Abstract
Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.
Highlights
The worldwide prevalence of obesity and its metabolic complications have increased substantially in recent decades
Expression of angiopoietin-like protein 2 (ANGPTL2) in adipose tissue and circulating levels of ANGPTL2 are higher in diet-induced obese mice than in control mice, and circulating levels of ANGPTL2 are closely related to adiposity, insulin resistance, and inflammation in mice [158]
As noted in the preceding text, obese subjects have higher levels of macrophage infiltration into adipose tissue compared with lean controls, leading to the increased levels of pro-inflammatory cytokines and circulating free fatty acids that are involved in the pathogenesis of dyslipidemia
Summary
The worldwide prevalence of obesity and its metabolic complications have increased substantially in recent decades. Excess fat accumulation promotes the release of free fatty acids into the circulation from adipocytes, which may be a critical factor in modulating insulin sensitivity [11,12]. Of body fat, since their basal adipose tissue lipolysis per kilogram of fat is lower in obese subjects than in lean subjects [13] This finding has been supported by other studies of adipocytes from obese subjects [14,15] and it was associated with down-regulation of hormone sensitive lipase and adipose triglyceride lipase, key enzymes involved in intracellular degradation of triglycerides [14,16,17,18]. We will review how the dysregulation of free fatty acids and inflammatory factors released by enlarged adipose tissue is associated with the pathogenesis of metabolic syndrome (insulin resistance, dyslipidemia and NAFLD). We will focus on the imbalance of pro-inflammatory and anti-inflammatory molecules secreted by adipose tissue which contribute to metabolic dysfunction
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