BEER-SHEVA, ISRAEL, July 14, 2009 Ben-Gurion University of the Negev (BGU) researchers, in a collaboration with colleagues from the University of Leipzig, Germany, have identified a signaling pathway that is operational in intra-abdominal fat, the fat depot that is most strongly tied to obesity-related morbidity.
The paper was just published in the Endocrine Society's the Journal of Clinical Endocrinology and Metabolism ( J. Clin. Endocrinol. Metab. 2009; 94:2507-251)
"Fat tissue in obesity is dysfunctional, yet, the processes that cause fat tissue to malfunction are poorly understood -- specifically, it is unknown how fat cells 'translate' stresses in obesity into dysfunction," said Dr. Assaf Rudich, senior lecturer from the Department of Clinical Biochemistry at Ben-Gurion University.
Fat tissue is no longer considered simply a storage place for excess calories, but in fact is an active tissue that secretes multiple compounds, thereby communicating with other tissues, including the liver, muscles, pancreas and the brain. Normal communication is necessary for optimal metabolism and weight regulation. However, in obesity, fat (adipose) tissue becomes dysfunctional, and mis-communicates with the other tissues. This places fat tissue at a central junction in mechanisms leading to common diseases attributed to obesity, like type 2 diabetes and cardiovascular diseases.
Fat tissue dysfunction is believed to be caused by obesity-induced fat tissue stress: Cells over-grow as they store increasing amounts of fat. This excessive cell growth may cause decreased oxygen delivery into the tissue; individual cells may die (at least in mouse models), and fat tissue inflammation ensues. Also, excess nutrients (glucose, fatty acids) can also result in increased metabolic demands, and this in itself can cause cellular stress.
The BGU and Leipzig teams established a setup for collecting fat tissue samples from people un
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American Associates, Ben-Gurion University of the Negev