Association of lifestyle factors, polymorphisms in adiponectin, perilipin and hormone sensitive lipase, and clinical markers in Japanese males.

According to recent genome-wide association studies, a number of single nucleotide polymorphisms is reported to be associated with diseases or several clinical markers. Among them, adiponectin (ADIPOQ) and perilipin (PLIN) polymorphisms are major factors of obesity. However, the association between lifestyle factor, these polymorphisms and obesity-related clinical markers in Japanese is not well researched. Therefore, the aim of present study is to investigate the association between lifestyle factor, polymorphisms of lipid metabolic genes, and clinical markers in 148 middle-aged Japanese males. The study revealed that ADIPOQ 45 T>G and ADIPOQ 276 G>T genotypes were significantly associated with triglyceride, total cholesterol, hemoglobin A1c (HbA1c) in blood and body mass index (BMI). PLIN4 11482 G>A and hormone sensitive lipase (LIPE)-60 C>G genotypes were respectively associated with BMI and serum triglyceride. Not only genetic factors but also lifestyle factors influence several clinical markers. The BMI of subjects who like sweets and have the GG allele in ADIPOQ 276 G>T was higher than that of subjects who don't like sweets. The habit of eating fruits and fish affected low-density lipoprotein-cholesterol of the GT allele and HbA1c of the TT allele in ADIPOQ 276 G>T. Those findings indicate improvement and conservation of lifestyle depending on genetic predisposition in ADIPOQ, PLIN and LIPE should be encouraged.

Continuous intake of polyphenolic compounds containing cocoa powder reduces LDL oxidative susceptibility and has beneficial effects on plasma HDL-cholesterol concentrations in humans.

BACKGROUND: Cocoa powder is rich in polyphenols such as catechins and procyanidins and has been shown in various models to inhibit LDL oxidation and atherogenesis. OBJECTIVE: We examined whether long-term intake of cocoa powder alters plasma lipid profiles in normocholesterolemic and mildly hypercholesterolemic human subjects. DESIGN: Twenty-five subjects were randomly assigned to ingest either 12 g sugar/d (control group) or 26 g cocoa powder and 12 g sugar/d (cocoa group) for 12 wk. Blood samples were collected before the study and 12 wk after intake of the test drinks. Plasma lipids, LDL oxidative susceptibility, and urinary oxidative stress markers were measured. RESULTS: At 12 wk, we measured a 9% prolongation from baseline levels in the lag time of LDL oxidation in the cocoa group. This prolongation in the cocoa group was significantly greater than the reduction measured in the control group (-13%). A significantly greater increase in plasma HDL cholesterol (24%) was observed in the cocoa group than in the control group (5%). A negative correlation was observed between plasma concentrations of HDL cholesterol and oxidized LDL. At 12 wk, there was a 24% reduction in dityrosine from baseline concentrations in the cocoa group. This reduction in the cocoa group was significantly greater than the reduction in the control group (-1%). CONCLUSION: It is possible that increases in HDL-cholesterol concentrations may contribute to the suppression of LDL oxidation and that polyphenolic substances derived from cocoa powder may contribute to an elevation in HDL cholesterol.

Effects of bezafibrate on lipoprotein subclasses and inflammatory markers in patients with hypertriglyceridemia--a nuclear magnetic resonance study.

BACKGROUND: Hypertriglyceridemia is often associated with elevated remnants, small dense LDL and decreased HDL-cholesterol (C). The objective of this study was to investigate the efficacy of bezafibrate on lipoprotein subfractions profile and inflammation markers in patients with hypertriglyceridemia. METHODS: Twenty-four hypertriglyceridemic subjects took bezafibrate, 400 mg daily, for 4 weeks. Lipoprotein subclasses were measured by nuclear magnetic resonance (NMR) spectroscopy. Inflammation markers including C-reactive protein (CRP), interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) were also determined. RESULTS: Bezafibrate lowered triglyceride (TG) by 59% and increased HDL-C by 20%. NMR analysis revealed that bezafibrate lowered large TG-rich lipoproteins and IDL by 81% and 46%, respectively. Small LDL was selectively decreased by 53% with increase in large to intermediate LDL, thus altering the LDL distribution towards the larger particles (mean diameter 19.9 to 20.7 nm, p = 0.0001). Small (HDL1) and intermediate (HDL3) HDL significantly increased by 168% and 70%, whereby resulting in a significant reduction of the mean HDL particle size from 9.0 to 8.7 nm (p = 0.026). None of inflammation makers showed significant change by bezafibrate. CONCLUSIONS: Bezafibrate effectively ameliorates atherogenic dyslipidemia by reducing remnants and small LDL as well as by increasing HDL particles in hypertriglyceridemic subjects.