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首页> 外文期刊>The Journal of Nutritional Biochemistry >Western diet consumption through early life induces microvesicular hepatic steatosis in association with an altered metabolome in low birth weight Guinea pigs
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Western diet consumption through early life induces microvesicular hepatic steatosis in association with an altered metabolome in low birth weight Guinea pigs

机译：通过早期生命的西方饮食消耗诱导微绒毛肝脏脂肪变性与低出生体重豚鼠的改变的代谢物

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摘要

Uteroplacental insufficiency-induced low birth weight (LBW) and postnatal high saturated fat/high sucrose-fructose diet (Western Diet, WD) consumption have been independently associated with the development of hepatic steatosis, while their additive effect on fatty acid, acylcarnitine and amino acid profiles in early adulthood have not been widely reported. We employed LBW, generated via uterine artery ablation, and normal birth weight (NBW) male guinea pigs fed either a WD or control diet (CD) from weaning to postnatal day 150 (early adulthood). Hepatic steatosis was absent in CD-fed offspring, while NBW/WD offspring displayed macrovesicular steatosis and LBW/WD offspring exhibited microvesicular steatosis, both occurring in a lean phenotype. Life-long consumption of the WD, irrespective of birth weight, was associated with an increase in hepatic medium- and long-chain saturated fatty acids, monounsaturated fatty acids, acylcarnitines, reduced oxidative phosphorylation complex III activity and polyunsaturated fatty acids, and molecular evidence of disrupted hepatic insulin signaling. In NBW/WD, hepatic C15:1 and C16:1n-6 fatty acids in phospholipids, C16, C18 and C18:1 acylcarnitines, concentrations of aspartate, phenylalanine, tyrosine and tryptophan and expression of carnitine palmitoyltransferase 1 alpha (CPT1 alpha) and uncoupling protein 2 (UCP2) genes were elevated compared to LBW/WD livers. Our results suggest that LBW and life-long WD combined are influential in promoting hepatic microvesicular steatosis in conjunction with a specific mitochondrial gene expression and metabolomic profile in early adulthood. (C) 2019 Elsevier Inc. All rights reserved.
机译：子宫内科功能诱导的低出生体重（LBW）和产后高饱和脂肪/高蔗糖 - 果糖饮食（西方饮食，WD）消费与肝脏脂肪变性的发育独立相关，同时对脂肪酸，酰基肉碱和氨基的添加剂作用已经过度报道了成年早期的酸性谱。我们使用通过子宫动脉消融产生的LBW，以及喂养WD或对照饮食（CD）的正常出生体重（NBW）雄性豚鼠从断奶前至后的第150天（成年早期）。在CD-FED后代不存在肝脏脂肪变性，而NBW / WD后代显示宏观分析和LBW / WD后代表现出微血管脂肪变性，两者都处于瘦肉表型。无论出生体重如何，WD的终生消耗与出生体重有关，与肝脏中链和长链饱和脂肪酸，单不饱和脂肪酸，酰基碱，降低氧化磷酸化复合体III活性和多不饱和脂肪酸的增加有关，以及分子证据破坏肝胰岛素信号传导。在NBW / WD，肝脏C15：1和C16：1N-6脂肪酸中的磷脂，C16，C18和C18：1酰基甘氨酸浓度，苯丙氨酸浓度，苯丙氨酸，酪氨酸和色氨酸和肉毒碱棕榈酰转移酶1α（CPT1α）的表达和表达与LBW / WD肝脏相比，升高了蛋白2（UCP2）基因。我们的研究结果表明，LBW和寿命长的WD在成年早期结合特定的线粒体基因表达和代谢组分，促进肝脏微绒毛脂肪变化是有影响力的。 （c）2019 Elsevier Inc.保留所有权利。

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