Premium
Effects of selenium on apoptosis and abnormal amino acid metabolism induced by excess fatty acid in isolated rat hepatocytes
Author(s) -
Zhang Zhigang,
Li Siyu,
Jiang Huijie,
Liu Biying,
Lv Zhanjun,
Guo Changming,
Zhang Haili
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700016
Subject(s) - insulin resistance , oxidative stress , apoptosis , palmitic acid , endocrinology , medicine , fatty acid , fatty acid metabolism , metabolism , antioxidant , chemistry , fatty liver , biology , lipotoxicity , insulin , biochemistry , disease
Scope Increased serum free fatty acid (FFA) occurs in subjects with non‐alcoholic fatty liver disease (NAFLD) and also triggers oxidative stress, apoptosis, and insulin resistance. Selenium (Se) is an antioxidant agent. However, the effect of Se on NAFLD or diabetes is still unclear. We investigated the effect of Se on apoptosis and abnormal amino acid metabolism initiated by excess FFA in isolated rat hepatocytes. Methods and results Primary hepatocytes from rats were isolated and exposed to excessive FFA (0.5 mM oleate/palmitic acid 2:1) and 0.1 μM Se. Se protected primary hepatocytes against oxidative stress and apoptosis induced by excess FFA, but did not play a role on abnormal amino acid metabolism and insulin resistance initiated by FFA in isolated rat hepatocytes. Conclusion Although Se had the capability of preventing the apoptosis initiated by ROS, insulin resistance failed to be reversed in hepatocytes exposed to FFA. This failure may be attributed to the limitation of Se in regulating branched chain amino acids abundance. This indicates that apoptosis and insulin resistance might be involved in different pathways when isolated hepatocytes were exposed to FFA and Se.