Alcohol Induced Lipid DYS-homeostasis in the Prefrontal Cortex of Diabetic Rats
Shallie Philemon Dauda, Adebukola Adenuga, Adejumo Esther Ngozi, Ihyar Alamun Clement, Shotunde Damilola Faith, Esegbue Peters
International Journal of Biochemistry Research & Review · pp. 559–567 · Published 23 Jul 2014
10.9734/IJBCRR/2014/6380Abstract
Aim: To investigate the potential importance of the association between alcohol consumption, diabetes andlipid homeostasisin the prefrontal cortex. Study Design: Twenty-four adult rats were randomly divided into four groups of six rats each viz; Group 1- Control, given rat pellets and water ad libitum; Group 2- Diabetic, diabetes was induced with a single dosage of 120mg/kg body weight followed by 50mg/kg body weight of alloxan weekly. Group 3- Diabetic and low alcohol intake (9% w/w). Group 4- Diabetic and high alcohol intake (20% w/w). Place and Duration of Study: This work was carried out in the Department of Anatomy; Olabisi Onabanjo University, Ago-Iwoye, Nigeria between February and April, 2012. Methodology: The skull was dissected and the brain removed and the prefrontal cortex excised, homogenized, centrifuged and the supernatant analyzed for lipid profile, AST and ALT. Results: Diabetes elevates the levels of ALT and AST significantly at P=0.05 when compared to the normal control group (67.33+/-0.15 versus 59.25+/-0.25 and 135.50±0.50 versus 75.50+/-0.50) respectively. The TG levels increase significantly at P=0.05 in the diabetic group compared to the normal control group (92.01+/-0.18 versus 72.62+/-0.52) whereas the total cholesterol and HDL levels decrease in the diabetic group when compared to normal control group (34.99+/-0.40 versus 37.28+/-0.23 and 150.90+/-0.33 versus 103.29+/-0.23 respectively). Concomitant alcohol intake lowered the levels of all parameters significantly at P=0.05. Conclusion: Our findings showed that, both low and high chronic alcohol intake in diabetes disturbed lipid homeostasis in the prefrontal cortex, probably by lowering ALT and AST levels or via the mechanism that suppresses the enzymes of lipid syntheses in the prefrontal cortex.
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