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Nutrition Diabetes Weight and Obesity

Compound Found in Heat-Processed Food Linked to Diabetes

11 years, 7 months ago

8500  0
Posted on Sep 28, 2012, 6 a.m.

Exposure to a compound produced when food is cooked with dry heat has been linked to the development of abdoinal obesity, insulin resistance, and type 2 diabetes in mice.

Researchers have linked exposure to a byproduct produced when food is cooked with dry heat with the development of abdominal obesity, insulin resistance, and type 2 diabetes in mice. Helen Vlassara, MD, Professor and Director of the Division of Experimental Diabetes and Aging at Mount Sinai School of Medicine, and colleagues discovered that mice chronically exposed to the advanced glycation endproduct (AGEs) methyl-glyoxal (MG), developed significant abdominal weight gain, early insulin resistance, and type 2 diabetes. The researchers fed one group of mice a diet high in MG over four generations, while the control group was fed a diet without MG. Both diets contained normal levels of calories and fat. Over four generations, the mice that ate the MG started to develop early insulin resistance and increased body fat, whereas the control group did not have either of these conditions. Further research revealed that MG caused a marked deficiency in protective mechanisms, such as the survival factor SIRT1 which controls inflammation and enhances the metabolism of glucose and insulin. MG ingestion also adversely affected the activity of an important anti-AGE receptor called AGER1, which protects SIRT1 and fights insulin resistance. "The study demonstrates how the prolonged ingestion of seemingly innocuous substances common in human food, such as MG, can reduce defenses and compromise native resistance to metabolic and other diseases," concluded Dr. Vlassara.

Cai W, Ramdas M, Zhu L, Chen X, Striker GE, Vlassara H. Oral advanced glycation endproducts (AGEs) promote insulin resistance and diabetes by depleting the antioxidant defenses AGE receptor-1 and sirtuin 1. Proc Natl Acad Sci U S A. 2012 Aug 20.

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