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Diabetes 53:2844-2854, 2004
© 2004 by the American Diabetes Association, Inc.

Pioglitazone Reduces Islet Triglyceride Content and Restores Impaired Glucose-Stimulated Insulin Secretion in Heterozygous Peroxisome Proliferator–Activated Receptor-{gamma}–Deficient Mice on a High-Fat Diet

Junji Matsui1, Yasuo Terauchi2, Naoto Kubota1,2, Iseki Takamoto1,2, Kazuhiro Eto1,2, Tokuyuki Yamashita1, Kajuro Komeda3, Toshimasa Yamauchi1,2, Junji Kamon1, Shunbun Kita1, Mitsuhiko Noda2,4, and Takashi Kadowaki1,2

1 Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
2 Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation (JST), Kawaguchi, Japan
3 Division of Laboratory Animal Science, Animal Research Center, Tokyo Medical University, Tokyo, Japan
4 Institute for Diabetes Care and Research, Asahi Life Foundation, Tokyo, Japan

Heterozygous peroxisome proliferator–activated receptor-{gamma} (PPAR-{gamma})-deficient (PPAR{gamma}+/–) mice were protected from high-fat diet–induced insulin resistance. To determine the impact of systemic reduction of PPAR-{gamma} activity on ß-cell function, we investigated insulin secretion in PPAR{gamma}+/– mice on a high-fat diet. Glucose-induced insulin secretion in PPAR{gamma}+/– mice was impaired in vitro. The tissue triglyceride (TG) content of the white adipose tissue, skeletal muscle, and liver was decreased in PPAR{gamma}+/– mice, but it was unexpectedly increased in the islets, and the increased TG content in the islets was associated with decreased glucose oxidation. Administration of a PPAR-{gamma} agonist, pioglitazone, reduced the islet TG content in PPAR{gamma}+/– mice on a high-fat diet and ameliorated the impaired insulin secretion in vitro. Our results demonstrate that PPAR-{gamma} protects islets from lipotoxicity by regulating TG partitioning among tissues and that a PPAR-{gamma} agonist can restore impaired insulin secretion under conditions of islet fat accumulation.

Address correspondence and reprint requests to Takashi Kadowaki, MD, PhD, Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. E-mail: kadowaki-3im{at}h.u-tokyo.ac.jp


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