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烟酸可增加高脂饮食喂养小鼠的脂联素水平并减少脂肪组织炎症。

Niacin increases adiponectin and decreases adipose tissue inflammation in high fat diet-fed mice.

机构信息

Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama, USA.

出版信息

PLoS One. 2013 Aug 13;8(8):e71285. doi: 10.1371/journal.pone.0071285. eCollection 2013.

Abstract

AIMS

To determine the effects of niacin on adiponectin and markers of adipose tissue inflammation in a mouse model of obesity.

MATERIALS AND METHODS

Male 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.

RESULTS

Niacin 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.

CONCLUSIONS

Niacin 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.

摘要

目的

在肥胖症小鼠模型中,确定烟酸对脂联素和脂肪组织炎症标志物的影响。

材料和方法

雄性 C57BL/6 小鼠被置于对照或高脂肪饮食(HFD)中,并在整个研究过程中维持在这种饮食上。在对照或高脂肪饮食 6 周后,开始给予载体或烟酸治疗,并维持 5 周。在 HCA2(-/-)(烟酸受体(-/-))小鼠中同时进行了相同的研究。

结果

烟酸使 HFD 喂养的野生型小鼠的抗炎脂联素血清浓度增加了 21%,但对瘦野生型或瘦或 HFD 喂养的 HCA2(-/-)小鼠没有影响。烟酸仅增加了 HFD 喂养的野生型小鼠的脂联素基因和蛋白表达。脂联素血清浓度、基因和蛋白表达的增加与脂肪组织中 PPARγ C/EBPα 或 SREBP-1c(已知正向调节脂联素基因转录的关键转录因子)表达的变化无关。此外,烟酸对脂肪组织 ERp44、Ero1-Lα 或 DsbA-L(涉及脂联素产生和分泌的关键内质网伴侣)的表达没有影响。然而,烟酸处理可减轻 HFD 诱导的野生型 HFD 喂养小鼠脂肪组织中 MCP-1 和 IL-1β 基因表达的增加。烟酸还降低了 HFD 喂养的野生型小鼠中促炎 M1 巨噬细胞标志物 CD11c 的表达。

结论

烟酸治疗通过增加脂联素和抗炎细胞因子的表达以及减少促炎细胞因子的表达,减轻了肥胖引起的脂肪组织炎症,这是一种依赖于烟酸受体的方式。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca68/3742781/5b945ced9d36/pone.0071285.g001.jpg

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