The autocrine and paracrine roles of adipokines

Abstract

Please cite this article as: Karastergiou, K., Mohamed-Ali, V., The autocrine and paracrine roles of adipokines, Molecular and Cellular Endocrinology (2008), doi:10.1016/j.mce.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Page 1 of 35A c c e p t e d M a n u s c r i p t Abstract.Obesity, defined by an excess of adipose tissue, is often associated with the development of various metabolic diseases. The increased and inappropriate deposition of this tissue contributes to hyperglycemia, hyperlipidemia, insulin resistance, endothelial dysfunction and chronic inflammation. Recent evidence suggests that factors expressed and secreted by the adipose tissue, adipokines, may contribute to the development of these abnormalities by mechanisms including inhibition of adipogenesis, adipocyte hypertrophy and death, immune cell infiltration and disruption of tissue metabolism. The presence of adipokine receptors in adipocytes renders these cells available to autocrine and paracrine effects of adipokines. In this review the reported local effects of adipokines on adipose tissue structure, inflammation and regulation of metabolic functions, in the face of over-nutrition and consequent obesity, are outlined. Elucidating the local regulation of white adipocyte development and function could help in the design of effective, tissue-specific therapies for obesity-associated diseases.

Apelin Enhances Brown Adipogenesis and Browning of White Adipocytes

“…An explosion of interest has been triggered because stimulating adipose browning may be a novel route to combat obesity and associated metabolic diseases. Increasing evidence is mounting to suggest that adipokines secreted by adipocytes play important roles in the self-modeling of adipose tissue (19,29,33). But their effects on browning are not well explored.…”

Immune dysfunction and chronic inflammation following spinal cord injury

“…12,35 Obesity is now classified as an inflammatory disorder due to the discovery that adipose tissue acts as an endocrine organ, possessing the ability to secrete proinflammatory mediators, termed adipokines, such as TNF (tumor necrosis factor)-α, IL (interleukin)-1 and IL-6. 36 As such, an abundance of adipose tissue, as seen in obesity, may result in the overproduction of proinflammatory mediators and contribute to a low-grade inflammatory state. Adipose tissue is also known to secrete adiponectin, a protein with a critical role in fatty acid oxidation and glucose regulation.…”

Lysophosphatidic acid impairs glucose homeostasis and inhibits insulin secretion in high-fat diet obese mice

“…In parallel with its lipid storage capacity, the adipose tissue produces various bioactive molecules (adipokines, reactive phospholipids, glycerol, NEFA). The export of these molecules from adipose tissue is often altered in obese individuals and some of them (TNF-α, resistin, monocyte chemotactic protein-1 [MCP-1]) exert deleterious effects on glucose metabolism and insulin sensitivity [3].…”