妊娠后期过量喂养奶牛改变肝脏ppar α调控通路,包括肝因子:对代谢和外周胰岛素敏感性的影响

Gene regulation and systems biology Pub Date : 2014-04-03 eCollection Date: 2014-01-01 DOI:10.4137/GRSB.S14116
M Jawad Khan, Carolina B Jacometo, Daniel E Graugnard, Marcio N Corrêa, Eduardo Schmitt, Felipe Cardoso, Juan J Loor
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引用次数: 67

摘要

研究了妊娠最后45 d饲喂控制饲粮(CON, 1.34 Mcal/kg)和高能量饲粮(OVE, 1.62 Mcal/kg)的奶牛肝脏代谢基因网络。共57个靶基因,包括ppar α-靶点/共调节因子、肝因子、生长激素(GH)/胰岛素样生长因子1 (IGF-1)轴、脂肪生成和脂蛋白代谢,在分娩前后-14、7、14和30天进行评估。OVE奶牛与CON奶牛相比,产后负能量平衡(NEB)更严重,血清非酯化脂肪酸(NEFA)、β-羟基丁酸(BHBA)和肝脏甘油三酯(TAG)浓度更高。乳汁合成速率无显著差异。OVE奶牛的肝脏通过上调脂肪酸氧化和生酮途径中ppar α-靶点以及糖异生基因的表达来响应产后NEB。产后肝因子(成纤维细胞生长因子21 (FGF21),血管生成素样4 (ANGPTL4))和载脂蛋白a - v (APOA5)在OVE组的上调幅度大于con组。OVE导致更高的血胰岛素准备,更低的NEFA:胰岛素,更高的脂肪生成基因表达,表明胰岛素敏感性未受损。在饲喂OVE的奶牛中,APOB、MTTP和PNPLA3缺乏变化,加上产后PLIN2的上调,导致了TAG的积累。NEFA和FGF21伴OVE的产后反应支持该肝因子在降低脂肪胰岛素敏感性中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Overfeeding Dairy Cattle During Late-Pregnancy Alters Hepatic PPARα-Regulated Pathways Including Hepatokines: Impact on Metabolism and Peripheral Insulin Sensitivity.

Overfeeding Dairy Cattle During Late-Pregnancy Alters Hepatic PPARα-Regulated Pathways Including Hepatokines: Impact on Metabolism and Peripheral Insulin Sensitivity.

Overfeeding Dairy Cattle During Late-Pregnancy Alters Hepatic PPARα-Regulated Pathways Including Hepatokines: Impact on Metabolism and Peripheral Insulin Sensitivity.

Overfeeding Dairy Cattle During Late-Pregnancy Alters Hepatic PPARα-Regulated Pathways Including Hepatokines: Impact on Metabolism and Peripheral Insulin Sensitivity.

Hepatic metabolic gene networks were studied in dairy cattle fed control (CON, 1.34 Mcal/kg) or higher energy (overfed (OVE), 1.62 Mcal/kg) diets during the last 45 days of pregnancy. A total of 57 target genes encompassing PPARα-targets/co-regulators, hepatokines, growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis, lipogenesis, and lipoprotein metabolism were evaluated on -14, 7, 14, and 30 days around parturition. OVE versus CON cows were in more negative energy balance (NEB) postpartum and had greater serum non-esterified fatty acids (NEFA), β-hydroxybutyrate (BHBA), and liver triacylglycerol (TAG) concentrations. Milk synthesis rate did not differ. Liver from OVE cows responded to postpartal NEB by up-regulating expression of PPARα-targets in the fatty acid oxidation and ketogenesis pathways, along with gluconeogenic genes. Hepatokines (fibroblast growth factor 21 (FGF21), angiopoietin-like 4 (ANGPTL4)) and apolipoprotein A-V (APOA5) were up-regulated postpartum to a greater extent in OVE than CON. OVE led to greater blood insulin prepartum, lower NEFA:insulin, and greater lipogenic gene expression suggesting insulin sensitivity was not impaired. A lack of change in APOB, MTTP, and PNPLA3 coupled with upregulation of PLIN2 postpartum in cows fed OVE contributed to TAG accumulation. Postpartal responses in NEFA and FGF21 with OVE support a role of this hepatokine in diminishing adipose insulin sensitivity.

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