| Autor: |
Hojnacki JL; Department of Biological Sciences, University of Lowell, MA 01854., Cluette-Brown JE, Mulligan JJ, Hagan SM, Mahony KE, Witzgall SK, Osmolski TV, Barboriak JJ |
| Jazyk: |
angličtina |
| Zdroj: |
Alcoholism, clinical and experimental research [Alcohol Clin Exp Res] 1988 Feb; Vol. 12 (1), pp. 149-54. |
| DOI: |
10.1111/j.1530-0277.1988.tb00150.x |
| Abstrakt: |
Male squirrel monkeys were fed increasing caloric percentages (0, 12, 24, and 36%) of ethanol (ETOH) substituted isocalorically for carbohydrate as part of a chemically defined liquid diet to assess how alcohol dose modifies plasma lipoproteins and liver function. A separate group of primates was used to define the dose at which elevations in plasma apolipoprotein B first occurred and to measure plasma alcohol levels. ETOH caused a dose-related, linear increase in high density lipoprotein (HDL) cholesterol which was primarily the result of increments in coronary protective HDL2 cholesterol. HDL2 total mass (lipid + protein) followed the pattern of HDL2 cholesterol. Animals fed the 12% regimen had plasma ETOH levels of approximately 49 mg/dl, the lowest low density lipoprotein (LDL) cholesterol, and the highest HDL2/HDL3 cholesterol ratio. Significant elevations in apolipoprotein B first appeared at 18% ETOH while higher doses (24 and 36%) caused increases in LDL cholesterol and HDL3, reduced HDL2/HDL3 ratios, and plasma alcohol levels of 142 and 202 mg/dl, respectively. Liver function tests were normal for all animals. Our results indicate that while a moderate ETOH caloric intake (12%) produces an antiatherogenic lipoprotein profile (decreases LDL/HDL, increases HDL2/HDL3), any coronary protection afforded by continued increases in HDL2 at higher doses may be attenuated by concurrent atherogenic alterations (increases LDL cholesterol, increases apolipoprotein B). |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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