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CTRP1 protects against diet-induced hyperglycemia by enhancing glycolysis and fatty acid oxidation

Authors
Han, SoraPark, Jeong SuLee, SunyiJeong, Ae LeeOh, Ki SookKa, Hye InChoi, Hyun-JiSon, Woo-ChanLee, Won-YoungOh, Suk JoongLim, Jong-SeokLee, Myeong-SokYang, Young
Issue Date
Jan-2016
Publisher
ELSEVIER SCIENCE INC
Keywords
Hyperglycemia; Insulin resistance; High-sucrose diet; High-fat diet; Glycolysis; Fatty acid oxidation
Citation
JOURNAL OF NUTRITIONAL BIOCHEMISTRY, v.27, pp.43 - 52
Journal Title
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Volume
27
Start Page
43
End Page
52
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/3594
DOI
10.1016/j.jnutbio.2015.08.018
ISSN
0955-2863
Abstract
Complement-C1q/tumor necrosis factor-alpha related protein 1 (CTRP1) is a 35-kDa glycoprotein that is secreted from various tissues. Although CTRP1 is highly increased in patients with type II diabetes and obesity, the metabolic roles of CTRP1 remain largely unknown. To unveil the physiological roles of CTRP1 in vivo, CTRP1 transgenic (TG) mice were challenged by a high-fat diet (HFD) and a high-sucrose drink (HS). Homeostatic model assessment-estimated insulin resistance values were decreased in HFD- or HS-fed CTRP1 TG mice compared with wild-type control mice. In this context, CTRP1 stimulated glucose uptake through the glucose transporter GLUT4 translocation to the plasma membrane and also increased glucose consumption by stimulating glycolysis. To analyze the roles of CTRP1 in lipid metabolism, acetyl-CoA carboxylase (ACC) and hormone-sensitive lipase levels were determined in CTRP1 TG mice, and the effect of CTRP1 on fatty acid oxidation was assessed in C2C12 myotubes. CTRP1 was found to inhibit ACC by phosphorylation and to stimulate fatty acid oxidation in C2C12 myotubes. Taken together, CTRP1 performs active catabolic roles in vivo. Therefore, CTRP1 seems to perform a defensive function against nutritional challenges. (C) 2015 Elsevier Inc. All rights reserved.
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