title: Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors.
abstract: There is significant debate regarding high-density lipoprotein cholesterol (HDL-C) and high-fiber, low-fat diets. The present study was designed to examine the effects of lifestyle modification on the inflammatory/anti-inflammatory properties of HDL in obese men (n = 22) with metabolic syndrome factors. Subjects were placed on a high-fiber, low-fat diet in a 3-wk residential program where food was provided ad libitum and daily aerobic exercise was performed. Fasting blood was drawn pre- and postintervention for serum lipids, lipid hydroperoxides, and the ability of subject HDL to alter low-density lipoprotein (LDL)-induced monocyte chemotactic activity (MCA) in a human artery wall coculture. Induction of MCA by control LDL in the absence of HDL was normalized to 1.0. Values >1.0 after HDL addition indicated proinflammatory HDL; values <1.0 indicated anti-inflammatory HDL. In addition, proteins involved in regulating HDL function, apolipoprotein A-I (apoA-I), paraoxonase 1 and 3, and platelet-activating factor acetylhydrolase were measured. After 3 wk, decreases in total-cholesterol, LDL-cholesterol, HDL-C, triglycerides, total cholesterol-to-HDL cholesterol ratio, and lipid hydroperoxides (all P < 0.05) were noted. The HDL inflammatory index decreased (P < 0.05) from pro- (1.14 +/- 0.11) to anti-inflammatory (0.94 +/- 0.09). ApoA-I level and paraoxonase activity did not change; however, platelet-activating factor acetylhydrolase activity increased (P < 0.05). Despite a quantitative reduction in HDL-C, HDL converted from pro- to anti-inflammatory. These data indicate that intensive lifestyle modification improves the function of HDL even in the face of reduced levels, suggesting increased turnover of proinflammatory HDL.
authors.affiliation: Department of Physiological Science, and 2Atherosclerosis Research Unit, University of California, Los Angeles, California 90095, USA. croberts@ucla.edu
authors.forename: Christian K
authors.initials: CK
authors.lastname: Roberts
authors.forename: Carey
authors.initials: C
authors.lastname: Ng
authors.forename: Susan
authors.initials: S
authors.lastname: Hama
authors.forename: Anna Jane
authors.initials: AJ
authors.lastname: Eliseo
authors.forename: R James
authors.initials: RJ
authors.lastname: Barnard
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000209:etiology* / Q000276:immunology / Q000517:prevention & control; D004035:Diet Therapy / Q000379:methods*; D005081:Exercise Therapy / Q000379:methods*; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D008075:Lipoproteins, HDL / Q000276:immunology*; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000276:immunology / Q000628:therapy; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000276:immunology* / Q000628:therapy*; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D008075:Lipoproteins, HDL