2011 ADA Posters 1261-2041.indd - Diabetes

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esistance and type 2 diabetes. By comprehensive proteomic profi ling of the human adipocyte secretome we identifi ed DPP4 as a novel adipokine. This study assessed the association of the adipokine DPP4 to the metabolic syndrome. Fully differentiated adipocytes exhibit a substantially higher release of DPP4, when compared to preadipocytes or macrophages. DPP4 release from adipocytes is increased after treatment with insulin and TNFα. Direct addition of DPP4 to adipocytes impairs insulin signaling at the level of insulin-stimulated Akt phoshorylation. A signifi cantly higher level of DPP4 protein expression was seen in visceral as compared to subcutaneous fat of obese patients. DPP4 expression in lean subjects was signifi cantly lower in both depots compared to the obese patients and with no regional difference. DPP4 serum concentrations signifi cantly correlated with adipocyte size, serum leptin and various clinical parameters related to the metabolic syndrome as BMI, fasting insulin and hs-CRP. Using adipose tissue explants from lean and obese subjects, we observed a 2-fold increase in DPP4 release in obesity that strongly correlated with adipocyte volume and parameters of the metabolic syndrome. DPP4 release from adipose tissue was decreased to the lean level after weight reduction of the obese patients induced by bariatric surgery. Both circulating DPP4 and DPP4 released from adipose tissue strongly correlated positively with an increasing risk score for the metabolic syndrome. DPP4 is a novel adipokine which may be linked to adipocyte hypertrophy and adipose tissue infl ammation. As DPP4 release strongly correlates with adipocyte size, adipose tissue could represent an important source of DPP4 in obesity. We therefore suggest that DPP4 may be critical in linking adipose tissue and the metabolic syndrome. & 1856-P Lipid Accumulation Products Index as a Better Predictor for Insulin Resistance and Glucose Intolerance Than BMI in Young Obese Women with Polycystic Ovary Syndrome JEE-YOUNG OH, HYE JIN LEE, YOUNG SUN HONG, YEON-AH SUNG, Seoul, Republic of Korea Elevated waist circumference and elevated triglycerides has been considered as a surrogate marker of cardiovascular risk. BMI may not to be the best marker for obesity-related disease. Lipid accumulation product (LAP) index, an ordinal scale combining waist circumference and triglycerides concentration, was suggested as a better marker for cardiovascular disease than BMI. We examined whether the LAP index is associated with cardiovascular risk factors and a better predictive marker than BMI in obese women with polycystic ovary syndrome (PCOS). We recruited 223 obese (BMI ³23kg/m 2 ) women with PCOS and 230 age-, and BMI-matched regular cycling control women by voluntary participation for the prevalence study. PCOS was diagnosed by using NICHD, and LAP index was calculated using the formula [waist circumference(cm)-58] x TG(mmol/L). Glucose intolerance was defi ned as IFG, IGT or diabetes, and insulin resistance as HOMA value greater than 90 percentile of obese controls. Mean age and BMI were 24±4 yr and 25.6±2.2 kg/m 2 in PCOS and 24±4 yr and 25.2±1.8 kg/m 2 in controls. LAP index was signifi cantly higher in women with PCOS than controls (32.2±21.9 vs. 23.6±15.6, P
Integrated Physiology/ Obesity POSTERS & 1859-P Liraglutide Provides Weight Maintenance and Additional Weight Loss after Low Calorie Diet-Induced Weight Loss in Obese Subjects without <strong>Diabetes</strong>: The SCALE Maintenance Study THOMAS A. WADDEN, PRISCILLA HOLLANDER, SAMUEL KLEIN, KEVIN NIS- WENDER, VINCENT WOO, PAULA HALE, TU DUYEN LE THI, LOUIS J. ARONNE, Philadelphia, PA, Dallas, TX, St. Louis, MO, Nashville, TN, Winnipeg, MB, Canada, Princeton, NJ, Copenhagen, Denmark, New York, NY Weight loss is diffi cult to achieve and sustain by lifestyle therapy alone. Liraglutide, a once-daily human glucagon-like peptide-1 analog approved for the treatment of T2DM, induced dose-dependent wt loss in obese subjects without diabetes in a phase 2 study, with highest effi cacy shown by a 3mg/d dose. The present randomized, placebo-controlled trial tested the ability of liraglutide (3mg/d) to maintain diet-induced wt loss. Subjects who lost >5% body wt after a 4–12 week run-in (RI) with a low-calorie diet (1200–1400kcal/d) and exercise counseling were randomized to receive liraglutide or placebo plus a 500kcal/d defi cit diet and exercise regimen for 56 weeks. Of 511 subjects entering RI, 422 were randomized 1:1 to the 2 arms. The mean RI wt loss for all randomized subjects was 6.0% (6.3kg). Over the next 56 weeks, additional wt loss occurred post-randomization (PR) (6.1% vs 0.05%, liraglutide vs placebo, p
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2011 ADA Posters 1261-2041.indd - Diabetes

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