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神经肽Y促进原代培养的人脂肪来源干细胞的成脂分化。

Neuropeptide Y promotes adipogenic differentiation in primary cultured human adipose-derived stem cells.

作者信息

Liu Min, Liu Hong, Liang Fang, Song Xiao-Qin, Hu Ping-An

机构信息

Department of Clinical Nutrition, the Third Xiangya Hospital of Central South University, Changsha 410013, Hunan, China.

Department of Endocrinology, the Third Xiangya Hospital of Central South University, Changsha 410013, Hunan, China.

出版信息

Endocr J. 2018 Jan 30;65(1):43-52. doi: 10.1507/endocrj.EJ17-0017. Epub 2017 Sep 28.

Abstract

Neuropeptide Y (NPY) is an important neurotransmitter in the control of energy metabolism. Several studies have shown that obesity is associated with increased levels of NPY in the hypothalamus. We hypothesized that the release of NPY has coordinated and integrated effects on energy metabolism in different tissues, such as adipocyte tissue, resulting in increased energy storage and decreased energy expenditure. Whether NPY has role in the molecular mechanism of human adipocyte tissue remains unclear. We established the model of human adipose derived stem cells (hADSCs) from human adipose tissue and differentiated it into adipocytes in the presence of NPY at different concentrations (10-10 mmol/L). We then assessed hADSCs proliferation and differentiation by quantifying lipid accumulation and examining the expression levels of related adipocyte markers after differentiation. Furthermore, the specific markers of white adipocyte tissue (WAT) in hADSCs were also analyzed. The results showed that low doses of NPY stimulated hADSCs proliferation (p < 0.05), while high doses of NPY inhibited hADSCs proliferation (p < 0.05). NPY significantly promoted lipid accumulation and increased the size of lipid droplets during human adipogenic differentiation; the levels of adipocyte markers PPAR-γ and C/EBPα were also increased. At the same time, NPY also increased the levels of WAT markers Cidec and RIP140 after adipocyte differentiation. The results suggested high dose NPY inhibits the proliferation of hADSCs while promotes adipocyte differentiation and increases the expression of WAT markers. This may be the reason why increased levels of NPY can lead to a rise in body weight.

摘要

神经肽Y(NPY)是能量代谢控制中的一种重要神经递质。多项研究表明,肥胖与下丘脑NPY水平升高有关。我们推测,NPY的释放对不同组织(如脂肪组织)的能量代谢具有协调和整合作用,导致能量储存增加和能量消耗减少。NPY在人类脂肪组织的分子机制中是否起作用仍不清楚。我们从人类脂肪组织建立了人脂肪来源干细胞(hADSCs)模型,并在不同浓度(10⁻¹⁰ mmol/L)的NPY存在下将其分化为脂肪细胞。然后,我们通过量化脂质积累和检测分化后相关脂肪细胞标志物的表达水平来评估hADSCs的增殖和分化。此外,还分析了hADSCs中白色脂肪组织(WAT)的特异性标志物。结果表明,低剂量的NPY刺激hADSCs增殖(p < 0.05),而高剂量的NPY抑制hADSCs增殖(p < 0.05)。NPY在人类脂肪生成分化过程中显著促进脂质积累并增加脂滴大小;脂肪细胞标志物PPAR-γ和C/EBPα的水平也有所增加。同时,NPY在脂肪细胞分化后还增加了WAT标志物Cidec和RIP140的水平。结果表明,高剂量NPY抑制hADSCs的增殖,同时促进脂肪细胞分化并增加WAT标志物的表达。这可能是NPY水平升高导致体重增加的原因。

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