Researchers Identify Role For Protein Linked To Obesity, Type 2 Diabetes

Main Category: Diabetes
Also Included In: Obesity / Weight Loss / Fitness;  Biology / Biochemistry
Article Date: 21 Dec 2012 - 0:00 PST Current ratings for:
Researchers Identify Role For Protein Linked To Obesity, Type 2 Diabetes

Researchers at UT Southwestern Medical Center have taken another step toward better understanding the metabolic functions of obesity and its connection to type 2 diabetes.

Dr. Philipp Scherer, Director of the Touchstone Center for Diabetes Research at UT Southwestern, led a group of researchers in a recent multicenter study published in Nature Medicine that successfully identified ways to manipulate the protein mitoNEET. This is the first time the protein has been effectively altered to expand fat tissue in a way that allows subjects - in this case, mice - to remain metabolically healthy.

MitoNEET is a key component of a cell's mitochondrion, which serves as the cell's energy powerhouse. When the levels of MitoNEET protein were elevated inside the fat cells of rodents, more fat was stored in the adipose tissue, thereby keeping toxic lipids away from other types of cells. This sequestration resulted in extremely obese yet metabolically healthy mice that displayed no signs of type 2 diabetes. In contrast, when MitoNEET levels were decreased, the mice became lean but unhealthy, and developed pre-diabetic conditions such as failure to metabolize glucose properly.

"The manipulation of mitochondrial activity in fat tissue is a very powerful approach to control how much excess energy we store in our bodies and where we store it. We have heretofore underestimated the importance of mitochondrial pathways in our fat cells and their influence on how we manage our weight," said Dr. Scherer, senior author of the three-year study and Professor of Internal Medicine and Cell Biology at UTSW.

The body stores fat in the white adipose tissue, and, ideally, individuals burn any excess calories through exercise and a healthy diet. The current research findings suggest that manipulating components of mitochondria in fat cells can be an effective way to funnel excess calories into "good" locations. This storage then thwarts their negative effect on other internal organs like the liver in which excess fat accumulation is toxic.

The obese mice in this study weighed 120 to 130 grams (4.23 to 4.58 ounces), whereas a normal adult mouse weighs 25 to 30 grams (.88 to 1.06 ounces). This difference is the equivalent of a 150-pound person increasing his or her weight to 700 pounds.

The researchers were careful to clarify that the findings were not meant to encourage obesity, even though the obese mice were considered metabolically healthy. The study instead provides a clearer understanding of the mitochondrion's importance to the metabolic dysfunction - that is characteristic of obese patients and those with type 2 diabetes.

"These results taught us a great deal about how fat cells sense, store, and burn energy," said Dr. Christine Kusminski, a postdoctoral researcher in Internal Medicine who served as the study's first author. "By learning more about the underlying mechanisms, we hope to develop ways to target these pathways for future drug development."

The researchers now hope to translate these findings into a clinical setting. The staff of the Touchstone Center is devoted to the study of cells and tissues that either contribute to or are affected by diabetes and related diseases, including the physiology of adipose tissue.

Other UT Southwestern researchers involved in the study were Dr. William L. Holland, Instructor in Internal Medicine; Dr. Kai Sun, Assistant Instructor in Internal Medicine; Dr. Jiyoung Park, Assistant Instructor in Internal Medicine; and Stephen B. Spurgin, a medical student. Scientists from the Albert Einstein College of Medicine, the University of Utah School of Medicine, and Merck Research Laboratories also contributed.

The investigation was funded by support from the National Institutes of Health, the American Heart Association, and fellowships from the Juvenile Diabetes Research Foundation and the Department of Defense.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Increase In Vision Impairment Linked To Higher Prevalence Of Diabetes

Editor's Choice
Academic Journal
Main Category: Eye Health / Blindness
Also Included In: Diabetes
Article Date: 12 Dec 2012 - 12:00 PST Current ratings for:
Increase In Vision Impairment Linked To Higher Prevalence Of Diabetes

Nonrefractive visual impairment, not due to needing glasses, has increased significantly among Americans in recent years, and the higher incidence of diabetes may be responsible.

The finding came from new research, conducted by a team at the Johns Hopkins University School of Medicine, Baltimore, and was published in JAMA, December 12 issue.

Background information in the report stated: "It is estimated that more than 14 million individuals in the United States aged 12 years and older are visually impaired (<20/40). Of these cases, 11 million are attributable to refractive error."

The most frequent reasons Americans experience nonrefractive visual impairment are:

Prior research has demonstrated that people with visual impairment often have diabetes. Since the eye is one of the main organs impacted by diabetes, patients can develop certain visual conditions.

"The prevalence of diagnosed diabetes has increased among adults in recent years, rising from 4.9 percent in 1990 to 6.5 percent in 1998, 7.9 percent in 2001, 10.7 percent in 2007, and 11.3 percent in 2010," the authors explained.

The researchers, led by Fang Ko, M.D., set out to evaluate the prevalence of nonrefractive visual impairment and the risk factors associated with the condition.

Data was gathered and analyzed from the National Health and Nutrition Examination Survey (NHANES), a representative sample of the American population.

Questionnaires, physical exams, and laboratory tests were given to 9,471 and 10,480 subjects aged 20 and older in 1999-2002 and 2005-2008 respectively.

Participants were considered to have nonrefractive visual impairment when their visual acuity was less than 20/40 when measured by an autorefractor - a tool which evaluates a person's refractive error.

Results showed that the prevalence of nonrefractive visual impairment increased 21%, from 1.4% in 1999-2002 to 1.7% in 2005-2008. They also found that non-Hispanic whites experienced a 40% increase, from 0.5% to 0.7%.

The factors that were linked to nonrefractive visual impairment included: povertyolder agelower education leveldiabetes diagnosed at least 10 years agoThe only risk factor that increased in prevalence between the 2 time periods analyzed was diabetes. The incidence of diabetes with more than 10 years since diagnosis increased 22% overall, from 2.8 percent to 3.6 percent. Among non-Hispanic whites aged 20-39, the prevalence of diabetes increased 133%, from 0.3% to 0.7%.

The researchers concluded:

"We report a previously unrecognized increase of visual impairment among U.S. adults that cannot be attributed to refractive error. If the current finding becomes a persisting trend, it could result in increasing rates of disability in the U.S. population, including greater numbers of patients with end-organ diabetic damage who would require ophthalmic care. These results have important implications for resource allocation in the debate of distribution of limited medical services and funding. Continued monitoring of visual disability and diabetes, as well as additional research addressing causes, prevention, and treatment, is warranted."

Written by Sarah Glynn
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our eye health / blindness section for the latest news on this subject. Prevalence of Nonrefractive Visual Impairment in US Adults and Associated Risk Factors, 1999-2002 and 2005-2008
Fang Ko, Susan Vitale, Chiu-Fang Chou, Mary Frances Cotch, Jinan Saaddine, David S. Friedman
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Genetic Variant Linked To Obesity And Insulin Resistance

Main Category: Diabetes
Also Included In: Obesity / Weight Loss / Fitness;  Genetics
Article Date: 28 Jun 2012 - 0:00 PDT Current ratings for:
Genetic Variant Linked To Obesity And Insulin Resistance

A large study in people at risk of diabetes has found a direct association between the presence of a small genetic alteration in a hormone receptor and increased body fat and insulin resistance. The results, to be presented Tuesday at The Endocrine Society's 94th Annual Meeting in Houston, suggest an adverse role for a previously described genetic variant, the BclI polymorphism.

"Our findings support the idea that even small variations in hormone receptor sensitivity can have metabolic implications, such as obesity or diabetes," said co-author Bastiaan Havekes, MD, PhD, of Maastricht University Medical Center, Maastricht, the Netherlands.

"Endocrinologists should not just focus on hormone levels themselves. Taking into account hormone receptor sensitivity could help in better understanding hormone-mediated effects on metabolism," he said.

The inherited BclI polymorphism occurs in the gene encoding for the glucocorticoid receptor, which controls the actions of glucocorticoids, steroid hormones that affect every system in the body. This small variant makes the receptor more sensitive to glucocorticoids, resulting in greater effects with similar hormone levels, Havekes said.

The effects of this change appear to be similar to, although much smaller than, the excessive glucocorticoid exposure that can occur from certain medications or diseases, Havekes said. Such excess exposure can result in weight gain, especially around the abdomen, as well as in disturbed blood sugar metabolism. This exposure most often occurs from long-term use of prednisone or other glucocorticoid medications, which are widely used to treat inflammatory diseases or to suppress the immune system. It also can result from endocrine diseases such as Cushing's syndrome. Cushing's causes overproduction in the body of the glucocorticoid cortisol, often called the "stress hormone."

Patients in this study, however, did not have known excess exposure to glucocorticoids, according to Havekes. He and his co-investigators studied 1,228 adults who participated in one of two Dutch studies focusing on diabetes in the general population. More than half of the study participants had either prediabetes (23 percent) or Type 2 diabetes (33 percent). All subjects underwent genetic testing for the BclI polymorphism.

The researchers found that 519 subjects did not carry the alternative form of the gene, or G-allele, for the BclI polymorphism on either chromosome. Another 540 subjects were heterozygous carriers, meaning the G-allele was present on one of the two chromosomes. The remaining 169 subjects were homozygous carriers and therefore carried the G-allele on both chromosomes.

Those who had the BclI polymorphism on each chromosome had a significantly higher body mass index and larger waist and hip circumferences than did noncarriers or heterozygous carriers, the authors reported. This was reflected by greater insulin resistance, meaning that insulin is less effective at lowering blood glucose (blood sugar).

"Determining an individual's genetic risk profile for metabolic disease is of paramount importance to prevent development of cardiovascular diseases," he said. "Future studies concerning cardiovascular risk profiling should perhaps consider the BclI polymorphism."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Waist Size, Regardless Of BMI, Linked To Diabetes Risk

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Academic Journal
Main Category: Diabetes
Also Included In: Obesity / Weight Loss / Fitness
Article Date: 07 Jun 2012 - 1:00 PDT Current ratings for:
'Waist Size, Regardless Of BMI, Linked To Diabetes Risk'

Waist circumference is strongly and independently linked to diabetes type two risk, even after accounting for body mass index (BMI), and should be measured more widely for estimating risk, researchers from the Medical Research Council (MRC) Epidemiology Unit, UK, reported in PLoS Medicine. The authors explained that overweight people with a large waist, over 102cm (40.2 inches) for men and over 88cm (34.6 inches) for women, have approximately the same or higher risk of eventually developing diabetes type 2 as obese individuals.

Dr Claudia Langenberg and team gathered data on over 340,000 individuals from eight European countries to determine what their future risk of developing diabetes type 2 might be.

Dr Claudia Langenberg, said:

"Type 2 diabetes is a serious and increasingly common disease. More than a third of the UK adult population is overweight and at increased risk of diabetes, but they are not systematically monitored for this risk. Our findings suggest that if their waist circumference is large, they are just as likely to develop the condition as if they were obese.

We do not suggest replacing BMI as a core health indicator, but our results show that measuring waist size in overweight patients allows doctors to 'zoom in' on this large population group and identify those at highest risk of diabetes. These people can then be offered lifestyle advice, which can reduce their risk of developing the disease."

Diabetes type 2 is a long-term condition that occurs when the person's body cannot produce enough insulin, or when the cells in the body do not react properly to insulin. The exact causes of type 2 diabetes are not precisely understood, but experts say that being obese or overweight are the main modifiable risk factors.

Langenberg and team set out to determine what the link between BMI, waist size and the likelihood of developing diabetes type 2 might be - they also aimed to find out what the risks were separately for men and women. They gathered data from the European Union funded InterAct Study, consisting of 12,403 individuals with diabetes type 2 who had developed the disease during a 15-year follow up.

They found that:
Overweight people with large waists have the same or higher risks of eventually developing type 2 diabetes as obese invidivuals7% of males with a large waist who were overweight eventually developed diabetes type 2 within ten years
4% of females with a large waist who were overweight eventually developed diabetes type 2 within ten years
Large-waisted overweight men and women were found to have either the same or higher risk of eventually developing diabetes type 2, compared to obese individuals
Normal weight men with a small waist had only a 1.6% chance of developing the disease
Normal weight women with a small waist had a 0.6% risk of developing the disease
Pear-shaped people - those who were overweight but had a small waist - were found to have a relatively low risk of developing diabetes type 2
Women with a BMI greater than 35 (obese women) with a large waist were nearly 32-times more likely to eventually develop diabetes type 2 compared to thin women with a small waist
Obese men with a large waists were 22-times more likely to develop the disease compare to their lean and small-waisted counterpartsPrincipal Investigator of the InterAct Study, Professor Nick Wareham, said:

"This is one of the most comprehensive studies of lifestyle and diabetes risk to date, not just in scale, but in the powerful prospective design which allows us to follow a population over a long period of time to see how and why disease develops. The results of this important research will help inform new strategies for the prevention of this devastating condition that affects almost three million people in the UK."

Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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Immune System Glitch Identified Which Is Linked To A Fourfold Higher Likelihood Of Death

Main Category: Immune System / Vaccines
Also Included In: Diabetes;  Heart Disease;  Respiratory / Asthma
Article Date: 06 Jun 2012 - 0:00 PDT Current ratings for:
'Immune System Glitch Identified Which Is Linked To A Fourfold Higher Likelihood Of Death'

Mayo Clinic researchers have identified an immune system deficiency whose presence shows someone is up to four times likelier to die than a person without it. The glitch involves an antibody molecule called a free light chain; people whose immune systems produce too much of the molecule are far more likely to die of a life-threatening illness such as cancer, diabetes and cardiac and respiratory disease than those whose bodies make normal levels. The study is published in the June issue of Mayo Clinic Proceedings.

Researchers studied blood samples from nearly 16,000 people 50 and older enrolled in a population-based study of plasma cell disorders in Olmsted County, Minn. They found that those who had the highest level of free light chains - the top 10 percent - were about four times more at risk of dying than those with lower levels. Even after accounting for differences in age, gender and kidney function, the risk of death was roughly twice as high.

The study suggests that high levels of free light chains are markers of increased immune system response to infection, inflammation or some other serious disorders, says lead researcher Vincent Rajkumar, M.D., a Mayo Clinic hematologist.

Researchers have known that high levels of free light chains are associated with increased risk of death among patients with plasma disorders, such as lymphomas and other blood cancers, but this is the first study to find that high levels of light chains are associated with increased mortality in the general population. Free light chain levels can be measured by using a serum free light chain assay, a simple blood test. This test is often used to monitor light chain levels in patients with plasma disorders such as myeloma to gauge how well they are responding to treatment.

However, Dr. Rajkumar cautions against administering this test with the intent of gauging one's risk of death.

"We do not recommend this test as a screening test, because it will only cause alarm," Dr. Rajkumar says. "We do not know why this marker is associated with higher rates of death. We do not have a way of turning things around. Therefore, I would urge caution in using this test until we figure out what to do about it and what these results mean."

Plasma cells are white blood cells that produce large amounts of antibodies and are key to fighting off infection. The antibodies are comprised of two different types of molecules tightly joined to each other: heavy chains and light chains. Most people produce at least a slightly excess amount of light chains that can be detected in the blood in the "free" state, unbound to heavy chains. Free light chains are not usually a threat to health, but excess levels serve as a marker of underlying immune system stimulation, kidney failure or plasma cell disorders such as myeloma.

Next steps for researchers include identifying the precise mechanisms by which excess free light chains are associated with a higher likelihood of death and determining if specific diagnostic or treatment options need to be pursued.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our immune system / vaccines section for the latest news on this subject. The study was funded by the National Institutes of Health. Freelite, the manufacturer of the serum free light chain assay, provided the serum free light chain assay reagents for this study.
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Risk Of Blood-Vessel Constriction Linked To Gum Disease May Be Increased By Specific Protein

Main Category: Dentistry
Also Included In: Cholesterol
Article Date: 20 Apr 2012 - 0:00 PDT Current ratings for:
'Risk Of Blood-Vessel Constriction Linked To Gum Disease May Be Increased By Specific Protein'

A protein involved in cellular inflammation may increase the risk of plaque containing blood vessels associated with inflammatory gum disease, according to research presented at the American Heart Association's Arteriosclerosis, Thrombosis and Vascular Biology 2012 Scientific Sessions in Chicago.

The protein, CD36, is found in blood cells, as well as many other cell types. Research has shown that CD36 may increase the harmful effects of "bad cholesterol," or low-density lipoprotein (LDL).

Investigators "knocked out," or deleted, the gene responsible for CD36 production, then induced plaque in blood vessels by feeding mice a high fat diet. Some animals were also infected with the bacteria associated with gum disease.

More fatty plaque accumulation occurred in the blood vessels of the animals that were infected with gum disease. In the animals with the deleted CD36 gene, however, vessels remained free of new plaque even when oral inflammation occurred.

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