Premium
Exercise training increases hepatic endoplasmic reticulum (er) stress protein expression in MTP‐inhibited high‐fat fed rats
Author(s) -
Chapados Natalie Ann,
Lavoie JeanMarc
Publication year - 2010
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1643
Subject(s) - endoplasmic reticulum , medicine , endocrinology , unfolded protein response , atf6 , triglyceride , microsome , treadmill , chemistry , cholesterol , biochemistry , enzyme
The purpose of the study was: (1) to determine the effects of microsomal triglyceride transfer protein (MTP) inhibition on endoplasmic reticulum (ER) stress in liver, and (2) to determine if this response is altered in exercise‐trained rats. Female Sprague‐Dawley rats (6 weeks) fed either a standard (SD) or a high‐saturated fat (HF; 43% as energy) diet were trained (Tr) or kept sedentary (Sed) for 6 week. Exercise training consisted of continuous running on a motor‐driven rodent treadmill 5 times/week. Ten days before the end of these interventions, rats were administrated (ip) daily a MTP inhibitor (MTPX) or a placebo (P). MTPX injection resulted in a large ( p < 0.01) liver triacylglycerol (TAG) accumulation in SD and HF‐fed rats (∼200 mg g −1 ), irrespective of the training status, while plasma TAG levels were largely (∼80%) decreased ( p < 0.01). MTPX injection in HF but not in SD‐fed animals resulted in an increase in BiP/GRP78, ATF6, PERK, and XBP‐1 mRNA levels, ( p < 0.01) indicating an increase in the unfolding protein response (UPR) to ER stress. Interestingly, exercise training in rats fed the HF diet resulted in a further increase in BiP/GRP78 and XBP‐1 mRNA levels in MTPX animals ( p < 0.01). It is concluded that: (1) ER stress induced by MTPX occurs only in HF‐fed rats despite the fact that liver TAG levels were largely increased in both dietary models; (2) the increase in gene expression of UPR markers with training may constitute a protective mechanism against ER stress in liver. Copyright © 2010 John Wiley & Sons, Ltd.