Various anthropometric indices can be used to estimate obesity, and it is important to determine which one is the best in predicting the risk of coronary heart disease (CHD) and to define the optimal cut-off point for the best index. This cross-sectional study investigated a consecutive sample of 11,247 adults, who had lived in rural areas of China and were older than 35 years of age. Eight obesity indices, including the body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), abdominal volume index (AVI), body adiposity index (BAI), body roundness index (BRI) and a body shape index (ABSI) were investigated. The risk of CHD was evaluated by the 10-year coronary event risk (Framingham risk score). Receiver operating characteristic (ROC) curve analyses were used to evaluate the predictive ability of the obesity indices for CHD risk. Of the whole population, 3636 (32.32%) participants had a risk score higher than 10%. Those who suffered medium or high CHD risk were more likely to have higher mean anthropometric indices, except for BMI in males. In the multivariate-adjusted logistic regression, all these anthropometric measurements were statistically associated with CHD risk in males. After adjusting for all the possible confounders, these anthropometric measurements, except for ABSI, remained as independent indicators of CHD risk in females. According to the ROC analyses, ABSI provided the largest area under the curve (AUC) value in males, and BMI showed the lowest AUC value, with AUC varying from 0.52 to 0.60. WHtR and BRI provided the largest AUC value in female, and similarly, BMI showed the lowest AUC value, with AUC varying from 0.59 to 0.70. The optimal cut-off values were as follows: WHtR (females: 0.54), BRI (females: 4.21), and ABSI (males: 0.078). ABSI was the best anthropometric index for estimating CHD risk in males, and WHtR and BRI were the best indicators in females. Males should maintain an ABSI of less than 0.078, and females should maintain a WHtR of less than 0.54 or a BRI of less than 4.21.

We aimed to investigate the effect of advanced glycation end products (AGEs) on the proliferation and migration ability of human umbilical vein endothelial cells (HUVECs). Cell proliferation was detected by methyl thiazolyl tetrazolium (MTT) assay, real-time cell analyzer and 5-Ethynyl-2′-deoxyuridine (EdU) staining. Cell migration was detected by wound-healing and transwell assay. AGEs significantly inhibited the proliferation and migration of HUVECs in a time-and dose-dependent way. Western blotting revealed that AGEs dramatically increased the expression of microtubule-associated protein 1 light chain 3 (LC3) II/I and p62. Immunofluorescence of p62 and acridine orange staining revealed that AGEs significantly increased the expression of p62 and the accumulation of autophagic vacuoles, respectively. Chloroquine (CQ) could further promote the expression of LC3 II/I and p62, increase the accumulation of autophagic vacuoles and promote cell injury induced by AGEs. In addition, AGEs reduced cathepsin D (CTSD) expression in a time-dependent way. Overexpression of wild-type CTSD significantly decreased the ratio of LC 3 II/I as well as p62 accumulation induced by AGEs, but overexpression of catalytically inactive mutant CTSD had no such effects. Only overexpression of wild-type CTSD could restore the proliferation of HUVECs inhibited by AGEs. However, overexpression of both wild-type CTSD and catalytically inactive mutant CTSD could promote the migration of HUVECs inhibited by AGEs. Collectively, our study found that AGEs inhibited the proliferation and migration in HUVECs and promoted autophagic flux, which in turn played a protective role against AGEs-induced cell injury. CTSD, in need of its catalytic activity, may promote proliferation in AGEs-treated HUVECs independent of the autophagy-lysosome pathway. Meanwhile, CTSD could improve the migration of AGEs-treated HUVECs regardless of its enzymatic activity.