Adiponectin in insulin resistance: lessons from translational research
Adiponectin is an adipose tissue-secreted endogenous insulin sensitizer, which plays a key role as a mediator of peroxisome proliferator-activated receptor γ action. Adiponectin alters glucose metabolism and insulin sensitivity, exhibits antiinflammatory and antiatherogenic properties, and has been...
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Published in | The American journal of clinical nutrition Vol. 91; no. 1; pp. 258 - 261S |
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Main Authors | , |
Format | Journal Article Conference Proceeding |
Language | English |
Published |
Bethesda, MD
American Society for Clinical Nutrition
01.01.2010
American Society for Nutrition American Society for Clinical Nutrition, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Adiponectin is an adipose tissue-secreted endogenous insulin sensitizer, which plays a key role as a mediator of peroxisome proliferator-activated receptor γ action. Adiponectin alters glucose metabolism and insulin sensitivity, exhibits antiinflammatory and antiatherogenic properties, and has been linked to several malignancies. Circulating concentrations of adiponectin are determined primarily by genetic factors, nutrition, exercise, and abdominal adiposity. Adiponectin concentrations are lower in subjects with obesity, metabolic syndrome, and cardiovascular disease. Adiponectin knockout mice manifest glucose intolerance, insulin resistance, and hyperlipidemia and tend to develop malignancies especially when on high-fat diets. Animal studies have also shown beneficial effects of adiponectin in rodents in vivo. Circulating concentrations of adiponectin are lower in patients with diabetes, cardiovascular disease, and several malignancies. Studies to date provide promising results for the diagnostic and therapeutic role of adiponectin in obesity, insulin resistance, diabetes, cardiovascular disease, and obesity-associated malignancies. |
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Bibliography: | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 ObjectType-Review-3 Supported by NIH/National Institute of Diabetes and Digestive and Kidney Diseases grants R01DK079929, R01DK058785, K24DK081913, and 5U01DK057154. Presented at the symposium “Novel Therapeutic Advances through the Development of Selective PPARγ Modulators from Bench to Bedside,” held at Experimental Biology 2009, New Orleans, LA, 21 April 2009. |
ISSN: | 0002-9165 1938-3207 1938-3207 |
DOI: | 10.3945/ajcn.2009.28449c |