Adipolin/C1qdc2/CTRP12 protein functions as an adipokine that improves glucose metabolism |
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Authors: | Enomoto Takashi Ohashi Koji Shibata Rei Higuchi Akiko Maruyama Sonomi Izumiya Yasuhiro Walsh Kenneth Murohara Toyoaki Ouchi Noriyuki |
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Institution: | Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan. |
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Abstract: | Obesity is a major risk factor for the development of insulin resistance and type 2 diabetes. Adipose tissue secretes various bioactive molecules, referred to as adipokines, whose dysregulation can mediate changes in glucose homeostasis and inflammatory responses. Here, we identify C1qdc2/CTRP12 as an insulin-sensitizing adipokine that is abundantly expressed by fat tissues and designate this adipokine as adipolin (adipose-derived insulin-sensitizing factor). Adipolin expression in adipose tissue and plasma was reduced in rodent models of obesity. Adipolin expression was also decreased in cultured 3T3-L1 adipocytes by treatment with inducers of endoplasmic reticulum stress and inflammation. Systemic administration of adipolin ameliorated glucose intolerance and insulin resistance in diet-induced obese mice. Adipolin administration also reduced macrophage accumulation and proinflammatory gene expression in the adipose tissue of obese mice. Conditioned medium from adipolin-expressing cells diminished the expression of proinflammatory cytokines in response to stimulation with LPS or TNFα in cultured macrophages. These data suggest that adipolin functions as an anti-inflammatory adipokine that exerts beneficial actions on glucose metabolism. Therefore, adipolin represents a new target molecule for the treatment of insulin resistance and diabetes. |
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Keywords: | Adipokines Adipose Tissue Glucose Metabolism Inflammation Obesity Adipolin |
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