期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 319, 期 1, 页码 E11-E25出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00263.2019
关键词
amino acid response; autophagy; histone modification; protein deficiency
资金
- University of Illinois at Urbana-Champaign (UIUC) Research Board [RB14148]
- Vision 20/20 Grant from the Division of Nutritional Sciences in College of Agricultural, Consumer, and Environmental Sciences at UIUC
The present study examined the mechanism of a low-protein (LP) diet on hepatic lipid metabolism during gestation and lactation. Timed-pregnant Sprague-Dawley rats were fed a control or an LP diet during gestation and lactation. LP dams had increased hepatic triglyceride accumulation and a significantly higher aspartate/alanine transaminase ratio, accompanied by a decrease in the circulating very low-density/low-density lipoprotein ratio. Microtubule-associated protein 1 light-chain 3 beta (LC3B) expression was stimulated in LP dams along with increased histone acetylation. LP diet induced colocalization of the LC3 binding motif interacting proteins apolipoprotein B (APOB) or microsomal triglyceride transfer protein (MTTP) with LC3B, suggesting autophagic degradation. Histone deacetylase 3 (HDAC3) is found necessary to prevent lipid accumulation in response to amino acid deprivation in HepG2 cells. LC3B-mediated APOB protein degradation is related to increases in lipid accumulation. HDAC3 regulated LC3B-induced lipid accumulation potentially through autophagic degradation of APOB and MTTP in response to amino acid limitation caused by a low-protein diet.
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