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Adiponectin: more than just another fat cell hormone?

Recent research has shown that adipose tissue is not simply an inert storage depot for lipids but is also an important endocrine organ that plays a key role in the integration of endocrine, metabolic, and inflammatory signals for the control of energy homeostasis. The adipocyte has been shown to secrete a variety of bioactive proteins into the circulation. These secretory proteins, which have been collectively named adipocytokines (1), include leptin (2), tumor necrosis factor (TNF)-α (3), plasminogen-activator inhibitor type 1 (PAI-1) (4), adipsin (5), resistin (6), and adiponectin (7). Adiponectin, the gene product of the adipose most abundant gene transcript 1 (apM1) (7), is a novel and important member of the adipocytokine family. Adiponectin cDNA was first isolated by large-scale random sequencing of the human adipose tissue cDNA library (7). It is a collagen-like protein that is exclusively synthesized in white adipose tissue, is induced during adipocyte differentiation, and circulates at relatively high (microgram/milliliter) concentrations in the serum. Both murine and human forms of adiponectin have been isolated independently by several groups, and various descriptive names have been given to the same compound by different investigators: adipocyte complement-related protein of 30 kilodalton (Acrp30) (8), Adipo Q (9), and gelatin binding protein of 28 kilodalton (GBP28) (10). The former two are murine analogs and the latter the human counterpart. Throughout this review, we will be referring to the protein by its most commonly used name, adiponectin.

Adiponectin has been postulated to play an important role in the modulation of glucose and lipid metabolism in insulin-sensitive tissues in both humans and animals. Decreased circulating adiponectin levels have been demonstrated in genetic and diet-induced murine models of obesity (11), as well as in diet-induced forms of human obesity (12). Low adiponectin levels have also been strongly implicated in the development of insulin resistance …