Abstract
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 significantly higher aspartate/alanine transaminase ratio, accompanied by a decrease in circulating very low-density/low-density lipoprotein ratio. LC3B (Microtubule Associated Protein 1 Light Chain 3 Beta) expression was stimulated in LP dams along with increased histone acetylation. LP diet-induced co-localization of the LC3 binding motif-interacting proteins APOB or MTTP with LC3B, suggesting autophagic degradation. 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. Conclusion: 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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