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Int. J. Mol. Sci. 2017, 18(8), 1770;

Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development

Department of Nutrition, Food Sciences and Physiology, University of Navarra, 31008 Pamplona, Spain
Centre for Nutrition Research, University of Navarra, 31008 Pamplona, Spain
Nutrition and Obesity Group, Department of Nutrition and Food Science, University of the Basque Country (UPV/EHU) and Lucio Lascaray Research Institute, 01006 Vitoria, Spain
Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition (CIBERobn), Institute of Health Carlos III, 01006 Vitoria, Spain
Navarra Institute for Health Research (IdiSNa), 31008 Pamplona, Spain
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Received: 17 July 2017 / Revised: 9 August 2017 / Accepted: 10 August 2017 / Published: 15 August 2017
(This article belongs to the Special Issue Adipokines)
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Adipose tissue releases bioactive mediators called adipokines. This review focuses on the effects of omentin, vaspin, cardiotrophin-1, Tumor necrosis factor-like Weak Inducer of Apoptosis (TWEAK) and nephroblastoma overexpressed (NOV/CCN3) on obesity and diabetes. Omentin is produced by the stromal-vascular fraction of visceral adipose tissue. Obesity reduces omentin serum concentrations and adipose tissue secretion in adults and adolescents. This adipokine regulates insulin sensitivity, but its clinical relevance has to be confirmed. Vaspin is produced by visceral and subcutaneous adipose tissues. Vaspin levels are higher in obese subjects, as well as in subjects showing insulin resistance or type 2 diabetes. Cardiotrophin-1 is an adipokine with a similar structure as cytokines from interleukin-6 family. There is some controversy regarding the regulation of cardiotrophin-1 levels in obese -subjects, but gene expression levels of cardiotrophin-1 are down-regulated in white adipose tissue from diet-induced obese mice. It also shows anti-obesity and hypoglycemic properties. TWEAK is a potential regulator of the low-grade chronic inflammation characteristic of obesity. TWEAK levels seem not to be directly related to adiposity, and metabolic factors play a critical role in its regulation. Finally, a strong correlation has been found between plasma NOV/CCN3 concentration and fat mass. This adipokine improves insulin actions. View Full-Text
Keywords: adipokines; omentin; vaspin; cardiotrophin-1; TWEAK and NOV/CCN3 adipokines; omentin; vaspin; cardiotrophin-1; TWEAK and NOV/CCN3

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Escoté, X.; Gómez-Zorita, S.; López-Yoldi, M.; Milton-Laskibar, I.; Fernández-Quintela, A.; Martínez, J.A.; Moreno-Aliaga, M.J.; Portillo, M.P. Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development. Int. J. Mol. Sci. 2017, 18, 1770.

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