical Congress (AACE)...

Although 66% of the patients had no improvement in diabetes with HCV eradication, 10% of the patients showed improvement but not sustained, and 24% experienced sustained improvement...

Monday, April 23, 2018

HCV, type 2 diabetes & fatty liver disease - Importance of diet and exercise

Importance of diet and exercise 

This Michigander is announcing winter might just be over. I am so done walking on my ugly, hated, overrated treadmill, looking forward to moving my morning routine outside.

If you too are feeling a bit of spring fever, or preparing for a lifestyle change, check out the links provided below and learn about the importance of diet and exercise for people with HCV, type 2 diabetes or fatty liver disease.

On The Radio
To get you started we begin with Dr Norman Swan, the host of Health Report, along with his guest Professor Mike Lean, lead author in a study investigating the impact of weight loss on type 2 diabetes, published in the Lancet 10 February 2018; Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The study found after a year, participants who lost weight (around 30 pounds) on a 800 calorie diet, no longer had type 2 diabetes. The diet may be too difficult or not recommended for some people, in the trial patients were followed closely, however, the outcome is amazing. The interview starts at 8:29, listen to the program, here, read the transcript below or visit Health Report.

Norman Swan: There's good news, for once, from the west of Scotland where a trial in general practice of an extremely low calorie diet has reversed type 2 diabetes in a large percentage of participants. Mike Lean is Professor of Human Nutrition at the University of Glasgow and is on the line. Welcome to the Health Report.

Mike Lean: Hello, how are you?

Norman Swan: Fine. You say in the paper that this is the first trial of its kind in type 2 diabetes, which is extraordinary.

Mike Lean: We've known about type 2 diabetes and thought of it as a distinct disease growing enormously in numbers and costing perhaps more than any other single disease for about 100 years, and it has been noted in a number of studies that some people if they lose enough weight will get rid of their diabetes. But no study has previously gone out to actually try and do that, to actually get as many people as possible to become non-diabetic, to get rid of their diabetes completely.

Norman Swan: So what did you do in this study?

Mike Lean: Well, this is not rocket science. What we did was we recruited people in primary care, in general practice, who were overweight, BMI over 27, so not enormously overweight but overweight, with type 2 diabetes. And we ask them to follow a formula diet, not a very low calorie but and 800-odd calorie diet for as long as it took, and it took quite a long time in some cases, to lose enough weight to become non-diabetic. And we aimed to get 15 kg weight loss because we knew from other observations that that was likely to do it. And of course not everybody managed, sadly, a lot of people found it really hard. A lot of people did manage. In the end we got about a quarter of our patients to lose that amount of weight. And those who lost 15 kg, almost 90% were no longer diabetic after a year, they were off all their medication, they were off all their diabetic medication and their antihypertensive medication, and they felt a lot better, their quality of life went up.

The remainder who didn't lose 15 kg, none of them got worse. Of those who lost over 10 kg, over half of them were non-diabetic. So you don't need to lose 15 kg but it's much better if you do. And I think what we've learnt from this is what we've regarded as a distinct disease, type 2 diabetes, is actually all part and parcel of obesity when you think about obesity as a disease process…

Norman Swan: We'll come back to the diet in a minute. And what was the recidivism rate, if you want to call it that, in terms of people gaining weight again and returning to diabetes?

Mike Lean: Yes, so that is of course…we've only published the one-year results and there's a lot more to find out. What we did find out was that the proportion of people with diabetes who wanted to have a go at this was very high. It was probably no great surprise because being diabetic is a penalty and it carries terrible medical risks as well as financial. The number within a year who put on any weight was really quite small, but we know very well from earlier studies that it's hard to maintain…the biggest problem is not losing the weight, it's actually maintaining it long term, and that's where our big research effort needs to go.

Norman Swan: So the diet itself…an 800 calorie diet is not something you try yourself at home because you can go into nutritional deficiency. This was a shakes and bars diet, wasn't it, it was a meal plan diet.

Mike Lean: That's correct, it was a formula diet which made sure it had all the vitamins and minerals, everything that was necessary, provided the patients actually followed this. And they didn't have to pay for it, they were given it for the study. And so they did that, so it was perfectly safe, there was no…

Norman Swan: That's my point, so it's one of these things you can buy in the chemist and it comes in various boxes, but we won't talk about the branding.

Mike Lean: The branding doesn't matter, all these things are pretty much the same. What matters is not what comes in the box or out of the packet, it's the support that is given with it, because people who go and get these type of diets from the chemist or from a supermarket generally do it for two or three or four weeks and then they peel off. If you are going to get rid of your diabetes you've got to stick in for probably 12 weeks if you do it full time. There are plenty of people who do it off and on for 12 weeks and need to carry on doing it off and on for a bit longer to lose their 10 or 15 kg. So there are different routes to getting there, you don't half to lose it all in one go but it works better if you do.

Norman Swan: What about complications, like if you lose weight fast when you are overweight you can get gallbladder disease…

Mike Lean: Ah, you're well informed!

Norman Swan: You can low blood sugar if you're on insulin, or diabetes complications. What sort of complications did people get?

Mike Lean: Well, the first thing was for this particular study we didn't include people who were already on insulin, partly because their likelihood of getting a remission is much lower. It had probably done damage to their pancreas by that stage. And what we did on day one was that we stopped all our anti-diabetes medication, so there's no risk of hypoglycaemia at all, and nobody had hypoglycaemia. And the same thing went for the blood pressure tablets, we stopped all their blood pressure tablets on day one because otherwise if you lose weight there is a risk of possible hypotension, and just to pick up your other point, there was one patient amongst the 150 who started, one who developed abdominal pains and we think that was probably by gallstones. That's a common complication of obesity, very common in people with diabetes anyway, and it can be made worse during weight loss.

Norman Swan: These are similar findings to bariatric surgery.

Mike Lean: Oddly the remission rate was actually a tiny bit better than bariatric surgery if you can lose 15 kg. If you lose 15 kg you will almost certainly get rid of your diabetes, whether or not it's done with surgery. There are of course many fewer hazards doing it without surgery. They produce very similar results, yes.

Norman Swan: Mike, thanks very much for joining us, a fascinating study.

Mike Lean: Thank you very much.

Norman Swan: Mike Lean is Professor of Human Nutrition at the University of Glasgow.

Fatty Liver Disease & Type 2 Diabetes 
"Given the increasing worldwide incidence of obesity and metabolic syndrome, non-alcoholic fatty liver disease (NAFLD) has become the most common cause of chronic liver disease. Recent developments in the field have shown that NAFLD not only is a “liver disease” but also is the underlying cause of an increasing number of extrahepatic manifestations; thus, it should be treated as a multisystem disease. NAFLD is most prominently linked to chronic kidney disease, mellitus type 2 and cardiovascular disease, as well as a number of other severe chronic diseases. These findings demonstrate that NAFLD ranks amongst the most serious public health problems of our time."

Also noted in the article; The prevalence of Nonalcoholic Steatohepatitis (NASH), in people who are obese and have type 2 diabetes may be as high as 40%, whereas it is less than 5% in people without type 2 diabetes.
Read the article, here.

Presented at Liver Congress 2018
Alcoholic liver disease replaces hepatitis C infection as leading cause of liver transplantation in patients without hepatocellular carcinoma in the USA
Two independent studies presented at the conference reported; that alcoholic liver disease has now replaced hepatitis C virus (HCV) infection as the leading cause of liver transplantation in the USA in patients without HCC. Non-alcoholic steatohepatitis (NASH) is also on the increase, now ranking second as a cause of liver transplantation due to chronic liver disease.
Read the article, here.

Hepatitis C & Diabetes
Several studies have demonstrated the risk for development of diabetes is increased in people with chronic hepatitis C infection (HCV), for instance people with HCV have a 2.3 fold increased chance of having type 2 diabetes. According to a 2013 study published in Alimentary Pharmacology Therapeutics; Chronic hepatitis C virus infection is independently associated with presence of metabolic conditions (insulin resistance, type 2 diabetes mellitus and hypertension) and congestive heart failure.

HCV Treatment & Type 2 Diabetes
The good news is with today's high sustained viral response rates using direct antiviral medications to treat HCV, people who successfully reach SVR, or achieve a cure, lower their risk for the development of type 2 diabetes, the recent study was published in the Journal of Viral Hepatitis [published online February 25, 2018]. A quick overview of the study can be found online, here.

Fatty liver is very common in hepatitis C virus (HCV) patients post-SVR
This particular study may be of interest to people with HCV, according to data published Mar 21, 2018 in the online journal World J Gastroenterology, evidence of steatosis was reported to be found in close to half of patients who achieve a sustained virologic response after treating with direct-acting antivirals. Full-text, here....

Tips - Eating Right
Eating better tied to lower risk of liver disease
April 27, 2018
(Reuters Health) - People who make an effort to improve their diet may be more likely to have less fat in their livers and a lower risk of liver disease than individuals who stick to unhealthy eating habits, a U.S. study suggests.

The Liver Loving Diet
"The Liver Loving Diet" is a book that will help you learn to eat well during all phases of liver disease. Karen Hoyt, the author, also blogs about living with and treating hepatitis C, cirrhosis, liver cancer and liver failure.

Mediterranean diet reduces liver fat, risk for NAFLD
March 30, 2018
Improved diet quality based on the Mediterranean-style diet score and Alternative Healthy Eating Index score correlated with less liver fat accumulation and a reduced risk for new-onset nonalcoholic fatty liver, according to a recently published study.
Continue reading @ Healio

Bottom Line
Spring is a great time to start again, experts agree two key elements in the prevention and management of type 2 diabetes and fatty liver disease is weight loss and exercise. In the end, its all good for your liver!

See you soon,

Wednesday, April 11, 2018

The link between hepatitis C virus and diabetes mellitus: Improvement in insulin resistance after HCV eradication
Updates published in Clinical Liver Disease (CLD)
Clinical Liver Disease (CLD) is a digital educational resource published on behalf of the American Association for the Study of Liver Diseases (AASLD).

Radiology in Liver Disease
The link between hepatitis C virus and diabetes mellitus: Improvement in insulin resistance after eradication of hepatitis C virus
Justine Hum M.D. Janice H. Jou M.D., M.H.S.
Pages: 73-76
First Published:6 April 2018
Watch a video presentation of this article
Watch the interview with the author
Full text

Controversies in HCV Management
Hepatitis C: Who should treat hepatitis C virus? The role of the primary care provider
Tram T. Tran M.D.
Pages: 66-68
First Published:6 April 2018
Watch a video presentation of this article
Watch the interview with the author
Full text

Friday, April 6, 2018

Prevalence and genotype distribution of hepatitis C virus infection among patients with type 2 diabetes mellitus.

Med Princ Pract. 2018 Apr 5. doi: 10.1159/000488985. [Epub ahead of print]
Published online: April 05, 2018

Prevalence and genotype distribution of hepatitis C virus infection among patients with type 2 diabetes mellitus.
Farshadpour F, Taherkhani R, Ravanbod MR, Eghbali SS.

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In this study, the prevalence of HCV infection in the diabetic patients in southern Iran was high and it was not associated with the biochemical measurements. Genotype 3a was the only genotype found in the diabetic population of this study, and all the HCV-infected diabetic patients were unaware of the infection due to asymptomatic nature of chronic HCV infection. Therefore, screening of all diabetic patients for HCV infection should be recommended to prevent the serious consequences associated with the coexistence of these two chronic diseases in a long run.

As Noted In The Study: After genotype 1a, genotype 3a is the most prevalent genotype in Iran, which is frequently observed among young Iranian patients and intravenous drug users; while genotypes 2 and 4 are uncommon in Iran [11, 27]. Overall, it is not obvious whether HCV genotype 3a observed in the present study is responsible for the occurrence of DM or whether it merely follows the predominant genotypic pattern of HCV in the region. However, this specific genotypic pattern of HCV infection in the diabetic patients of the present study is unlikely to be ascribable to chance alone and, therefore, merits further attention.

This study was conducted to determine the prevalence and genotype distribution of HCV infection among patients with type 2 diabetes mellitus (DM).

Materials (Subjects) and Methods
A total of 556 consecutive patients with confirmed type 2 DM attending the diabetic clinic of Bushehr University of Medical Sciences and 733 non-diabetic subjects as control group were included in this study. Levels of FBS, ALT, AST, TCH and TG were measured by enzymatic colorimetric method, and the presence of anti-HCV antibodies were determined by ELISA. Semi-nested RT-PCR followed by sequencing was performed for all the anti-HCV seropositive samples. The data were analyzed using the Statistical Package for the Social Sciences 17.

Seroprevalence of HCV in diabetic patients was 1.98% (11/556), which was higher than HCV prevalence among the non-diabetic controls (4/733, 0.54%) (P=0.032). No significant differences in ALT, AST, FBS, TG and TCH levels were found between HCV seropositive and seronegative diabetic patients, although HCV seropositive diabetic patients tended to have higher ALT, AST and TCH levels but lower TG and FBS levels than seronegative patients. In the logistic regression analysis, only AST level was significantly associated with HCV seropositivity. Hence, AST level of 41-80 IU/L was the only significant predictive variable for HCV seropositivity in the diabetic patients (odds ratio, 4.89; 95% CI: 1.06-22.49; P= 0.041). Of 11 HCV seropositive diabetic patients, 10 (91%) had HCV viremia with genotype 3a.

Patients with type 2 DM had a higher prevalence of HCV infection than controls, and this HCV seropositivity was independent of biochemical parameters.

Thursday, April 5, 2018

Does Pioglitazone Have the Same Effects on NASH in Patients With vs Without Diabetes?

AGA Blog
Does Pioglitazone Have the Same Effects on NASH in Patients With vs Without Diabetes?
Dr. Kristine Novak
Patients with prediabetes and nonalcoholic steatohepatitis (NASH) benefit nearly as much from pioglitazone therapy as those with type-2 diabetes, researchers report in the April issue of Clinical Gastroenterology and Hepatology. The diabetes drug reduced fibrosis in non-diabetic patients with NASH, the clinical study found, although to a lesser extent than in patients..
Read more

Monday, March 26, 2018

Editorial: diabetes, obesity and clinical inertia—the recipe for advanced NASH

We should screen patients with diabetes for “diabetic hepatopathy” (NAFLD), in the same way, we do today for diabetic retinopathy or nephropathy, considering NASH as the “new” complication of T2DM. Earlier treatment will likely benefit patients as evidence shows that the majority of patients that lose ≥8%‐10% of body weight,1 or about two‐thirds of prediabetics/diabetics treated with pioglitazone,8 experience resolution of NASH. Breaking clinical inertia by targeting obese patients with T2DM is a reasonable first step to curb the looming epidemic of NASH‐cirrhosis among us.

Editorial: diabetes, obesity and clinical inertia—the recipe for advanced NASH

J. Leey K. Cusi
First published: 25 March 2018

Linked content
This article is linked to Patel et al and Patel and Hunt papers. To view these article visit and

The prevalence of NAFLD continues to rise, with T2DM and obesity being major risk factors for advanced NASH, cirrhosis and HCC.1 The prevalence of diabetes in adults ≥18 years in the USA is 12.2%, but doubles to 25.2% in those aged ≥65 (CDC, July 2017). This epidemic is particularly concerning at the Veterans Health Administration (VHA) that looks after an ageing population. At our Veterans Administration Medical Center (Gainesville, Florida), the prevalence of diabetes in 2016 among primary care clinics was 29%. Obesity is also a problem: 41% of all veterans are obese.2 Calls to systematically screen obese patients with T2DM are gaining traction.3 Despite veterans being a high‐risk population, and NAFLD being identified as a significant problem,4 a cohesive early screening/treatment strategy is still lacking within the VHA and at a national level.

In a recent issue, Patel5 makes an even stronger case for action. They examine risk factors for advanced NASH in 399 patients identified with a liver biopsy between 2005 and 2015. The strength of the study was the large sample size with patients divided into well‐defined categories across the spectrum of NAFLD. Shortcomings were the lack of centralised pathology reading and inclusion of few females. However, the study had two important take home messages: the relevance of T2DM as the major risk factor for advanced NASH and the need to reverse clinical inertia. Both diabetes and clinical inertia, combined with obesity, appeared to be the perfect mix for disease progression, cirrhosis and even HCC. For instance, while 37% of patients with NAFL steatosis had T2DM, this climbed to 66% and 80% with NASH‐fibrosis and NASH‐cirrhosis respectively. Relative to controls, diabetics had a 4‐fold increase in the odds of being in the group of NASH‐without‐fibrosis, but eightfold in the NASH‐fibrosis and 12‐fold in the NASH‐cirrhosis groups. No other risk factor was as significant as diabetes; although most patients were obese and obesity‐related metabolic defects and “lipotoxicity”6 contributed to advanced NASH. Of note, 68% of women and 56% of men with T2DM in the VHA are obese.2 The study5 also highlights the need to educate healthcare providers about NAFLD. Even for a study between 2005 and 2015, lifestyle or pharmacological interventions were unacceptably low. The value of weight loss for NASH is well‐established,1 but only 12.3%‐19.5% of patients were offered diet/exercise and ≤2.6% had bariatric surgery. Considering ~30%‐40% of veterans have obesity/T2DM, still today few are offered the VHA behavioural modification programme and weight loss medications remain restricted. Medications proven to be effective for NASH, such as pioglitazone or vitamin E,1 were rarely prescribed (≤10%) in the study.5 The thiazolidinedione has been reported to be safe and effective in RCTs in NASH since 2006,7 including patients with7, 8 and without T2DM.1, 4 Pioglitazone may benefit even patients with advanced NASH‐fibrosis.9

In summary, Patel's work5 makes the case for screening obese patients with T2DM. It is ill‐advised to wait on long‐term outcome studies before supporting such a strategy as ~70% of obese patients with T2DM have NAFLD, and ~20% moderate‐to‐severe NASH‐fibrosis.4 We should screen patients with diabetes for “diabetic hepatopathy” (NAFLD), in the same way, we do today for diabetic retinopathy or nephropathy, considering NASH as the “new” complication of T2DM.10 Earlier treatment will likely benefit patients as evidence shows that the majority of patients that lose ≥8%‐10% of body weight,1 or about two‐thirds of prediabetics/diabetics treated with pioglitazone,8 experience resolution of NASH. Breaking clinical inertia by targeting obese patients with T2DM is a reasonable first step to curb the looming epidemic of NASH‐cirrhosis among us.

Alimentary Pharmacology & Therapeutics

Monday, March 19, 2018

Diabetes medicine reduces liver fat in nonalcoholic fatty liver disease

Diabetes medicine reduces liver fat in nonalcoholic fatty liver disease

Chicago, IL - In people with type 2 diabetes, nonalcoholic fatty liver disease (NAFLD) is common and can progress to a severe liver disease known as nonalcoholic steatohepatitis (NASH). Now a study has found that empagliflozin, a newer treatment for type 2 diabetes, reduces liver fat in patients with NAFLD and diabetes. Results of the randomized controlled study, called the E-LIFT Trial, will be presented Monday at the Endocrine Society’s 100th annual meeting in Chicago, Ill., during a late-breaking abstracts session.

Diabetes medications in the same class as empagliflozin have decreased liver fat in rodents with a buildup of fat in the liver, but in humans the effect of empagliflozin on liver fat has not been previously reported, said the study’s senior investigator, Ambrish Mithal, M.D., chair of the Division of Endocrinology and Diabetes at Medanta The Medicity Hospital, Gurugram, India.

“Despite the fact that NASH may progress to cirrhosis of the liver and liver cancer, there are no approved medications for treating NASH or NAFLD, and agents like metformin, pioglitazone and vitamin E have had limited success in reducing liver fat,” Mithal said. “Our results suggest that empagliflozin may help in treating NAFLD.”

The study, funded by the Endocrine and Diabetes Foundation India in New Delhi, included 50 patients who were 40 years or older and had type 2 diabetes and NAFLD. The patients were randomly assigned to receive empagliflozin (10 milligrams per day) plus their standard medical treatment for type 2 diabetes, such as metformin and/or insulin, or to receive only their standard treatment without empagliflozin (control group). All patients were aware of their group assignment.

At the beginning of the study and 20 weeks later, the patients had blood tests of their liver enzyme levels, which are typically elevated in NAFLD. They also underwent measurement of their liver fat using a new, robust technique called magnetic resonance imaging (MRI)-derived proton density fat fraction.

After 20 weeks of treatment, the liver fat of patients receiving empagliflozin decreased from an average of 16.2 to 11.3 percent, whereas the control group had only a decrease from 16.4 to 15.6 percent, a statistically significant difference between groups, the researchers reported.

“While our findings do not prove that empagliflozin will help treat NAFLD or prevent NASH, the initial results are promising and open up the possibility that empagliflozin may provide additional benefits for patients with diabetes,” Mithal said.

Approved by the U.S. Food and Drug Administration in 2014 for adults with type 2 diabetes, empagliflozin is in a drug class called sodium-glucose cotransporter 2, or SGLT-2, inhibitors. Empagliflozin primarily acts by increasing glucose excretion through the urine, thereby reducing blood glucose levels and body weight, research studies show.

Saturday, March 17, 2018

Progression of diabetes, heart disease, and stroke multimorbidity in middle-aged women: A 20-year cohort study

Research Article

Progression of diabetes, heart disease, and stroke multimorbidity in middle-aged women: A 20-year cohort study

Xiaolin Xu , Gita D. Mishra, Annette J. Dobson, Mark Jones Published: March 13, 2018

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The prevalence of diabetes, heart disease, and stroke multimorbidity (co-occurrence of two or three of these conditions) has increased rapidly. Little is known about how the three conditions progress from one to another sequentially through the life course. We aimed to delineate this progression in middle-aged women and to determine the roles of common risk factors in the accumulation of diabetes, heart disease, and stroke multimorbidity.

Methods and findings
We used data from 13,714 women aged 45–50 years without a history of any of the three conditions. They were participants in the Australian Longitudinal Study on Women's Health (ALSWH), enrolled in 1996, and surveyed approximately every 3 years to 2016. We characterized the longitudinal progression of the three conditions and multimorbidity. We estimated the accumulation of multimorbidity over 20 years of follow-up and investigated their association with both baseline and time-varying predictors (sociodemographic factors, lifestyle factors, and other chronic conditions).
Over 20 years, 2,511 (18.3%) of the women progressed to at least one condition, of whom 1,420 (56.6%) had diabetes, 1,277 (50.9%) had heart disease, and 308 (12.3%) had stroke; 423 (16.8%) had two or three of these conditions. Over a 3-year period, the age-adjusted odds of two or more conditions was approximately twice that of developing one new condition compared to women who did not develop any new conditions. For example, the odds for developing one new condition between Surveys 7 and 8 were 2.29 (95% confidence interval [CI], 1.93–2.72), whereas the odds for developing two or more conditions was 6.51 (95% CI, 3.95–10.75). The onset of stroke was more strongly associated with the progression to the other conditions (i.e., 23.4% [95% CI, 16.3%–32.2%] of women after first onset of stroke progressed to other conditions, whereas the percentages for diabetes and heart disease were 9.9% [95% CI, 7.9%–12.4%] and 11.4% [95% CI, 9.1%–14.4%], respectively). Being separated, divorced, or widowed; being born outside Australia; having difficulty managing on their available income; being overweight or obese; having hypertension; being physically inactive; being a current smoker; and having prior chronic conditions (i.e., mental disorders, asthma, cancer, osteoporosis, and arthritis) were significantly associated with increased odds of accumulation of diabetes, heart disease, and stroke multimorbidity. The main limitations of this study were the use of self-reported data and the low number of events.

Stroke was associated with increased risk of progression to diabetes or heart disease. Social inequality, obesity, hypertension, physical inactivity, smoking, or having other chronic conditions were also significantly associated with increased odds of accumulating multimorbidity. Our findings highlight the importance of awareness of the role of diabetes, heart disease, and stroke multimorbidity among middle-aged women for clinicians and health-promotion agencies.

Author summary
Why was this study done?
  • In an aging population, it is common for women to experience two or more of diabetes, heart disease, and stroke.
  • Few published studies have investigated how women progress from a “healthy” state to having one of diabetes, heart disease, and stroke and then to multimorbidity.
  • No prospective evidence is available on the roles of time-varying common risk factors (i.e., high blood pressure or obesity) in the accumulation of multimorbidity from diabetes, heart disease, and stroke—information that may be important for health promotion and risk modification.
What did the researchers do and find?
  • In this national prospective cohort study, 13,714 middle-aged Australian women (45–50 years old) were recruited in 1996 and have been followed for 2 decades. We collected data on their health conditions, including diabetes, heart disease, and stroke, as well as potential risk factors every 3 years until 2016.
  • From early to late middle age, many more women developed a single condition than multimorbidity. However, the odds ratio for accumulation of multimorbidity (i.e., from none or one to two or three, or from two to three of diabetes, heart disease, or stroke) was much higher than the odds of developing only one new condition, compared to women who did not develop any new condition over 3 years.
  • Nearly one-quarter of women who were initially diagnosed with stroke subsequently progressed to other conditions, a much higher percentage than those who were initially diagnosed with diabetes (9.9%) or heart disease (11.4%).
  • Women who were obese, had hypertension, were physically inactive, were smokers, or had other chronic conditions had higher odds of accumulating diabetes, heart disease, and stroke multimorbidity over the following 3-year period than women without these characteristics.
What do these findings mean?
  • To our knowledge, this is the first study to delineate the accumulation of diabetes, heart disease, and stroke multimorbidity and investigate its association with both baseline and time-varying predictors in a prospective cohort study.
  • These findings suggest that health promotion, interventions for modifying lifestyle factors (obesity, high blood pressure, physical inactivity, and smoking), and treatment of other chronic conditions would be potentially beneficial for preventing the accumulation of diabetes, heart disease, and stroke multimorbidity.
  • For women who have had a stroke, health promotion, intervention, and treatment would be particularly important, as they appear most likely to progress to other conditions
Continue to full text article:

Thursday, March 1, 2018

Scientists say diabetes is five separate diseases, and treatment could be tailored to each form

Diabetes is actually five separate diseases, research suggests
By James Gallagher Health and science correspondent
BBC News

The results, published in The Lancet Diabetes and Endocrinology, showed the patients could be separated into five distinct clusters.

Cluster 1 - severe autoimmune diabetes is broadly the same as the classical type 1 - it hit people when they were young, seemingly healthy and an immune disease left them unable to produce insulin

Cluster 2 - severe insulin-deficient diabetes patients initially looked very similar to those in cluster 1 - they were young, had a healthy weight and struggled to make insulin, but the immune system was not at fault

Cluster 3 - severe insulin-resistant diabetes patients were generally overweight and making insulin but their body was no longer responding to it

Cluster 4 - mild obesity-related diabetes was mainly seen in people who were very overweight but metabolically much closer to normal than those in cluster 3

Cluster 5 - mild age-related diabetes patients developed symptoms when they were significantly older than in other groups and their disease tended to be milder

Friday, February 9, 2018

Salk researchers discover how liver responds so quickly to food

Salk researchers discover how liver responds so quickly to food

LA JOLLA--(February 9, 2018) Minutes after you eat a meal, as nutrients rush into your bloodstream, your body makes massive shifts in how it breaks down and stores fats and sugars. Within half an hour, your liver has made a complete switch, going from burning fat for energy to storing as much glucose, or sugar, as possible. But the speed at which this happens has flummoxed scientists--it's too short a time span for the liver's cells to activate genes and produce the RNA blueprints needed to assemble new proteins to guide metabolism.

Now, Salk researchers have uncovered how the liver can have such a speedy response to food; liver cells store up pre-RNA molecules involved in glucose and fat metabolism.

"The switch from fasting to feeding is a very quick switch and our physiology has to adapt to it in the right time frame," says  Satchidananda Panda, a professor in the Salk Institute's Regulatory Biology Laboratory and lead author of the paper, published February 6, 2018 in Cell Metabolism. "Now we know how our body quickly handles that extra rush of sugar."

It was known that a RNA-binding protein called NONO was implicated in regulating daily ("circadian") rhythms in the body. But Panda, along with first author Giorgia Benegiamo, a former graduate student in the Panda lab, and their collaborators wondered whether NONO had a specific role in the liver. They analyzed levels of NONO in response to feeding and fasting in mice. After the animals ate, speckled clumps of NONO suddenly appeared in their liver cells, newly attached to RNA molecules. Within half an hour, the levels of corresponding proteins--those encoded by the NONO-bound RNA--increased.

"After mice eat, it looks as if NONO brings all these RNAs together and processes them so they can be used to make proteins," says Panda.

When mice lacked NONO, it took more than three hours for levels of the same proteins, involved in processing glucose, to increase. During that time lag, blood glucose levels shot up to unhealthy levels. Since blood glucose levels are also heightened in diabetes, the researchers think that the mice without NONO may act as a model to study some forms of the disease.

"Understanding how glucose storage and fat burning are regulated at the molecular level will be important for the development of new therapies against obesity and diabetes," says Benegiamo.

Questions still remain about how exactly NONO is triggered to attach to the pre-RNA molecules after a meal. And Panda is hoping to assemble a more complete list of all the pre-RNAs that NONO binds to--in both the liver and other parts of the body. NONO has been found at high levels in the brain and muscle cells, so the researchers are planning studies to see whether is reacts similarly in those organs to food.

Cell Metabolism
The RNA-Binding Protein NONO Coordinates Hepatic Adaptation to Feeding
Giorgia Benegiamo, Ludovic S. Mure, Galina Erikson, Hiep D. Le, Ermanno Moriggi, Steven A. Brown and Satchidananda Panda

Thursday, February 8, 2018

Regulation of insulin resistance and type II diabetes by hepatitis C virus infection: A driver function of circulating miRNAs.

J Cell Mol Med. 2018 Feb 7. doi: 10.1111/jcmm.13553. [Epub ahead of print]

Regulation of insulin resistance and type II diabetes by hepatitis C virus infection: A driver function of circulating miRNAs.
Singhal A1, Agrawal A2, Ling J1.

Hepatitis C virus (HCV) infection is a serious worldwide healthcare issue. Its association with various liver diseases including hepatocellular carcinoma (HCC) is well studied. However, the study on the relationship between HCV infection and the development of insulin resistance and diabetes is very limited. Current research has already elucidated some underlying mechanisms, especially on the regulation of metabolism and insulin signalling by viral proteins. More studies have emerged recently on the correlation between HCV infection-derived miRNAs and diabetes and insulin resistance. However, no studies have been carried out to directly address if these miRNAs, especially circulating miRNAs, have causal effects on the development of insulin resistance and diabetes. Here, we proposed a new perspective that circulating miRNAs can perform regulatory functions to modulate gene expression in peripheral tissues leading to insulin resistance and diabetes, rather than just a passive factor associated with these pathological processes. The detailed rationales were elaborated through comprehensive literature review and bioinformatic analyses. miR-122 was identified to be one of the most potential circulating miRNAs to cause insulin resistance. This result along with the idea about the driver function of circulating miRNAs will promote further investigations that eventually lead to the development of novel strategies to treat HCV infection-associated extrahepatic comorbidities.

Full text:

Wednesday, January 24, 2018

Treating Insulin Resistance in Hepatitis C-Infected Patients With Diabetes

Treating Insulin Resistance in Hepatitis C-Infected Patients With Diabetes
Elizabeth Kukielka, PharmD
Publish Date: Wednesday, January 24, 2018
Both insulin resistance (IR) and type 2 diabetes mellitus (T2DM) are more prevalent in patients with chronic hepatitis C virus (HCV) infection compared with the general population. 
As this is one of the first studies to demonstrate the benefit of treating HCV-positive patients who also have IR with both standard HCV therapy and metformin to achieve SVR, more studies are needed to confirm the results and help determine a standard regimen for patients with HCV and IR, researchers noted.

Full Text

Tuesday, December 12, 2017

Impact of HCV eradication on insulin resistance (IR), and the control of type 2 diabetes.

What We Know
Achieving Sustained Virologic Response (SVR) in patients treated with direct-acting antivirals (DAAs) is associated with the reversal of fibrosis, reduces the risk of liver transplant, liver cancer, and risk of other complications of chronic liver disease, including extrahepatic manifestations of HCV. The hepatitis C virus is associated with various extrahepatic manifesations, some of these include systemic manifestations such as thyroid disease, cardiovascular disease, renal disease, eye disease (sicca syndrome), skin disease (PCT, vasculitis, and lichen planus), lymphomas, and type II diabetes mellitus. As for the latter, previous research has demonstrated a significant association between hepatitis C - type 2 diabetes - and insulin resistance.

The Stats
According to The World Health Organization (WHO) people infected with HCV are at risk for liver related complications, worldwide around 399 000 people die each year from hepatitis C, mostly from cirrhosis and hepatocellular carcinoma.

Extrahepatic Consequences of HCV
However, because these estimates do not included extrahepatic consequences of HCV infection the risks of morbidity and mortality are underestimated, according to a systematic review investigating the relationship between HCV infection and glucose abnormalities; Diabetes mellitus, insulin resistance and hepatitis C virus infection: A contemporary review, published in World J Gastroenterol.

New In The Journals
Learn more about the impact of HCV eradication on insulin resistance (IR), and the control of type 2 diabetes by viewing this collection of recent articles.

Journal of Medical Virology
Volume 90, Issue 2 February 2018 Pages 320–327
Authors Alessia Ciancio, Roberta Bosio, Simona Bo, Marianna Pellegrini, Marco Sacco, Edoardo Vogliotti, Giulia Fassio, Andrea G. F. Bianco Mauthe Degerfeld, Monica Gallo, Chiara Giordanino, Lodovico Terzi di Bergamo, Davide Ribaldone, Elisabetta Bugianesi, Antonina Smedile, Mario Rizzetto, Giorgio Maria Saracco
First published: 14 November 2017
Full publication history DOI: 10.1002/jmv.24954
Many studies showed insulin resistance amelioration in HCV-patients achieving Sustained Virologic Response (SVR) but results on glycemic control in diabetic patients are unclear. This study aimed to assess fasting glucose (FG) and glycated hemoglobin (HbA1c) values before and after therapy with direct-acting antivirals (DAAs) in HCV-patients with type 2 diabetes mellitus (T2DM). Of the 122 consecutively recruited patients with chronic hepatitis C and T2DM, 110 patients were treated with DAAs and 12 remained untreated. Clinical, biochemical, virological, and metabolic features were collected both at baseline and at 12 weeks after the end of therapy (EOT) or after a comparable period of time in untreated patients. A total of 101 patients obtained a SVR (Group 1), while nine were relapsers. Group 2 (21 patients) was composed by the nine relapsers and the 12 untreated patients. A significant reduction of mean FG (134.3 ± 41.32 mg/dL vs 152.4 ± 56.40 mg/dL, P = 0.002) and HbA1c values (46.51 ± 16.15 mmoL/moL vs 52.15 ± 15.43 mmoL/moL, P <  0.001) was found in Group 1 but not in Group 2 (140.6 ± 47.87 mg/dL vs. 145.31 ± 30.18 mg/dL, P = 0.707, and 55.31 ± 20.58 mmoL/moL vs. 53.38 ± 9.49 mmoL/moL, P = 0.780). In Group 1, 20.7% of patients could reduce or suspend their antidiabetic therapy compared to none in Group 2 (P = 0.03), despite the significant weight increase observed in Group 1. SVR induced a significant amelioration of glycemic control in diabetic HCV-patients, despite a significant weight increase; larger prospective studies are needed to verify whether these results are maintained over the long-term.
View Full Text Article: Downloaded and shared by @HenryEChang on Twitter

Journal of Gastroenterology and Hepatology
Luigi E Adinolfi,Riccardo Nevola,Barbara Guerrera,Giovanni D’Alterio,Aldo Marrone,Mauro Giordano, Luca Rinaldi
Accepted manuscript online: 11 December 2017
DOI: 10.1111/jgh.14067
Abstract Background and Aim
Chronic hepatitis C (HCV), particularly genotype 1, is associated with insulin resistance (IR) and diabetes. We evaluated the impact of HCV clearance by all-oral direct-acting antiviral (DAAs) treatments on IR and glycemic control.

Included in this prospective case-control study were 133 consecutive HCV-genotype 1 patients with advance liver fibrosis (F3-F4) without type 2 diabetes. Sixty-eight treated with DAAs and 65 untreated. Liver fibrosis was assessed by transient elastography. Pre-, end- and 3 months post-treatment withdrawal IR homeostasis was assessed by HOMA-IR, QUICKI and HOMA-B.

At baseline, treated and untreated patients showed similar liver fibrosis levels, HOMA-IR was 4.90±4.62 and 4.64±5.62, respectively. HOMA-IR correlated with HCV RNA levels. At the end of treatment, all patients cleared HCV RNA, regardless of liver fibrosis and BMI, a reduction in HOMA-IR at 2.42±1.85 was showed (p<0.001), in addition, increased insulin sensitivity, decreased insulin secretion, reduction of serum glucose and insulin levels were observed. Data were confirmed 3 months after treatment withdrawal in the 65 patients who cleared HCV. No variation occurred in untreated patients. Overall, 76.5% of SVR patients showed IR improvements, of which 41.2% normalized IR. Improvement of IR was strict associated with HCV clearance, however, patients with the highest levels of fibrosis remain associated with some degree of IR.

The data underline a role of HCV in development of IR and that viral eradication reverses IR and improves glycemic control and this could prevent IR-related clinical manifestations and complications.
Subscription required to view full text article

Diabetes Care
Diabetes Care 2017 Sep - Justine Hum,1 Janice H. Jou,1 Pamela K. Green,2 Kristin Berry,2 James Lundblad,3 Barbara D. Hettinger,3 Michael Chang,1 and George N. Ioannou2,4 1Division of Gastroenterology, Portland Veterans Affairs Medical Center, Portland, OR 2Health Services Research and Development, Veterans Affairs Puget Sound Healthcare System, Seattle, WA 3Division of Endocrinology, Portland Veterans Affairs Medical Center, Portland, OR 4Division of Gastroenterology, Veterans Affairs Puget Sound Healthcare System and University of Washington, Seattle, WA

Hepatitis C virus (HCV) infection is associated with diabetes and may worsen glycemic control in patients with diabetes. We aimed to investigate whether eradication of HCV infection with direct-acting antiviral (DAA) agents is associated with improved glycemic control in patients with diabetes.

In summary, glycemic control improves in patients with diabetes after DAA-induced SVR. Patients not only have an improvement in HbA1c level after achieving SVR, they are also less likely to require insulin. These endocrine benefits of SVR provide additional justification for considering antiviral treatment in all patients with diabetes. ....hepatitis C virus (HCV) infection is associated with a higher prevalence of type 2 diabetes mellitus (T2DM) . In addition, HCV proteins increase the release of proinflammatory cytokines such as interleukin-6 and tumor necrosis factor-α, which then upregulate gluconeogenesis and enhance lipid accumulation in the liver

Future studies are needed to confirm our findings, to determine how durable the SVR-induced improvement in glycemic control is over time, and to assess the long-term effect on complications of diabetes such as nephropathy, neuropathy, and cardiovascular disease.
View Full Text Article: Available at NATAP

Medpage Today
Commentary: Improvement in Glycemic Control of Type 2 Diabetes After Successful Treatment of Hepatitis C Virus
Researchers at the VA health system—the largest provider of integrated hepatitis C care in the country—recently tested the role of viral eradication on the control of type 2 diabetes
By Kristin Bundy
Researchers at the VA health system—the largest provider of integrated hepatitis C care in the country—recently tested the role of viral eradication on the control of type 2 diabetes (T2D). Previous data demonstrated that the risk of developing T2D is about 4 times higher in people infected with the hepatitis C virus (HCV) than those without. Investigators wanted to know: Could HCV suppression lead to better control of T2D?
Continue reading: Available at Medpage Today

Nature - Scientific Reports
Yun Soo Hong, Yoosoo Chang, Seungho Ryu, Miguel Cainzos-Achirica, Min-Jung Kwon, Yiyi Zhang, Yuni Choi, Jiin Ahn, Sanjay Rampal, Di Zhao, Roberto Pastor-Barriuso, Mariana Lazo, Hocheol Shin, Juhee Cho & Eliseo Guallar
Published online:04 2017
In conclusion, in this large study of men and women at low risk of diabetes, we found that serologic evidence of HBV and HCV infection was associated with the prevalence of diabetes. In addition, HBV infection was associated with the risk of incident diabetes in prospective analyses, but we could not reliably evaluate the prospective association between HCV infection and diabetes due to the small number of infected participants. Our studies add to the growing body of evidence suggesting that diabetes is an additional metabolic complication of HBV and HCV infection.

On This Blog

Saturday, December 2, 2017

Behind the Headlines - Some type 1 diabetes cases in adults misdiagnosed as type 2

What is Behind the Headlines?
Each day the NHS Choices team selects health stories that are making headlines. These, along with the scientific articles behind the stories, are sent to Bazian, a leading provider of evidence-based healthcare information. Bazian's clinicians and scientists analyse the research and produce impartial evidence-based assessments, which are edited and published by NHS Choices. The following article was published December 1, 2017; analysis by Bazian and edited by NHS Choices.

Some type 1 diabetes cases in adults misdiagnosed as type 2 
Friday December 1 2017

“Doctors 'wrong to assume type 1 diabetes is childhood illness',” says The Guardian.

This follows a study looking at a large number of adults in the UK to see if they had diabetes and if so, which type of the condition they had.

Type 1 diabetes is an autoimmune condition where the body destroys the insulin-producing cells of the pancreas, so is reliant on life-long insulin injections. Type 2 diabetes is a condition where the person produces limited insulin, or their body can't use it so well. It can be managed in the early stages with changes to diet and medication.

Type 1 diabetes is often thought of as a “childhood illness” as most people are diagnosed at a young age. For this reason, people who develop diabetes as adults are often assumed to have type 2. Perhaps the most famous example is Prime Minister Theresa May who was, at first, misdiagnosed with type 2 diabetes in 2013, when in fact further tests revealed she had type 1.

This study looked at 13,250 people diagnosed with diabetes at a range of ages. Of all people who developed type 1 diabetes, surprisingly 42% were not diagnosed until after the age of 30.

However, only 4% of all newly diagnosed diabetes in the over 30s were type 1. Therefore, although type 1 diabetes starting in adulthood is uncommon, it still highlights the need for healthcare professionals to be aware that not all people who develop diabetes in adulthood automatically have type 2.

Making sure that people receive the correct diagnosis, and therefore the correct treatment, is crucial.

If you have been diagnosed with type 2 diabetes but are not responding to treatment, it may be worth discussing the possibility of further testing with your doctor.

Where did the story come from?
The study was carried out by researchers from the University of Exeter using data from a nationwide study called UK Biobank. It was funded by The Wellcome Trust and Diabetes UK. It was published in the peer-reviewed medical journal The Lancet: Diabetes and Endocrinology.

The story was covered by the BBC and The Guardian, both of which accurately covered the key findings and explained the importance of receiving a correct diagnosis to ensure people are given the right treatments.

What kind of research was this? 
This researchers used data from a large, ongoing cohort study called UK Biobank which started in 2006. The study aimed to see how people with genes predisposing them to type 1 diabetes developed the condition in later life rather than in childhood or teenage years as usual.

UK Biobank involves more than half a million adults across the country, and has followed them up for a number of years. As well as attending health screening sessions, participants have also given blood samples from which genetic information can be recorded. For this research, a snapshot was taken of people from UK Biobank who were of white European descent, and who had genetic data available.

A cohort study that followed people from childhood throughout their lives may have been able to look at this in more detail. But the size and coverage of the UK Biobank study make this a useful starting point to look at whether people with genetic risk factors for type 1 diabetes are diagnosed in adulthood or childhood.

What did the research involve? 
The study involved a sample of 379,511 people from the UK Biobank study, of whom a subgroup had diabetes. All were of white European background and had genetic data available. None of the people were related to each other.

The researchers assessed all people for genetic variants known to be associated with type 1 diabetes. They then gave each person a genetic risk score for their risk of developing type 1 diabetes.

Self-reports of a diabetes diagnosis were assessed by questionnaire at study enrolment or later follow-up. People provided information about the age they received a diagnosis, and whether they used insulin within one year of diagnosis (reliance on insulin would indicate type 1). They also reported any hospital admissions for diabetic ketoacidosis (a serious complication of diabetes), and general health such as body mass index.

For the analysis, the researchers compared people with ‘high risk’ or ‘low risk’ for type 1 diabetes based on the results of the risk score. They limited analysis to cases of type 1 or type 2 diabetes occurring in people aged 60 or under at time of diagnosis, as after that point any new cases are almost certain to be type 2 diabetes.

What were the basic results? 
In the study sample there were 13,250 people with diabetes, 55% of whom had high genetic risk scores and the remainder had low risk scores.

There were 1,286 cases (9.7%) of type 1 diabetes, and all of these occurred in people with the high risk score:
18% of those with a high risk score were diagnosed with type 1 diabetes, the remainder with type 2
42% of those in the high risk group diagnosed with type 1 (537) were diagnosed between the ages of 31 and 60, with the remainder diagnosed under the age of 30 (as is more usual)
of all people aged under 30 at time of diabetes diagnosis (all risk categories), 74% had type 1 diabetes
of all people aged 31 to 60 at time of diabetes diagnosis, 4% had type 1 diabetes
across all ages of life, people with a high genetic risk score were more likely to be diagnosed with any type of diabetes than people with a low risk score

All people diagnosed with type 1 after the age of 30 needed insulin treatment, compared to only 16% of people diagnosed with type 2 (who started insulin later, after 7 years on average). They also had a lower body mass index (BMI) than those with type 2.

How did the researchers interpret the results?
The researchers stated their findings have “clear clinical implications”, alerting healthcare professionals to the fact that type 1 diabetes can occur in the over-30s. They recommend that recognition of late-onset type 1 diabetes is an important area of improvement for both medicine and research.

This study gives us an important insight into the way in which type 1 diabetes has been mislabelled as a “childhood condition”. It suggests that a number of people with genetic risk factors are also diagnosed in midlife, when most new diabetes diagnoses would be thought to be type 2.

However, there are a few points to note:
The study shows that of all people diagnosed with diabetes after age 30, the vast majority (96%) were still type 2 diagnoses. Therefore, though practitioners need to be aware, this only accounts for a small proportion of all diagnoses.

Even among people with hereditary risk factors for type 1 diabetes, most diagnoses were still type 2.
The diagnosis of diabetes was based on people's own reports, rather than looking at medical records.

People are unlikely to be wrong about whether they have the condition or not, but there may be some uncertainty as to whether they self-reported the correct type, age at which they were diagnosed, or when they started insulin.

The study only looked at people from a white European background. Type 1 and type 2 diabetes prevalence and risk factors may differ in people from other ethnic backgrounds, so this study’s results cannot be generalised to everyone.

When the UK Biobank study started in 2006, the majority of people taking part were aged 40 or over. This means that they were children in the 1980s or earlier. Since that time, the diagnosis of diabetes may have improved. It would also mean that people who suffered complications from the disease and died in earlier life would not have been included.

The study can't tell us how many of these people with type 1 in later life may have been misdiagnosed initially, or had insulin treatment delayed when they needed this to start with.

People who commit to take part in studies like UK Biobank might be more active about monitoring and managing their health than people in the general population. Therefore people in this study may have had slightly different experiences when getting diagnoses, or have different lifestyle behaviours that could affect their risk of conditions like diabetes.

Nonetheless, this study highlights the fact that type 1 diabetes can begin in adulthood as well as in childhood. Adults diagnosed with diabetes must receive the correct diagnosis to get the right treatment as soon as possible. If you are concerned that you may have been misdiagnosed, ask the doctor in charge of your care for advice.


Tuesday, November 28, 2017

Critical link between obesity and diabetes has been identified

Critical link between obesity and diabetes has been identified

DALLAS - Nov. 28, 2017 - UT Southwestern researchers have identified a major mechanism by which obesity causes type 2 diabetes, which is a common complication of being overweight that afflicts more than 30 million Americans and over 400 million people worldwide.

Researchers found that in obesity, insulin released into the blood by the pancreas is unable to pass through the cells that form the inner lining of blood vessels. As a result, insulin is not delivered to the muscles, where it usually stimulates most of the body's glucose to be metabolized. Blood glucose levels rise, leading to diabetes and its related cardiovascular, kidney and vision problems, said Dr. Philip Shaul, Director of the Center for Pulmonary and Vascular Biology in the Department of Pediatrics at UT Southwestern.

"It was totally unpredicted that a major problem in obesity is the delivery of circulating insulin to your muscle. It was even more surprising that this problem involves immunoglobulins, which are the proteins that make up circulating antibodies," said Dr. Chieko Mineo, Associate Professor of Pediatrics, who is a co-senior author on the report with Dr. Shaul.

The researchers found that obese mice have an unexpected chemical change in their immunoglobulins. "The abnormal immunoglobulins then act on cells lining blood vessels to inhibit an enzyme needed to transfer insulin from the bloodstream into the muscle," said Dr. Shaul, who holds the Associates First Capital Corporation Distinguished Chair in Pediatrics. "Type 2 diabetes patients have the same chemical change, and if we give a mouse immunoglobulins from a type 2 diabetic individual, the mouse becomes diabetic."

The findings reported in The Journal of Clinical Investigation may lead to new tools for diabetes risk screening and new avenues for diabetes prevention or treatment. The researchers identified an agent that they could administer to mice that prevents the chemical change in immunoglobulins that occurs with obesity and preserves healthy glucose status. The researchers plan to test this strategy in humans in the near future.

Funding for the study came from the American Diabetes Association, the American Heart Association, The Hartwell Foundation, the Cancer Prevention and Research Institute of Texas (CPRIT) and the National Institutes of Health (NIH). Further research on both adults and children is under way with support from The Hartwell Foundation and the National Institutes of Health.

Other researchers involved were Dr. Keiji Tanigaki, senior research scientist and first author; Dr. Wanpen Vongpatanasin, Director of the Hypertension Section and holder of the Norman and Audrey Kaplan Chair in Hypertension Research at UT Southwestern; Dr. Jennifer Kohler, Associate Professor of Biochemistry; Dr. William Holland, Assistant Professor of Internal Medicine in the Touchstone Diabetes Center at UT Southwestern; and collaborators from the University of Texas at Dallas, University of Alabama, University of Georgia, and Imperial College London.

Wednesday, November 15, 2017

Listen: With Stricter Guidelines, Do You Have High Blood Pressure Now?

November 14, 201712:56 PM ET
Heard on All Things Considered
You may not have had high blood pressure Sunday, but you may have it today. Even if your blood pressure hasn't changed a smidge. What's up?

The rules shifted Monday. It used to be that we encouraged people to adopt healthy behavior to keep their blood pressure down but didn't label someone as having hypertension until systolic blood pressure (the top number) exceeded 140 millimeters of mercury and/or the diastolic blood pressure (the bottom number) exceeded 90 mm Hg. Lots of people watch those numbers closely.

Now the American College of Cardiology and the American Heart Association have updated blood pressure guidelines that move the goal post for many people.
Continue reading......

NIH blood pressure study supports important part of new AHA/ACC hypertension guidelines
Today the AHA and the ACC issued the first comprehensive new high blood pressure guidelines in more than a decade that indicate high blood pressure should be treated earlier with lifestyle changes and in some patients with medication – at 130/80 mm Hg rather than 140/90. An important component of these guidelines was informed by the results of the Systolic Blood Pressure Intervention Trial (SPRINT), a clinical study sponsored in part by the NHLBI and designed to determine the best way to treat blood pressure in adults with hypertension, 50 years or older, who are at high risk for heart disease.

SPRINT, which began in the fall of 2009, included more than 9,300 participants, recruited from about 100 medical centers and clinical practices throughout the United States. It remains the largest study of its kind to date to examine how maintaining systolic blood pressure at a lower than previously recommended level would impact cardiovascular and kidney diseases.