Human resistin and the RELM of Inflammation in diabesity.

Fatima Al Hannan,Kevin Gerard Culligan

doi:10.1186/s13098-015-0050-3

Fatima Al Hannan, Kevin Gerard Culligan

Open Access

https://doi.org/10.1186/s13098-015-0050-3

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Abstract

The initial discovery of resistin and resistin-like molecules (RELMs) in rodents suggested a role for these adipocytokines in molecular linkage of obesity, Type 2 Diabetes mellitus and metabolic syndrome. Since then, it became apparent that the story of resistin and RELMs was very much of mice and men. The putative role of this adipokine family evolved from that of a conveyor of insulin resistance in rodents to instigator of inflammatory processes in humans. Structural dissimilarity, variance in distribution profiles and a lack of corroborating evidence for functional similarities separate the biological functions of resistin in humans from that of rodents. Although present in gross visceral fat deposits in humans, resistin is a component of inflammation, being released from infiltrating white blood cells of the sub-clinical chronic low grade inflammatory response accompanying obesity, rather than from the adipocyte itself. This led researchers to further explore the functions of the resistin family of proteins in inflammatory-related conditions such as atherosclerosis, as well as in cancers such as endometrial and gastric cancers. Although elevated levels of resistin have been found in these conditions, whether it is causative or as a result of these conditions still remains to be determined.

Highlights

Obesity is increasing worldwide at such an alarming rate that is has been classified as an epidemic [1]
Recent advances in the understanding of obesity have identified a causative genetic influence over obesity [3], along with other contributing factors such as excessive calorific intake, sedentary lifestyle and a diet high in saturated fat. Such is the tightness of this pathophysiological association between obesity and Type 2 Diabetes mellitus (T2DM) diabetes that the term Diabesity has been coined to represent obesity-associated diabetes [4]
Human resistin was found to be produced in immunocompetent cells [50, 72], including those that resided around adipose tissue, providing a chronic, sub-clinical low-grade inflammation in diabesity [12]

Summary

Introduction

Obesity is increasing worldwide at such an alarming rate that is has been classified as an epidemic [1]. Adipocytes and chronic Low grade inflammation In lean individuals, white adipose tissue (WAT) storage of triglycerides is systematically regulated, controlling the release of anti-inflammatory cytokines such as Adiponectin [24], Transforming Growth Factor (TGF)-β and interleukin (IL)-1 [25], which aid in the homeostasis of inflammation, metabolic control and vascular function [25]. The increase in inflammatory mediators acts as a positive feedback mechanism, further recruiting inflammatory cells to obese adipose tissue.

Results

Conclusion