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The unfolded protein response is not involved in trans‐10, cis‐ 12 CLA induced hepatic steatosis in the mouse
Author(s) -
Hussein Mahmoud,
Giesy Sarah,
Krumm Christopher,
Long Oiaoming,
Bauman Dale,
Boisclair Yves
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.637.24
Subject(s) - steatosis , lipogenesis , hyperinsulinemia , medicine , endocrinology , conjugated linoleic acid , unfolded protein response , chemistry , adipose tissue , linoleic acid , biology , insulin resistance , fatty acid , biochemistry , insulin , endoplasmic reticulum
Chronic intake of trans ‐10, cis ‐12 conjugated linoleic acid ( t 10, c 12 CLA) reduces adiposity in mice. However, it also causes hyperinsulinemia and increases lipogenic gene expression and lipid accumulation in liver. Recently, components of the unfolded protein response (UPR) have been shown to mediate a portion of the effects of hyperinsulinemia on hepatic lipogenesis. To determine whether UPR contributes to the effect of CLA on hepatic steatosis, C57BL/6J female mice were offered diets supplemented with either 1% oleic acid or t 10, c 12 CLA for 4 weeks. As expected, t 10, c 12 CLA reduced adipose tissue mass and simultaneously increased plasma insulin and hepatic lipid deposition. t 10, c 12 CLA increased the hepatic expression of key enzymes involved in fatty acid synthesis, esterification and uptake. t 10, c 12 CLA, however, did not alter the mRNA expression or protein level of the key UPR components, IRE1α, spliced XBP1, CHOP, BiP and SEL1L. We conclude that the UPR is not involved in mediating the effects of t 10, c 12 CLA on hepatic steatosis.