Pharmacological effects of lipid-lowering drugs on circulating adipokines

The cardioprotective effects of lipid-lowering drugs have been primarily attributed to their effects on blood lipid metabolism.However,emerging evidence indicates that lipid-lowering drugs also modulate the synthesis and secretion of adipose tissue-secreted proteins referred to as adipokines.Adipoki...

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Published in:World journal of diabetes Vol. 1; no. 4; pp. 116 - 128
Main Authors: Wanders, Desiree, Plaisance, Eric P, Judd, Robert L
Format: Journal Article
Language:English
Published: United States Baishideng Publishing Group Co., Limited 15-09-2010
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Summary:The cardioprotective effects of lipid-lowering drugs have been primarily attributed to their effects on blood lipid metabolism.However,emerging evidence indicates that lipid-lowering drugs also modulate the synthesis and secretion of adipose tissue-secreted proteins referred to as adipokines.Adipokines influence energy homeostasis and metabolism and have also been shown to modulate the vascular inflammatory cascade.The purpose of this review will be to examine the reported effects of commonly used lipid-lowering drugs(statins,fibrates,niacin and omega-3-fatty acids) on the circulating concentrations of leptin,adiponectin,tumor necrosisfactor-α(TNF-α),Retinol binding protein 4(RBP4) and resistin.Overall,the lipid-lowering drugs reviewed have minimal effects on leptin and resistin concentrations.Conversely,circulating adiponectin concentrations are consistently increased by each lipid-lowering drug reviewed with the greatest effects produced by niacin.Studies that have examined the effects of statins,niacin and omega-3-fatty acids on TNF-α demonstrate that these agents have little effect on circulating TNF-α concentrations.Niacin and fibrates appear to lower RBP4 but not resistin concentrations.The results of the available studies suggest that a strong relationship exists between pharmacological reductions in blood lipids and adiponectin that is not obvious for other adipokines reviewed.
Bibliography:Desiree Wanders,Robert L Judd,Department of Anatomy,Physiology and Pharmacology,College of Veterinary Medicine,Auburn University,Auburn,AL 36849,United States Eric P Plaisance,Laboratory of Nutrient Sensing and Adipocyte Signaling,Pennington Biomedical Research Center,Baton Rouge,LA 70808,United States
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Author contributions: Wanders D, Plaisance EP and Judd RL contributed equally to this paper.
Correspondence to: Robert L Judd, PhD, Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, 219 Greene Hall, Auburn, AL 36849, United States. juddrob@auburn.edu
ISSN:1948-9358
1948-9358
DOI:10.4239/wjd.v1.i4.116