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- Title
RAGE Regulates Obesity & Hyperglycemia Induced by High-Fat Feeding in Mice.
- Authors
Song, Fei; Lerner, Shulamit; Rosario, Rosa; Schmidt, Ann Marie; Ferrante Jr., Anthony W.
- Abstract
Recent studies highlight the role of inflammatory responses in high-fat (HF) diet-induced obesity and hyperglycemia. The multi-ligand receptor RAGE (Receptor for Advanced Glycation Endproducts) transduces the impact of its pro-inflammatory ligands, S100/calgranulins and High Mobility Group Box-1. We tested the hypothesis that genetic deletion of RAGE modulates the response to HF-feeding in mice. Male RAGE null (RAGE 0) or wild-type (WT) C57BL/6 mice, age 6 wks, were assigned to either regular chow (REG) (11.8% kcal) or HF chow (60% kcal) and followed for 16 wks. At sacrifice, there were no significant differences in metabolic or physical characteristics between REG-fed WT vs RAGE 0 mice (table). On HF, WT mice displayed significantly increased fasting glucose, leptin, leptin/% body fat, and cholesterol levels vs. RAGE 0 mice. RAGE 0 mice displayed significantly lower body mass, lean mass, and % body fat on I-IF vs WT mice (table). Food consumption, kcal/body mass, was not different between WT and RAGE 0 mice on HF. These data implicate RAGE in the development of obesity and consequent hyperglycemia induced by HF-feeding. Blockade of RAGE may suppress the maladaptive impact of HF on body mass and metabolism. Studies are underway to dissect the mechanisms underlying these findings.
- Publication
Diabetes, 2007, Vol 56, pA451
- ISSN
0012-1797
- Publication type
Academic Journal