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Mice Lacking Adiponectin Show Decreased Hepatic ... - Jbc
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281:2654-2660. doi: 10.1074/jbc.M505311200 originally published online December 2, 2005 Access the most updated version of this article at doi: 10.1074/jbc.M505311200 Find articles, minireviews, Reflections and Classics on similar topics on the JBC Affinity Sites. Alerts: When this article is cited When a correction for this article is posted Click here to choose from all of JBC's e-mail alerts This article cites 33 references, 9 of which can be accessed free at http://www.jbc.org/conte.
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2002 FAQ
Chronic reduction in adiponectin is frequently observed in obese patients, contributing to the pathogenesis of different obesity-related diseases. A reduction in adiponectin also has an impact on the central nervous system (CNS) and can lead to brain aging and cognitive impairment.
Adiponectin contributes to the control of glucose uptake and lipids metabolism, by reducing gluconeogenesis and enhancing glycolysis and fatty acid oxidation in the liver. These metabolic effects happen through interactions with AdipoR1 and hepatic AdipoR2.
Adiponectin is a fat-derived hormone that appears to play a crucial role in protecting against resistance/diabetes and atherosclerosis. Decreased adiponectin levels are thought to play a central role in the development of type 2 diabetes, obesity and cardiovascular disease in humans.
In healthy liver, adiponectin controls the metabolism of both glucose and lipids, decreasing gluconeogenesis and stimulating glycolysis and fatty acid oxidation. These metabolic effects occur through the binding of gAd to AdipoR1 and fAd to the specific hepatic receptor AdipoR2.
Clinical Significance As a widely studied biomarker, adiponectin has been shown to play a role in various endocrine and metabolic disorders. Continued research regarding the role it plays as a biomarker has the potential to elucidate further the pathogenesis and treatment of disease.
Adiponectin targets the liver, heart, pancreatic β cells, kidney, potentially muscle, and many other cell types in various tissues. Adiponectin strongly suppresses hepatic gluconeogenesis by inhibiting genes involved in glucose production.
In addition, adiponectin is one of the hormones with the highest plasma concentrations. Weight loss or caloric restriction leads to increasing adiponectin levels, and this increase is associated with increased sensitivity.
There is an evidence that adiponectin decreases hepatic and systematic IR and attenuates liver inflammation and fibrosis. Adiponectin generally predicts steatosis grade and severity of NAFLD, but it remains to be addressed to what extent this is a direct effect or related to the presence of more severe IR.
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