Literature DB >> 28851736

Short-term changes in diet composition do not affect in vivo hepatic protein synthesis in rats.

Andrea Lee Estrada1, William Max Hudson1, Paul Y Kim2, Claire Marie Stewart1, Frederick F Peelor3, Yuren Wei1, Dong Wang1, Karyn L Hamilton3, Benjamin F Miller3, Michael J Pagliassotti1.   

Abstract

Protein synthesis is critical to protein homeostasis (proteostasis), and modifications in protein synthesis influence lifespan and the development of comorbidities associated with obesity. In the present study, we examined the acute response of liver protein synthesis to either high-fat or high-sucrose diets in order to elucidate nutrient-mediated regulation of hepatic protein synthesis in the absence of body fat accumulation. Total and endoplasmic reticulum-associated protein syntheses were assessed by use of the stable isotope, deuterium oxide (2H2O), in rats provided a control diet or diets enriched in polyunsaturated fat, saturated fat, or sucrose for 2, 4, or 7 days. The three experimental diets increased hepatic triglycerides 46-91% on day 7 and fasting insulin levels 83-117% on day 7, but did not result in differences in body weight when compared with control ( n = 6/diet/time). The fraction of newly synthesized proteins in total liver lysates and microsomes was not significantly different among dietary groups ( n = 3/diet/time). To determine whether the experimental diets provoked a transcriptional response to enhance the capacity for protein synthesis, we also measured a panel of genes linked to amino acid transport, synthesis, and processing. There were no significant differences in any of the genes measured among groups. Therefore, dietary treatments that have been linked to impaired proteostasis and that promote hepatic steatosis and insulin resistance, did not result in significant changes in total or ER-associated protein synthesis in the liver over a 7-day period.

Entities:  

Keywords:  endoplasmic reticulum; insulin resistance; liver; proteostasis; steatosis

Mesh:

Substances:

Year:  2017        PMID: 28851736      PMCID: PMC5899216          DOI: 10.1152/ajpendo.00209.2017

Source DB:  PubMed          Journal:  Am J Physiol Endocrinol Metab        ISSN: 0193-1849            Impact factor:   4.310


  45 in total

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