2101-P: Adipose Tissue Insulin Resistance in Overweight and Lean Patients with Impaired Glucose Tolerance or Type 2 Diabetes

Abstract

Background: When adipose tissue shows insulin resistance, insulin is unable to suppress lipolysis. Several Western studies have revealed a relationship between obesity and the antilipolytic effect of insulin. However, it is unclear whether a distinctly different degree of obesity between Westerner and Japanese could lead to a different outcome of the insulin antilipolytic effect. Thus, we investigated the impact of adipose tissue insulin resistance in Japanese patients with impaired glucose tolerance (IGT) and type 2 diabetes (T2D). Methods: Twenty Japanese patients with T2D and 20 participants without diabetes were recruited (January 2014 to March 2015). A 75-g oral glucose tolerance test (OGTT) was performed and plasma glucose, serum insulin, and free fatty acid (FFA) levels were measured during this test. Insulin resistance was estimated using the Matsuda index, HOMA-IR, and the adipocyte insulin resistance index (Adipo-IR). Glucose-stimulated insulin secretion was evaluated based on the insulinogenic index (II). The definition of overweight was BMI ≥ 25 kg/m 2 . Results: We included patients with IGT (n=19) and T2D (n=19). BMI in all patients was 26.0 ± 6.2 kg/m 2 . In T2D, HbA1c was higher and II was lower compared with those in IGT. No statistically significant difference in other parameters, such as BMI, FFA, insulin resistance, were observed between T2D and IGT. In overweight IGT, Adipo-IR was significantly higher (overweight IGT, 4.0 [2.0-9.4] vs, lean IGT, 1.0 [0.8-2.3], p Conclusion: Overweight status in IGT, but not in T2D, could be related to worsening Adipo-IR. These findings suggest that encouraging weight loss to the ideal weight for IGT patients might reduce the risk of worsening adipose tissue insulin resistance, and progression of IGT to T2DM. Disclosure A. Miya: None. A. Nakamura: Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Mitsubishi Tanabe Pharma Corporation, Novartis Pharmaceuticals Corporation, Ono Pharmaceutical Co., Ltd. H. Kameda: None. K. Cho: None. H. Miyoshi: Research Support; Self; Astellas Pharma Inc., AstraZeneca, Daiichi Sankyo Company, Limited, Eli Lilly and Company, Kowa Pharmaceutical Europe Co. Ltd., Mitsubishi Tanabe Pharma Corporation, MSD, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi, Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Speaker9s Bureau; Self; Astellas Pharma Inc., AstraZeneca, Eli Lilly and Company, Kissei Pharmaceutical Co., Ltd., Kowa Pharmaceutical Europe Co. Ltd., Mitsubishi Tanabe Pharma Corporation, MSD, Novartis Pharmaceuticals Corporation, Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi, Sumitomo Dainippon Pharma Co., Ltd., Takeda Pharmaceutical Company Limited. T. Atsumi: Research Support; Self; Astellas Pharma Inc., Bayer Yakuhin, Ltd., Chugai Pharmaceutical Co., Ltd., Daiichi Sankyo Company, Limited, Eisai Co., Ltd., Mitsubishi Tanabe Pharma Corporation, Takeda Pharmaceutical Company Limited. Speaker9s Bureau; Self; AbbVie Inc., Astellas Pharma Inc., Bristol-Myers Squibb Company, Chugai Pharmaceutical Co., Ltd., Eisai Co., Ltd., Eli Lilly and Company, Mitsubishi Tanabe Pharma Corporation, Pfizer Inc., Takeda Pharmaceutical Company Limited, UCB, Inc.