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High Dietary Glucose Intake Increases Hepatic Triglyceride Content and Oxidative Stress: Contributions of Angiotensin Receptor
Author(s) -
Montez Priscilla,
Max Thorwald A.,
Rodriguez Ruben,
Viscarra Jose,
Vázquez-Medina José Pablo,
Nakano Daisuke,
Nishiyama Akira,
Ortiz Rudy M
Publication year - 2012
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.26.1_supplement.714.8
Subject(s) - medicine , endocrinology , chemistry , olmesartan , oxidative stress , triglyceride , insulin resistance , nitrotyrosine , angiotensin ii , insulin , cholesterol , receptor , blood pressure , nitric oxide synthase , nitric oxide
Excessive glucose intake exacerbates the deposition of adipose and plasma lipid levels and can subsequently increase organ‐specific oxidative damage during insulin resistance. To test our hypothesize that angiotensin receptor contributes to increased hepatic triglyceride content and oxidative stress following increased glucose intake in a model of metabolic syndrome, we studied 5 groups of rats: 1) LETO (lean control strain), 2) OLETF (15 wk), 3) OLETF + ARB (10 mg olmesartan mg/kg/d), 4) OLETF + high glucose (HG; 5% in water) and 5) OLETF + ARB + HG. HG had increased plasma triglycerides (TG) (35%), plasma glycerol (87%), free fatty acids (FFA) (28%) and body mass (BM) (37%), indicative of dislipidemia, as well as increased (74%) hepatic lipid peroxidation (4‐HNE). ARB treatment in HG reduced plasma TG (15%), plasma glycerol (23%), FFA (14%), BM (12%), and hepatic TG content (42%). ARB treatment in HG also decreased hepatic nitrotyrosine and increased UCP2 protein expression (59%), aconitase (40%) and antioxidant enzyme activities 50–120% suggesting that AT1 activation contributes to protein oxidation, lipid metabolism, fat deposition and lipid‐associated hepatic oxidative stress. Thus, besides the antihypertensive effects of ARB treatment, ARBs can also improve the condition of metabolic syndrome by improving the lipid profile and reducing adiposity and oxidative stress. Funded by NIH NCMHD 9T37MD001480 & P20MD005049.