Fantuzzi / Mazzone Adipose Tissue and Adipokines in Health and Disease

1. Auflage 2007
ISBN: 978-1-59745-370-7
Verlag: Humana Press
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 400 Seiten, eBook

Reihe: Nutrition and Health

The aim of Adipose Tissue and Adipokines in Health and Disease is to provide comprehensive information regarding adipose tissue, its physiological functions and its role in disease. This volume contains a collection of information spanning the entire range of adipose tissue studies, from basic anatomical and physiological research to epidemiology and clinical aspects, in one place. This book is indispensable for basic researchers and clinicians interested in the fields of obesity, metabolic diseases, inflammation and immunity, and specialists in each of the pathologies associated with obesity.

Zielgruppe

Professional/practitioner

Autoren/Hrsg.

Fantuzzi, Giamila

Mazzone, Theodore

Weitere Mitwirkende

Goldberg, A.P.

Fried, S.K.

Inhaltsverzeichnis

Adipose Tissue: Structure and Function.- The Adipose Organ.- Metabolism of White Adipose Tissue.- Leptin.- Adiponectin.- Adipokines as Regulators of Immunity and Inflammation.- Vasoactive Factors and Inflammatory Mediators Produced in Adipose Tissue.- Regulation of the Immune Response by Leptin.- Leptin in Autoimmune Diseases.- Leptin and Gastrointestinal Inflammation.- Adiponectin and Inflammation.- Interactions Between Adipocytes and Immune Cells.- Macrophages, Adipocytes, and Obesity.- Interactions of Adipose and Lymphoid Tissues.- Adipose Tissue and Mast Cells.- Bone Marrow Adipose Tissue.- Weight Gain and Weight Loss.- The Epidemiology of Obesity.- Environmental Aspects of Obesity.- Developmental Perspectives on the Origins of Obesity.- Genetics of Obesity.- Inherited and Acquired Lipodystrophies.- Mechanisms of Cachexia.- Effect of Weight Loss on Disease.- Adipose Tissue and Disease.- Adipose Tissue and Insulin Resistance.- Adipokines in Non-Alcoholic Fatty Liver Disease.- Adiposity and Cancer.- Obesity and the Heart.- Obesity and Asthma.- Adiposity and Kidney Disease.- Obesity and Joint Disease.

Leseproben

Adipose Tissue and Insulin Resistance (p. 281-282)

Stephen E. Borst

21 Abstract

Adiposity, especially visceral adiposity, is an important risk factor for the development of insulin resistance and type 2 diabetes. In addition to its role in storing energy, adipose tissue also secretes into the circulation a number of hormones and other factors that can alter the response to insulin in distant tissues, such as liver and muscle. Many of these factors are cytokines, which have been associated with the immune system.

Fat-derived hormones that can enhance insulin signaling include leptin, adiponectin, and possibly visfatin. Those impairing insulin signaling include tumor necrosis factor- , resistin, and several of the interleukins. Obesity has also been identified as a low-grade inflammatory state. Several possible mechanisms are discussed whereby rapid growth of adipose tissue might trigger a local inflammatory response. It is suggested that this inflammatory response and associated release of cytokines may constitute the link between obesity and insulin resistance.

Key Words: Tumor necrosis factor, resistin, adiponectin, interleukins, free fatty acids, subcutaneous fat, visceral fat, insulin signaling.

INTRODUCTION

Obesity and type 2 diabetes are the most common metabolic diseases in Western society, together affecting as much as half of the adult population (1). Not only is the prevalence of these conditions high, but it also continues to increase. Insulin resistance a prediabetic condition, characterized by a failure of target organs to respond normally to insulin. Insulin resistance includes a central component (incomplete suppression of hepatic glucose output) and a peripheral component (impaired insulin-mediated glucose uptake in skeletal muscle and adipose tissue) (2). When increased insulin secretion is no longer sufficient to prevent hyperglycemia, the subject progresses from insulin resistance to type 2 diabetes. Insulin resistance is associated with other conditions such as central obesity, hypertension, and dyslipidemia, all risk factors for cardiovascular disease. The constellation of these metabolic abnormalities has been termed metabolic syndrome.

Obesity is a well-recognized risk factor for the development of insulin resistance and metabolic syndrome. In addition to the total amount of fat, distribution of adipose tissue also important, with most studies concluding that visceral fat contributes considerably more to insulin resistance than does subcutaneous fat (3). However, one report, by Misra al., documented a robust correlation between posterior abdominal subcutaneous fat and insulin resistance (4). Underscoring the importance of visceral fat is the report by Klein et al. that liposuction, resulting in a substantial reduction of subcutaneous fat, did not enhance insulin responsiveness in insulin-resistant subjects (5). In rats, we (6) and others (7) have found that surgical removal of visceral fat reverses insulin resistance.

Traditionally, adipose tissue has been regarded largely as a depot for stored fat. More recently, it has become clear that adipose tissue plays an active role in energy metabolism and is the source of hormones, cytokines, and metabolites that play an important role in whole-body metabolism (8). The role of these substances may be either autocrine or endocrine. Adipose tissue, especially visceral fat, is the source of a number of substances that might play a role in the development of insulin resistance. Among the latter are tumor necrosis factor (TNF)- , adiponectin, interleukin (IL)-6, resistin, and free fatty acids. The difference in the metabolic effects of visceral versus subcutaneous fat may be attributed both to differences in the hormones secreted by the two types of fat and to the fact that hormones secreted by visceral fat reach the liver in high concentration. The latter is due to the fact that visceral fat drains into the portal circulation, whereas subcutaneous fat drains into the systemic circulation (8). This review will focus on the regulation of insulin responsiveness by adipokines and on evidence supporting the hypothesis that these hormones play a role in the pathophysiology of insulin resistance.