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Review
. 2017 Aug 15;18(8):1770.
doi: 10.3390/ijms18081770.

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

Xavier Escoté  1   2 , Saioa Gómez-Zorita  3   4 , Miguel López-Yoldi  5   6 , Iñaki Milton-Laskibar  7   8 , Alfredo Fernández-Quintela  9   10 , J Alfredo Martínez  11   12   13   14 , María J Moreno-Aliaga  15   16   17   18 , María P Portillo  19   20
Affiliations
Review

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

Xavier Escoté et al. Int J Mol Sci. .

Abstract

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.

Keywords: TWEAK and NOV/CCN3; adipokines; cardiotrophin-1; omentin; vaspin.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of the metabolic actions of omentin-1 in adipose tissue (data obtained from isolated human adipocytes) suggesting an improvement in insulin sensitivity and hypothalamus (data obtained from animal studies) suggesting increased food intake. Akt: protein kinase b, IRS: insulin receptor substrate, CART: amphetamine-regulated transcript, CRH: corticotropin-releasing hormone.
Figure 2
Figure 2
Schematic representation of the metabolic actions of cardiotrophin-1. This adipokine promotes body weight and fat mass losses, reduces hyperglycemia and increases insulin sensitivity by coordinately acting on key metabolic tissues (hypothalamus, adipose tissue, liver, intestine and muscle). SGLT-1: sodium-dependent glucose transporter 1.
Figure 3
Figure 3
Schematic representation of the effects of omentin, vaspin, cardiotrophin-1, TWEAK and NOV/CCN3 on insulin signaling cascade that explain positive effects of these adipokines on glycemic control. Akt: protein kinase b; AMPK: AMP activated protein-kinase; AS160: Akt substrate of 160 kDa; GLUT: glucose transporter; IRS: insulin receptor substrate; LKB1: liver kinase B1; mTOR: mammalian target of rapamicin; P: inorganic phosphorous; PI3K: phosphatidylinositol 3-kinase; RAB-10: Ras-related protein RAB-10.
Figure 4
Figure 4
Schematic representation of the main tissues and organs involved in the effects of omentin, vaspin, cardiotrophin-1, TWEAK and NOV/CCN3 on insulin resistance and obesity. On the left side of the figure, target tissues and organs involved in the effects of adipokines on insulin resistance. On the right side of the figure, target tissues and organs involved in the anti-obesity action of adipokines.
See this image and copyright information in PMC

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