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Individual Differences in Hyperlipidemia and Vitamin E Status in Response to Chronic Alcohol Self‐Administration in Cynomolgus Monkeys
Author(s) -
Lebold Katie M.,
Grant Kathleen A.,
Freeman Willard M.,
Wiren Kristine M.,
Miller Galen W.,
Kiley Caitlin,
Leonard Scott W.,
Traber Maret G.
Publication year - 2011
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2010.01364.x
Subject(s) - medicine , endocrinology , hyperlipidemia , triglyceride , vitamin e , oxidative stress , cholesterol , chemistry , vitamin , alcohol , lipid peroxidation , tocopherol , antioxidant , biochemistry , diabetes mellitus
Background: Chronic ethanol self‐administration induces oxidative stress and exacerbates lipid peroxidation. α‐Tocopherol is a potent lipid antioxidant and vitamin that is dependent upon lipoprotein transport for tissue delivery. Methods: To evaluate the extent to which vitamin E status is deranged by excessive alcohol consumption, monkeys voluntarily drinking ethanol (1.36 to 3.98 g/kg/d for 19 months, n = 11) were compared with nondrinkers ( n = 5, control). Results: Three alcohol‐drinking animals developed hyperlipidemia with plasma triglyceride levels (1.8 ± 0.9 mM) double those of normolipidemic (NL) drinkers (0.6 ± 0.2) and controls (0.6 ± 0.3, p < 0.05); elevated plasma cholesterol (3.6 ± 0.5 mM) compared with NL drinkers (2.3 ± 0.2, p < 0.05) and controls (2.9 ± 0.3); and lower plasma α‐tocopherol per triglycerides (14 ± 6 mmol/mol) than controls (27 ± 8) and NL drinkers (23 ± 6, p < 0.05). Hyperlipidemic monkey liver α‐tocopherol (47 ± 15 nmol/g) was lower than NL drinkers (65 ± 13) and controls (70 ± 15, p = 0.080), as was adipose α‐tocopherol (84 ± 37 nmol/g) compared with controls (224 ± 118) and NL drinkers (285 ± 234, p < 0.05). Plasma apolipoprotein (apo) CIII increased compared to baseline at both 12 and 19 months in the normolipidemic ( p = 0.0016 and p = 0.0028, respectively) and in the hyperlipidemic drinkers ( p < 0.05 and p < 0.05, respectively). Plasma apo H concentrations at 19 months were elevated hyperlipidemics ( p < 0.05) relative to concentrations in control animals. C‐reactive protein (CRP), a marker of inflammation, was increased compared to baseline at both the 12‐ and 19‐month time points in the normolipidemic ( p = 0.005 and p = 0.0153, respectively) and hyperlipidemic drinkers ( p = 0.016 and p = 0.0201, respectively). Conclusion: A subset of alcohol‐drinking monkeys showed a predisposition to alcohol‐induced hyperlipidemia. The defect in lipid metabolism resulted in lower plasma α‐tocopherol per triglycerides and depleted adipose tissue α‐tocopherol, and thus decreased vitamin E status.