Background: The predictive potentials of neck circumference (NC) for cardio-metabolic risks remain uncertain. The aim of this study was to investigate whether NC independently contributes to the prediction of cardio-metabolic risks beyond body mass index (BMI), waist circumference (WC) and waist to hip ratio (WHpR) in a large Chinese population.Methods: A total of 4201 participants (2508 men and 1693 women) aged 20-85 were recruited from the Health Examination Centre between May 2009 and April 2010, anthropometric indices, biochemical and clinical parameters were measured. Receiver operating characteristic, partial correlation and logistic regression analyses were employed to evaluate the association of the anthropometric indices to cardio-metabolic risks separately by gender.Results: Neck circumference was positively correlated with SBP and DBP (r=0.250 and 0.261), fasting blood glucose (FBP) (r=0.177), TG (r=0.240), TC (r=0.143) and LDL-C (r=0.088) and negatively correlated with HDL-C (r=-0.202) in males (all P<0.01). Similar results were found in females with the exception of TC. The AUCs of NC for metabolic abnormalities ranged from 0.558 (Increased LDL-C) to 0.683 (MS-rf) in men and 0.596 (Increased LDL-C) to 0.703 (MS-rf) in women (P<0.01). The NC of ≥37 cm for men and ≥33 cm for women were the best cut-off points for metabolic syndrome. The adjusted ORs (95% CIs) of NC in men and women respectively were 1.29 (1.12-1.48) and 1.44 (1.20-1.72) for metabolic syndrome risk factors (MS-rf), 1.15 (1.01-1.32) and 1.22 (1.03-1.46) for high BP, 1.16 (1.02-1.33) and 1.42 (1.18-1.71) for increased TG, and 1.26 (1.06-1.50) and 1.32 (1.06-1.65) for increased FBP; the adjusted OR of NC in women for decreased HDL-C was 1.29 (1.10-1.51).Conclusions: Neck circumference was significantly associated with cardio-metabolic risk factors and independently contributed to the prediction of cardio-metabolic risks beyond the classical anthropometric indices in adults of China.
Background: Betaine is a methyl donor and has been considered as a lipotropic effect substance. But its mechanism remains unclear. Hepatic steatosis is associated with abnormal expression of genes involved in hepatic lipid metabolism. DNA methylation contributes to the disregulation of gene expression. Here we hypothesized that betaine supplement and subsequent DNA methylation modifications alter the expression of genes that are involved in hepatic lipid metabolism and hence alleviate hepatic triglyceride accumulation. Methods: Male wild-type (WT) C57BL/6 mice (n = 6) were fed with the AIN-93 G diet. ApoE−/− mice (n = 12), weight-matched with the WT mice, were divided into two groups (n = 6 per group), and fed with the AIN-93 G diet and AIN-93 G supplemented with 2% betaine/100 g diet. Seven weeks after the intervention, mice were sacrificed. Liver betaine, choline, homocysteine concentration were measured by HPLC. Liver oxidants activity and triglyceride level were assessed by ultraviolet spectrophotometry. Finally, hepatic PPAR alpha gene and its target genes expression levels and the methylation status of the PPAR alpha gene were determined. Results: ApoE−/− mice had higher hepatic triglyceride and lower GSH-Px activity when compared with the WT mice. Betaine intervention reversed triglyceride deposit, enhanced SOD and GSH-Px activity in the liver. Interestingly, mice fed on betaine-supplemented diet showed a dramatic increase of hepatic choline concentration and a decrease of betaine and homocysteine concentration relative to the WT mice and the ApoE−/− mice absent with betaine intervention. Expression of PPAR alpha and CPT1 were decreased and expression of FAS was markedly increased in ApoE−/− mice. In parallel, PPAR alpha promoter methylation level were slightly increased in ApoE−/− mice though without significance. Betaine supplement upregulated expression of PPAR alpha and its target genes (CPT1, CYP2E1) and reversed hypermethylation of PPAR alpha promoter of ApoE−/− mice. Furthermore, PPAR alpha methylation was positively correlated with hepatic betaine concentration. Conclusions: Our findings indicate that betaine supplement could alleviate hepatic triglyceride accumulation and improve antioxidant capacity by decreasing PPAR alpha promoter methylation and upregulating PPAR alpha and its target genes mRNA expression.