Abstract

AimsTo determine the effects of niacin on adiponectin and markers of adipose tissue inflammation in a mouse model of obesity.Materials and MethodsMale C57BL/6 mice were placed on a control or high-fat diet (HFD) and were maintained on such diets for the duration of the study. After 6 weeks on the control or high fat diets, vehicle or niacin treatments were initiated and maintained for 5 weeks. Identical studies were conducted concurrently in HCA2 −/− (niacin receptor−/−) mice.ResultsNiacin increased serum concentrations of the anti-inflammatory adipokine, adiponectin by 21% in HFD-fed wild-type mice, but had no effect on lean wild-type or lean or HFD-fed HCA2 −/− mice. Niacin increased adiponectin gene and protein expression in the HFD-fed wild-type mice only. The increases in adiponectin serum concentrations, gene and protein expression occurred independently of changes in expression of PPARγ C/EBPα or SREBP-1c (key transcription factors known to positively regulate adiponectin gene transcription) in the adipose tissue. Further, niacin had no effect on adipose tissue expression of ERp44, Ero1-Lα, or DsbA-L (key ER chaperones involved in adiponectin production and secretion). However, niacin treatment attenuated HFD-induced increases in adipose tissue gene expression of MCP-1 and IL-1β in the wild-type HFD-fed mice. Niacin also reduced the expression of the pro-inflammatory M1 macrophage marker CD11c in HFD-fed wild-type mice.ConclusionsNiacin treatment attenuates obesity-induced adipose tissue inflammation through increased adiponectin and anti-inflammatory cytokine expression and reduced pro-inflammatory cytokine expression in a niacin receptor-dependent manner.

Highlights

  • The incidence of obesity in the U.S has reached epidemic proportions within the last 30 years

  • Niacin had no effect on adipose tissue expression of ERp44, Ero1-La, or DsbA-L

  • Niacin reduced the expression of the pro-inflammatory M1 macrophage marker CD11c in HFDfed wild-type mice

Read more

Summary

Introduction

The incidence of obesity in the U.S has reached epidemic proportions within the last 30 years. Obesity is associated with an increased risk of metabolic and cardiovascular disease (CVD), with CVD being one of the leading causes of morbidity and mortality in the U.S [1]. Niacin clinically utilized as a monotherapy is an effective pharmacological intervention for the treatment of atherogenic dyslipidemia due to its ability to reduce carotid intima media thickness, improve endothelial function, and reduce CVD morbidity and mortality, presumably by improving blood lipid and lipoprotein characteristics. Along with producing modest reduction in circulating very low-density lipoprotein (VLDL), LDL-C, TG, and lipoprotein(a) concentrations, niacin is an effective pharmacological tool for increasing HDL-C concentrations [3,4,5,6]

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call