Abstract
Abundant evidence has demonstrated that obesity is a state of low-grade chronic inflammation that triggers the release of lipids, aberrant adipokines, pro-inflammatory cytokines, and several chemokines from adipose tissue. This low-grade inflammation underlies the development of insulin resistance and associated metabolic comorbidities such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD). During this development, adipose tissue macrophages accumulate through chemokine (C-C motif) receptor 2 and the ligand for this receptor, monocyte chemoattractant protein-1 (MCP-1), is considered to be pivotal for the development of insulin resistance. To date, the chemokine system is known to be comprised of approximately 40 chemokines and 20 chemokine receptors that belong to the seven-transmembrane G protein-coupled receptor family and, as a result, chemokines appear to exhibit a high degree of functional redundancy. Over the past two decades, the physiological and pathological properties of many of these chemokines and their receptors have been elucidated. The present review highlights chemokines and chemokine receptors as key contributing factors that link obesity to insulin resistance, T2DM, and NAFLD.
Highlights
Obesity is a state of chronic low-grade systemic inflammation that contributes to the development of metabolic diseases such as type 2 diabetes mellitus (T2DM), nonalcoholic fatty liver disease (NAFLD), cardiovascular disease, and several types of cancer [1,2,3,4]
The present review summarizes the various roles of chemokines and chemokine receptors during tissue inflammation with a special focus on the latest findings regarding chemokine systems that represent a link between inflammation in adipose tissue and the liver and the pathologies of insulin resistance, T2DM, and NAFLD
It has become increasingly evident that chemokines and chemokine receptors play an important role in obesity-induced insulin resistance and comorbid diseases such as T2DM, cardiovascular disease, and NAFLD and nonalcoholic steatohepatitis (NASH)
Summary
Obesity is a state of chronic low-grade systemic inflammation that contributes to the development of metabolic diseases such as type 2 diabetes mellitus (T2DM), nonalcoholic fatty liver disease (NAFLD), cardiovascular disease, and several types of cancer [1,2,3,4]. ATMs are a prominent source of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, that can block insulin action in the liver, adipose tissue, and skeletal muscle via autocrine and/or paracrine signaling. This can cause systemic insulin resistance through endocrine signals, which represents a potential link between inflammation and insulin resistance [6,7]. Obesity-associated systemic inflammation in both humans and rodents is characterized by the infiltration of macrophages into adipose tissue and the liver in conjunction with an increase in body weight [8,9,10] Both of these factors are positively correlated with insulin resistance. Immune Cell Activity during Obesity-Induced Inflammation and Insulin Resistance
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