Grilled, seared foods may add to waistlines, disease risk

December 12, 2012 by Brian Wallheimer in Medicine & Health / Medical research
Kee-Hong Kim found that the chemicals created by some cooking methods, including grilling, may allow immature fat cells to survive and accumulate lipids, blocking a cellular process that would normally kill those cells. Credit: Purdue Agricultural Communication photo/Tom Campbell




Kim wanted to see whether glycated proteins affect the speed at which precursor, or immature, fat cells turn into mature fat cells. Using a cell culture, Kim saw no change in how quickly those accumulated lipids, which is stored as fat in cells, but he did notice something else.

"Older animals don't generally accumulate new fat cells. Those lose their ability to become mature as we age," Kim said. "But when exposed to glycated proteins, immature fat cells started to differentiate and accumulate lipids like they would in a younger animal.


Kim found that the of glycated proteins - advanced glycation end products, or AGEs - interfere with that should kill immature fat cells in older animals. That means those animals, or people, may accumulate more fat cells than they should, and those cells store compounds that can lead to inflammation and certain types of diseases.

AGEs interact with a protein called p53, which usually begins cell death and aging programs for immature fat cells. With p53 disrupted, the immature survive and can accumulate lipids.





More information: An Advanced Glycation End Products (AGEs)-The Receptor for AGEs Axis Restores Adipogenic Potential of Senescent Preadipocytes through Modulation of p53 Protein Function, Chih-Yu Chen, Allison Martorano Abell, Yang Soo Moon, and Kee-Hong Kim

Impaired adipogenic potential of senescent preadipocytes is a hallmark of adipose aging and aging-related adipose dysfunction. While advanced glycation end products (AGEs) derived from both foods and endogenous non-enzymatic glycation, and AGEs-associated signaling pathways are known to play a key role in aging and its-related diseases, the role of AGEs in adipose aging remains elusive. We show a novel pro-adipogenic function of AGEs in replicative senescent preadipocytes and mouse embryonic fibroblasts, as well as primary preadipocytes isolated from aged mice. Using glycated bovine serum albumin (BSA) as a model protein of AGEs, we examined that glycated BSA restores impaired adipogenic potential of senescent preadipocytes in vitro and ex vivo. However, glycated BSA showed no effect on adipogenesis in non-senescent preadipocytes. AGEs-induced the receptor for AGEs (RAGE) expression is required for the pro-adipogenic function of AGEs in senescent preadipocytes. This is through RAGE-dependent impairment of p53 expression and p53 function in regulating p21 expression in senescent preadipocytes. We also observed a direct binding between RAGE and p53 in senescent preadipocytes. Taken together, our findings reveal a novel pro-adipogenic function of AGEs-RAGE axis in p53-regulated adipogenesis of senescent preadipocytes, providing new insights into aging-dependent adiposity by diet-driven and/or endogenous glycated proteins.

Provided by Purdue University

"Grilled, seared foods may add to waistlines, disease risk" December 12, 2012 http://medicalxpress.com/news/2012-12-grilled-seared-foods-waistlines-disease.html