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Oral N‐acetylcysteine prevents the impairment of muscle and liver insulin signaling pathway induced by a high‐sucrose diet in the rat
Author(s) -
Blouet Clemence,
Mariotti François,
AzzoutMarniche Dalila,
Tomé Daniel,
Huneau JeanFrançois
Publication year - 2006
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.20.4.a594-d
Subject(s) - medicine , endocrinology , insulin , oxidative stress , acetylcysteine , glutathione , protein kinase b , chemistry , homeostasis , sucrose , insulin receptor , glucose homeostasis , insulin resistance , phosphorylation , antioxidant , biochemistry , enzyme
A high‐sucrose (HS) diet increases oxidative stress and impairs glucose homeostasis. This study was designed to investigate the capacity of moderate or high NAC intake to reduce oxidative stress, increase insulin sensitivity and improve insulin signaling in HS‐fed rats. Male Wistar rats (32) were assigned for 6 weeks to a standard starch diet (S) or to HS diets either enriched with 5.5 g.kg−1 NAC (C1), 16 g.kg−1 NAC (C2) or not enriched (C0). Results are expressed as means ± SEM. On week 5, glucose and insulin AUC following an oral glucose challenge were significantly higher in C0 rats compared to S rats. This increase was dose‐dependently prevented by NAC. The resulting HOMA indexes were similar in S and C2 rats, and significantly lower than those of C1 and C0 rats (300 ± 51, 303 ± 102, 597 ± 105 and 708 ± 88 for S, C2, C1 and C0, respectively). Phosphorylation of IRS‐1 (pTyr) and Akt (pSer) in muscle 5 min. after iv insulin injection were halved in C0 rats compared to S rats, whereas no difference was observed between C2 and S rats. In the liver, no difference was observed between groups regarding IRS‐1 pTyr, whereas Akt pSer was lower in C0 rats compared to both S and C2 rats. Tissue glutathione ratio and plasma protein carbonyl content were higher in C0 rats compared to S rats. This increase was dose‐dependently prevented by NAC. Taken together, these data show that cysteine supplementation limits the HS‐induced impairment of the insulin signaling pathway, and suggest that this could be mediated by a reduction in oxidative stress.