Abstract
Context and objective. Lipoproteins are involved in the pathophysiology of several metabolic diseases. Here we focus on the interplay between lipoprotein metabolism and adiponectin with the extension of alcohol intake. Design and subjects. Eighty-three low-to-moderate and 80 heavy alcohol drinkers were studied. Plasma adiponectin, other biochemical and extensive lipoprotein data were measured. Self-organizing maps were applied to characterize lipoprotein phenotypes and their interrelationships with biochemical measures and alcohol consumption. Results. Alcohol consumption and plasma adiponectin had a strong positive association. Heavy alcohol consumption was associated with decreased low-density lipoprotein cholesterol (LDL-C). Nevertheless, two distinct lipoprotein phenotypes were identified, one with elevated high-density lipoprotein cholesterol (HDL-C) and decreased very-low-density lipoprotein triglycerides (VLDL-TG) together with low prevalence of metabolic syndrome, and the other vice versa. The HDL particles were enlarged in both phenotypes related to the heavy drinkers. The low-to-moderate alcohol drinkers were characterized with high LDL-C and C-enriched LDL particles. Conclusions. The analyses per se illustrated the multi-faceted and non-linear nature of lipoprotein metabolism. The heavy alcohol drinkers were characterized either by an anti-atherogenic lipoprotein phenotype (with also the highest adiponectin concentrations) or by a phenotype with pro-atherogenic and metabolic syndrome-like features. Clinically this underlines the need to distinguish the differing individual risk for lipid-related metabolic disturbances also in heavy alcohol drinkers.
Declaration of interest: The authors state no conflict of interest and have received no payment in preparation of this manuscript.
Acknowledgements
We thank Sari Pyrhönen, Marja-Leena Kytökangas, and Saara Korhonen for their skillful technical assistance and the staff of the Alcoholism Treatment Unit of Oulu for their valuable help. In addition, all the study subjects are warmly thanked. This study received funding from the Aarne Koskelo Foundation (M.L.H.), the Academy of Finland research funding (M.J.S.), the Academy of Finland's Responding to Public Health Challenges Research Programme (SALVE) (M.J.S., M.A.K.), the Finnish Cardiovascular Research Foundation (S.M.K., M.J.S., M.L.H., M.A.K.), the Finnish Cultural Foundation (S.M.K., V.P.M.), the Finnish Foundation for Alcohol Studies (M.J.S.), the Jenny and Antti Wihuri Foundation (S.M.K., V.P.M.), the Maud Kuistila Memorial Foundation (S.M.K.), the North Ostrobothnia Regional Fund of the Finnish Cultural Foundation (M.L.H.), the Orion-Farmos Research Foundation (S.M.K.), the Paavo Nurmi Foundation (M.L.H.), and the Sigrid Jusélius Foundation (S.M.K., M.J.S., M.L.H.).