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Brain Natriuretic Peptide Stimulates Lipid Metabolism through Its Receptor NPR1 and the Glycerolipid Metabolism Pathway in Chicken Adipocytes

机译:脑利钠肽通过其受体NPR1和鸡脂肪细胞中的糖脂代谢途径刺激脂质代谢。

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摘要

Brain natriuretic peptide (BNP) is related to lipid metabolism in mammals, but its effect and the molecular mechanisms underlying it in chickens are incompletely understood. We found that the level of natriuretic peptide precursor B (NPPB, which encodes BNP) mRNA expression in high-abdominal-fat chicken groups was significantly higher than that of low-abdominal-fat groups. Partial correlations indicated that changes in the weight of abdominal fat were positively correlated with NPPB mRNA expression level. In vitro, compared with the control group, preadipocytes with NPPB interference showed reduced levels of proliferation, differentiation, and glycerin in media. Treatments of cells with BNP led to enhanced proliferation and differentiation of cells and glycerin concentration, and mRNA expression of its receptor natriuretic peptide receptor 1 (NPR1) was upregulated significantly. In cells exposed to BNP, 482 differentially expressed genes were identified compared with controls without BNP. Four genes known to be related to lipid metabolism (diacylglycerol kinase; lipase, endothelial; 1-acylglycerol-3-phosphate O-acyltransferase 1; and 1-acylglycerol-3-phosphate O-acyltransferase 2) were enriched in the glycerolipid metabolism pathway and expressed differentially. In conclusion, BNP stimulates the proliferation, differentiation, and lipolysis of preadipocytes through upregulation of the levels of expression of its receptor NPR1 and key genes enriched in the glycerolipid metabolic pathway.
机译:脑钠肽(BNP)与哺乳动物的脂质代谢有关,但其作用及其在鸡中的分子机制尚不完全清楚。我们发现高腹脂鸡组的利钠肽前体B(NPPB,编码BNP)mRNA表达水平显着高于低腹脂组。部分相关性表明,腹部脂肪重量的变化与NPPB mRNA表达水平呈正相关。在体外,与对照组相比,受到NPPB干扰的前脂肪细胞在培养基中的增殖,分化和甘油水平降低。用BNP处理细胞可增强细胞的增殖和分化以及甘油的浓度,其受体利钠肽受体1(NPR1)的mRNA表达也显着上调。与不含BNP的对照相比,在暴露于BNP的细胞中鉴定出482个差异表达的基因。已知与脂质代谢有关的四个基因(甘油甘油激酶;脂肪酶,内皮; 1-酰基甘油-3-磷酸O-酰基转移酶1;和1-酰基甘油-3-磷酸O-酰基转移酶2)在甘油脂代谢途径中富集,并且差异表达。总之,BNP通过上调其受体NPR1和富含甘油脂代谢途径的关键基因的表达水平来刺激前脂肪细胞的增殖,分化和脂解。

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