Abstract
Obesity is an immunometabolic disease associated with chronic inflammation and the dysregulation of pro- and anti-inflammatory cytokines. One hallmark of obesity is reduced concentrations of the anti-inflammatory adipokine, adiponectin. Pharmacologic doses of niacin produce multiple metabolic benefits, including attenuating high-fat diet (HFD)-induced adipose tissue inflammation and increasing adiponectin concentrations. To determine if adiponectin mediates the anti-inflammatory effects of niacin, male C57BL/6J (WT) and adiponectin null (Adipoq-/-) mice were maintained on a low-fat diet (LFD) or HFD for 6 weeks, before being administered either vehicle or niacin (360 mg/kg/day) for 5 weeks. HFD-fed mice had increased expression of genes associated with macrophage recruitment (Ccl2) and number (Cd68), and increased crown-like structure (CLS) number in adipose tissue. While niacin attenuated Ccl2 expression, there were no effects on Cd68 or CLS number. The absence of adiponectin did not hinder the ability of niacin to reduce Ccl2 expression. HFD feeding increased gene expression of inflammatory markers in the adipose tissue of WT and Adipoq-/- mice. While niacin tended to decrease the expression of inflammatory markers in WT mice, niacin increased their expression in HFD-fed Adipoq-/- mice. Therefore, our results indicate that the absence of adiponectin alters the effects of niacin on markers of adipose tissue inflammation in HFD-fed mice, suggesting that the effects of niacin on tissue cytokines may involve adiponectin.
Highlights
Obesity is a chronic low-grade inflammatory disease characterized by increased inflammatory cytokines, circulating immune cells, and immune cells within adipose tissue [1,2,3,4,5,6].Specific pathophysiologic features of human and rodent models of obesity include increased numbers of adipose tissue macrophages (ATMs) and a shift in macrophage polarity from an alternatively activated (M2) to a classically activated (M1) state [7]
Chronic obesity and adipose tissue inflammation are associated with increases in serum MCP-1, TNFα, IL-6 [8,11,12,13], and C-reactive protein (CRP) [14], and the increased circulation of pro-inflammatory mononuclear cells [1,15]
Using wild-type (WT) and Adipoq-/- mice, we show that niacin decreased high-fat diet (HFD)-induced body weight gain in an adiponectin-dependent manner, but the effects of niacin on inflammatory markers differed between genotypes
Summary
Obesity is a chronic low-grade inflammatory disease characterized by increased inflammatory cytokines, circulating immune cells, and immune cells within adipose tissue [1,2,3,4,5,6].Specific pathophysiologic features of human and rodent models of obesity include increased numbers of adipose tissue macrophages (ATMs) and a shift in macrophage polarity from an alternatively activated (M2) to a classically activated (M1) state [7]. Obesity is a chronic low-grade inflammatory disease characterized by increased inflammatory cytokines, circulating immune cells, and immune cells within adipose tissue [1,2,3,4,5,6]. Obesity and chronic adipose tissue inflammation are associated with the development of metabolic syndrome, insulin resistance, type 2 diabetes, and low-grade systemic inflammation [8,9,10]. Chronic obesity and adipose tissue inflammation are associated with increases in serum MCP-1, TNFα, IL-6 [8,11,12,13], and C-reactive protein (CRP) [14], and the increased circulation of pro-inflammatory mononuclear cells [1,15]. Decreases in adiponectin precede the development of insulin resistance [18].
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