Roles of chronic low-grade inflammation in the development of ectopic fat deposition.

Lulu Liu,Mei Mei,Shumin Yang,Qifu Li

doi:10.1155/2014/418185

Abstract

Pattern of fat distribution is a major determinant for metabolic homeostasis. As a depot of energy, the storage of triglycerides in adipose tissue contributes to the normal fat distribution. Decreased capacity of fat storage in adipose tissue may result in ectopic fat deposition in nonadipose tissues such as liver, pancreas, and kidney. As a critical biomarker of metabolic complications, chronic low-grade inflammation may have the ability to affect the process of lipid accumulation and further lead to the disorder of fat distribution. In this review, we have collected the evidence linking inflammation with ectopic fat deposition to get a better understanding of the underlying mechanism, which may provide us with novel therapeutic strategies for metabolic disorders.

Highlights

Ectopic fat deposition refers to an excessive accumulation of lipids in nonadipose tissues, such as liver, muscle, and pancreas [1]
In terms of adipose tissue, inflammatory cytokines could decrease the lipid storage capacity by inhibiting preadipocytes differentiation and increasing lipolysis, which might further contribute to excessive fat accumulation in nonadipose tissues (Figure 1)
Our results showed that chronic systemic inflammation induced by casein injection exacerbated lipid accumulation in the liver of mice fed with normal chow diet (NCD) and high fat diet (HFD), with upregulated mRNA and protein expression of sterol regulatory element-binding protein 1 (SREBP-1), acetyl-CoA carboxylase enzymes (ACC), and fatty acid synthase (FAS) in liver, which indicated that chronic systemic inflammation increased lipogenesis in liver, resulting in hepatic lipid deposition [26]

Summary

Introduction

Ectopic fat deposition refers to an excessive accumulation of lipids (mainly triglycerides) in nonadipose tissues, such as liver, muscle, and pancreas [1]. In recent years, increasing evidence have shown that chronic low-grade inflammation is closely related to ectopic fat deposition and metabolic diseases; for example, elevated inflammatory factors are often observed in patients with ectopic fat deposition, such as fatty liver and fatty pancreas [3, 4]. This inflammatory condition is linked with overnutrition; a recent study reported elevated C-reactive protein (CRP) in nonobese or overweight subjects with nonalcoholic fatty liver disease, revealing that inflammation may play a critical and direct role, independent of excessive lipid from diet, in the development of ectopic fat accumulation [5]. Since ectopic fat accumulation involves both adipose tissue and nonadipose tissue, the purpose of the present review was to summarize the important evidence linking inflammation with ectopic lipid deposition in both adipose tissue and nonadipose tissue, in order to improve our understanding of the mechanism of ectopic lipid deposition

Inflammation Causes Decreased Capacity of Fat Storage in Adipose Tissue

Effect of Inflammation on Nonadipose Tissue

Conclusion