2011 ADA Posters 1261-2041.indd - Diabetes

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estrictive and GI bypass models, respectively. By using SG and RYGB mouse models, we tested whether the effects of bariatric surgery in the treatment of obesity and insulin resistance are associated with the regulation of infl ammation in visceral adipose tissue (VAT) and liver in DIO mice. SG induced weight loss, reduced fat mass and improved glucose tolerance in glucose tolerance tests within 4 wks, but the effects were not completely sustained. However, RYGB resulted in a sustained prevention of weight gain and improved liver steatosis and insulin resistance through 12 wks. Both RYGB and SG inhibited CD11b macrophages and Th1 (CD3 + /IFNg + ) subsets in liver by -60% and -42%, respectively, as well as in VAT (-85% and -64%, respectively) and enhanced Th2 (CD3 + /IL-10 + ) subsets in liver (+100%), but not in VAT at 7 days post-surgery. RYGB, but not SG, suppressed phosphorylation of IRS- 1/Ser 307 , inhibited (-47%) M1 (CD11c) macrophage polarization, promoted (+78.5%) M2 (CD206) macrophage polarization and enhanced (+100%) CD3 + / FoxP3 + regulatory T cells in the liver. RYGB, but not SG, reduced circulating insulin (-85%), leptin (-45%) and IL-6 (-64%) by one week post-surgery. Our study suggests that SG induces weight loss and improves glucose tolerance in the short term; however, RYGB persistently improves insulin resistance. Early positive effects of RYGB and SG in the improvements of insulin resistance appear to be modulated by the inhibition of infl ammation in liver and VAT. RYGB specifi cally inhibits infl ammatory M1 macrophages, enhances M2 macrophages and promotes regulatory T cell subsets in the liver. Supported by: NIH grants to D.W. and N.A., JDRF grant to D.Y. & 1807-P Depletion of α/β T Cells Attenuates Obesity-Associated Infl ammation and Metabolic Abnormalities ILVIRA M. KHAN, XIAOYUAN PERRARD, JERRY PERRARD, AMIR MANSOORI, C. WAYNE SMITH, HUAIZHU WU, CHRISTIE M. BALLANTYNE, Houston, TX Recent investigations have linked obesity with low-grade chronic infl ammation in adipose tissue (AT), which causes AT dysfunction, thus contributing to obesity associated metabolic abnormalities. Diet-induced obesity is correlated with accumulation of “classically activated” (M1) macrophages in AT, which secret proinfl ammatory cytokines and impair insulin signaling and lipid storage in adipocytes. In addition, obesity alters T cell numbers in AT. However, the role of T cells in metabolic complications of obesity is less defi ned. Using mouse model of diet-induced obesity, we found that both αβ and γδ T cells reside in perigonadal AT of lean mice. However, only αβ T cells were signifi cantly increased in AT of obese mice (25.05 + 4.38%) compared with lean controls (8.89 + 3.60%, n=7/group, P
Integrated Physiology/ Obesity POSTERS versus controls, despite similar intake), which may be attributed in part to an increased locomotor activity (p
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2011 ADA Posters 1261-2041.indd - Diabetes

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