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富含饱和脂肪酸的饮食在发育期关键期损害营养不良大鼠肝脏线粒体生物能学

Saturated Fatty Acid-Enriched Diet-Impaired Mitochondrial Bioenergetics in Liver From Undernourished Rats During Critical Periods of Development.

机构信息

Laboratory of Nutrition, Physical Activity and Phenotypic Plasticity, Federal University of Pernambuco-UFPE, Vitória de Santo Antão, PE 55608-680, Brazil.

Laboratoire de Recherche en Cardiovasculaire, Métabolisme, Diabétologie et Nutrition (CarMeN), INSERM U1060, INRA U1397, Université Claude Bernard Lyon1, 69921 Oullins, France.

出版信息

Cells. 2019 Apr 10;8(4):335. doi: 10.3390/cells8040335.

DOI:10.3390/cells8040335
PMID:30974751
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6523252/
Abstract

The nutritional transition that the western population has undergone is increasingly associated with chronic metabolic diseases. In this work, we evaluated a diet rich in saturated fatty acids (hyperlipidic, HL) after weaning of the offspring rats submitted to maternal protein restriction on the hepatic mitochondrial bioenergetics. Wistar rats were mated and during gestation and lactation, mothers received control diets (NP, normal protein content 17%) or low protein (LP, 8% protein). After weaning, rats received either NL (normolipidic) or HL (+59% SFA) diets up to 90 days of life. It was verified that all respiratory states of hepatic mitochondria showed a reduction in the LP group submitted to the post-weaning HL diet. This group also presented greater mitochondrial swelling compared to controls, potentiated after Ca addition and prevented in the presence of EGTA (calcium chelator) and cyclosporin A (mitochondrial permeability transition pore inhibitor). There was also an increase in liver protein oxidation and lipid peroxidation and reduction in catalase and glutathione peroxidase activities in the LP group fed HL diet after weaning. Our data suggest that adult rats subjected to maternal protein restriction were more susceptible to hepatic mitochondrial damage caused by a diet rich in saturated fatty acids post-weaning.

摘要

西方人群经历的营养转型与慢性代谢性疾病的发生日益相关。在这项工作中,我们评估了断奶后幼鼠的高脂肪饮食(富含饱和脂肪酸,HL)对其肝脏线粒体生物能量学的影响,这些幼鼠的母亲在孕期和哺乳期接受了蛋白质限制饮食(LP,蛋白质含量 8%)或正常蛋白饮食(NP,正常蛋白含量 17%)。断奶后,幼鼠接受 NL(正常脂质)或 HL(+59% SFA)饮食,直至 90 天。结果发现,所有呼吸状态下的肝脏线粒体在接受断奶后 HL 饮食的 LP 组中均显示出减少。与对照组相比,该组还表现出更大的线粒体肿胀,在添加 Ca 后加剧,并且在 EGTA(钙螯合剂)和环孢素 A(线粒体通透性转换孔抑制剂)存在的情况下被阻止。在断奶后接受 HL 饮食的 LP 组中,还观察到肝蛋白氧化和脂质过氧化增加,以及过氧化氢酶和谷胱甘肽过氧化物酶活性降低。这些数据表明,在哺乳期接受蛋白质限制的成年大鼠在断奶后更容易受到富含饱和脂肪酸饮食引起的肝脏线粒体损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/bba276a2768a/cells-08-00335-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/cb393754c8ac/cells-08-00335-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/dba3a4510770/cells-08-00335-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/d1bb21e9b686/cells-08-00335-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/ffe6756fe68c/cells-08-00335-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/bba276a2768a/cells-08-00335-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/cb393754c8ac/cells-08-00335-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/dba3a4510770/cells-08-00335-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/d1bb21e9b686/cells-08-00335-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/ffe6756fe68c/cells-08-00335-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af63/6523252/bba276a2768a/cells-08-00335-g005.jpg

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