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Diabetes 55:S32-S38, 2006
DOI: 10.2337/db06-S005
© 2006 by the American Diabetes Association
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Section I: The Adipocyte Connection

Adiponectin-Dependent and -Independent Pathways in Insulin-Sensitizing and Antidiabetic Actions of Thiazolidinediones

Naoto Kubota1,2,3, Toshimasa Yamauchi1,2, Kazuyuki Tobe1,2, and Takashi Kadowaki1,2,3

1 Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
2 CREST of Japan Science and Technology Agency, Saitama, Japan
3 Clinical Nutrition Program, National Institute of Health and Nutrition, Tokyo, Japan

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

Abbreviations: AMPK, AMP-activated protein kinase; EGP, endogenous glucose production; FFA, free fatty acid; GIR, glucose infusion rate; HMW, high-molecular-weight; TNF, tumor necrosis factor; TZD, thiazolidinedione

The first 300 words of the full text of this article appear below.

The metabolic syndrome has become one of the major public health challenges worldwide (1,2) and is thought to result from obesity and obesity-linked insulin resistance, the combination of which promotes diabetes, hypertension, hyperlipidemia, and cardiovascular diseases (1,2). Obesity, defined as increased adipose tissue mass, is mainly characterized by adipocyte hypertrophy, especially in adulthood (1,2). Adipose tissue serves as the site of triglyceride storage and free fatty acid (FFA)/glycerol release in response to changing energy demands (1). Adipose tissue also participates in the regulation of energy homeostasis as an important endocrine organ that secretes a number of biologically active "adipokines," such as FFA (3), tumor necrosis factor (TNF)-{alpha} (4), resistin (5), and leptin (6). Although the association of obesity and insulin resistance has been recognized, the mechanisms by which obesity causes systemic insulin resistance largely remain unclear. One such mechanism is upregulation of insulin resistance–inducing adipokines, such as FFA, TNF-{alpha}, and resistin (Fig. 1). In contrast to such insulin resistance–causing adipokines, adiponectin, as well as leptin, is one of the adipokines that directly sensitizes the body to insulin, and its expression and serum levels are known to be upregulated by thiazolidinediones (TZDs), a group of insulin sensitizers. In this review, we describe recent progress in research into the role of adiponectin in amelioration of insulin resistance and diabetes by TZDs.


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  		FIG. 1. TZDs decrease insulin resistance–causing adipokines via generation of small adipocytes. TZDs promote adipocyte differentiation and increase the number of small adipocytes and decrease the number of large adipocytes. Generation of small insulin-sensitive adipocytes by TZDs lowers circulating serum FFA levels and downregulates the production and secretion of TNF-{alpha} and resistin, subsequently ameliorating insulin resistance.

 

   TZDS DECREASE PRODUCTION AND SECRETION OF INSULIN RESISTANCE–CAUSING ADIPOKINES VIA GENERATION OF SMALL ADIPOCYTES
 
TZDs have . . . [Full Text of this Article]


   TZDS INCREASE EXPRESSION AND SECRETION OF A MAJOR INSULIN-SENSITIZING ADIPOKINE, ADIPONECTIN
 

   TZDS INCREASE HIGH-MOLECULAR–WEIGHT ADIPONECTIN
 

   LOW DOSE OF PIOGLITAZONE IMPROVES DIABETES AND INSULIN RESISTANCE IN OB/OB MICE, BUT NOT IN ADIPO–/–OB/OB MICE
 

   HIGH DOSES OF PIOGLITAZONE IMPROVE DIABETES AND INSULIN RESISTANCE IN OB/OB AND ADIPO–/– OB/OB MICE
 

   HIGH-DOSE, BUT NOT LOW-DOSE, PIOGLITAZONE DECREASES ADIPOCYTE SIZE, SERUM FFA LEVELS, AND EXPRESSION LEVELS OF TNF-{alpha} AND RESISTIN IN OB/OB AND ADIPO–/–OB/OB MICE
 

   ADIPONECTIN-DEPENDENT AND -INDEPENDENT PATHWAYS IN INSULIN SENSITIZING AND ANTI-DIABETIC ACTIONS OF TZDS (HYPOTHESIS)
 

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