Regular Article
Secretion of Adiponectin and Regulation of apM1 Gene Expression in Human Visceral Adipose Tissue

https://doi.org/10.1006/bbrc.2001.5904Get rights and content

Abstract

Adiponectin (ApN) is thought to play a major role in the pathogenesis of the Metabolic Syndrome. Production of ApN and regulation of its related gene (apM1) have not yet been studied in human visceral adipose tissue. ApN was mainly associated with adipocyte membranes and abundantly secreted in medium from isolated adipocytes. apM1 gene expression, restricted to the adipocyte fraction of adipose tissue, decreased spontaneously when adipose explants were cultured in basal medium for 24 h while the expression of other adipose genes barely changed (PPARγ, GAPDH) or increased (PAI-1). Unexpectedly, the fall of apM1 mRNA was prevented by the addition of actinomycin D, an inhibitor of transcription, or cycloheximide, an inhibitor of protein synthesis, and by reducing the amount of adipose tissue cultured per dish, thereby suggesting that a newly synthesized factor released by adipose tissue destabilizes apM1 mRNA. apM1 gene expression was also negatively regulated by glucocorticoids and positively by insulin and IGF-1. This regulation could contribute to the decreased apM1/ApN levels in insulin-resistant patients with obesity and the Metabolic Syndrome.

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      Adiponectin is an adipose tissue derived protein hormone with a potential antidiabetic, antiinflammatory, and antiatherogenic activities (Wabu et al., 2010; Maeda et al., 2002). Plasma adiponectin concentrations are inversely proportional to adiposity and decreased in insulin resistance, Type 2 Diabetes Mellitus and obesity, (T2DM) (Hotta et al., 2000; Halleux et al., 2001). Maeda et al. (2002) reported that over nutrition causes hypoadiponectinemia and increased TNF-α level which results in insulin resistance.

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