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Sunday, January 6, 2013

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
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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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Wednesday, July 25, 2012

Researchers Investigate 'Healthy' Obesity Gene

Main Category: Obesity / Weight Loss / Fitness
Also Included In: Genetics; Diabetes
Article Date: 05 Jun 2012 - 0:00 PDT

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Why is it that some obese people are healthier than others? This was one of the main questions Dr. Chaodong Wu of the College of Agriculture and Life Sciences - Texas A&M University System - and a group of researchers tried to answer in a recent study.

The study, which will appear in a July issue of the Journal of Biological Chemistry, used genetically modified mice to investigate the genetic aspects of why some obese people do not develop certain medical problems typically associated with obesity, especially Type 2 diabetes.

Wu noted that Xin Guo, a Ph.D. candidate in the college's department of nutrition and food sciences, contributed significantly to the study.

"Previous research had indicated that a regulatory enzyme which is encoded by the gene PFKFB3 protects against diet-induced fat tissue inflammation and systemic insulin resistance," said Wu, who also has a Texas AgriLife Research appointment. "Increasing evidence shows that fat deposition, or amount, is not directly associated with the inflammation or insulin resistance in the development of obesity-related metabolic diseases."

Wu said the inducible 6-phosphorofructo-2-kinase (iPFK2) enzyme links metabolic and inflammatory responses and may underlie what he refers to as "healthy" obesity.

"While many obese people develop Type 2 diabetes, heart conditions and other chronic health problems associated with being significantly overweight, other obese people do not," he said. "And while obesity in general is not healthy, some obese people do not develop the diseases more commonly associated with a less-than-healthy diet. Furthermore, a number of thinner people may have the sort of health problems more typically associated with obesity."

Wu said he and the other researchers theorized that these diseases are associated with the cellular inflammatory response brought on by obesity.

"We also thought this gene could conceivably be targeted for use in the treatment of diabetes, especially Type 2, commonly associated with obesity," he said. "We wanted to find out what might happen to a subject if that particular gene was activated."

Wu and his fellow researchers used laboratory mice to explore the effect of a targeted adipocyte overexpression of the gene/enzyme combination on diet-induced inflammatory responses and insulin sensitivity.

"We were trying to find out what it is in adipose, or fat, tissue that may trigger a negative response that leads to disease - and how to modulate that response," he said. "In our study, we learned overexpression of the iPFK2 enzyme increases fat deposition, suppresses inflammatory responses and improves insulin sensitivity in both adipose and live tissues."

As an extension of this research, Wu said, it may be possible to identify a pharmacological agent or bioactive agent which may have the desired effect on this gene toward reducing obesity-related cellular inflammatory response.

"We're hoping that, as one of its outcomes, this research will help lead to finding bioactive compounds or some type of supplement that might be taken to help activate this gene toward the promotion of health," he said. "It would also be a good idea to compare and contrast this research with studies done on what constitutes a healthy diet and the effect of such a diet at a cellular level. "

Wu said that would allow for screening bioactive compounds in a healthy diet to determine to what degree these might be applicable for the treatment of disease brought on by unhealthy obesity in an animal model.

"As a further extension, one might study different types of obese people and try to isolate additional specific genes that determine a healthy versus an unhealthy obesity and find a way to modulate the expression of those genes toward disease prevention and health promotion," he said. "Once you find the link between the gene and the obese status of the individual, then you could work with experts in chemical research to produce or replicate whatever pharmacological or bioactive compound is needed to treat unhealthy obesity."

Wu said it is important to determine positively to what degree obesity as a health problem is due to a person's genetic makeup as it relates to their ability to store fat, as well as what type of fat - saturated or non-saturated - the individual may store.

"Fat composition is more important than fat deposition, or content," he said. "We know fat cells secrete some of their own bioactive compounds that we may be able to isolate and identify for use in promoting health."

Wu said it will be necessary to discover the role of certain genes in the composition and deposition of fats beyond what has already been identified as being stored in the adipose tissue of mice.

"Then we may be able to produce a dietary supplement or other bioactive compound that would have a positive health effect," he said. "This could be used as a targeted treatment for obesity-related diseases such as Type 2 diabetes in a way that would have limited or minimal side effects."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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