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This meta-analysis aimed to study the relationship between abdominal obesity and the risk of CVD by waist circumference (WC), waist:hip ratio (WHR) and waist:height ratio (WHtR). We systematically searched PubMed, Embase and Web of Science. Prospective studies that estimated cardiovascular events by WC, WHR and WHtR were included in this study. Pooled relative risks with 95 % CI were calculated using random effects models. A total of thirty-one studies were included in the meta-analysis, including 669 560 participants and 25 214 cases. Compared the highest with the lowest category of WC, WHR and WHtR, the summary risk ratios were 1·43 (95 % CI, 1·30, 1·56, P < 0·001), 1·43 (95 % CI, 1·33, 1·54, P < 0·001) and 1·57 (95 % CI, 1·37, 1·79, P < 0·001), respectively. The linear dose–response analysis revealed that the risk of CVD increased by 3·4 % for each 10 cm increase of WC, and by 3·5 and 6·0 % for each 0·1 unit increase of WHR and WHtR in women, respectively. In men, the risk of CVD increased by 4·0 % for each 10 cm increase of WC, and by 4·0 and 8·6 % for each 0·1 unit increase of WHR and WHtR, respectively. Collectively, abdominal obesity is associated with an increased risk of CVD. WC, WHR and WHtR are good indicators for the prediction of CVD.
Hepcidin, a key regulator of Fe homeostasis, is an ideal drug target for treating patients with Fe disorders such as haemochromatosis, anaemia of chronic inflammation and Fe-deficiency anaemia. However, whether (and how) traditional Chinese black foods (e.g. black soyabeans) target hepcidin and improve Fe-deficiency anaemia remains unclear. Herein, we report that black soyabean seed coat extract (BSSCE) can potently inhibit the in vitro and in vivo expression of hepcidin. In the present study, in cells treated with 200 μg/ml BSSCE, hepcidin expression was found to be reduced to only 6 % of the control levels (P< 0·01). An AIN-76A diet containing 2 % BSSCE was fed to 8-week-old male C57BL/6 mice for 0, 1, 7, 15 or 30 d; importantly, compared with the day 0 group, the day 7 group exhibited nearly a 50 % decrease in hepatic hepcidin expression (P< 0·01), a 35 % decrease in splenic Fe concentrations (P< 0·05) and a 135 % increase in serum Fe concentrations (P< 0·05). Mechanistically, the effect of BSSCE on hepcidin expression was mediated via a reduction in the phosphorylation levels of mothers against decapentaplegic homolog proteins (Smad)1/5/8. Consequently, the mice in the day 30 group exhibited large increases in erythrocyte counts (111 % v. day 0, P< 0·01), Hb concentrations (109 %, P< 0·01) and haematocrit values (108 %, P< 0·01). In conclusion, these results indicate that black soyabean extract regulates Fe metabolism by inhibiting the expression of hepcidin. This finding can be used to optimise the intervention of patients with hepcidin-related diseases, including Fe-deficiency anaemia.
Systemic Fe overload can contribute to abnormal glucose metabolism and the onset of type 2 diabetes (T2D). Although hepcidin is the master regulator of systemic Fe homeostasis, few studies have systematically evaluated the associations of serum hepcidin concentrations with Fe metabolism parameters and risks for the development of T2D. In this regard, whether hepcidin concentrations are associated with T2D remains controversial. We measured serum hepcidin and ferritin concentrations in a case–control study of 1259 Han Chinese participants to evaluate the possible associations of serum hepcidin concentrations with Fe metabolism parameters and risks of T2D. Individuals with diabetes (n 555) and control participants (n 704) were recruited and serum hepcidin and ferritin concentrations were quantified. Additionally, selected biochemical and anthropometric variables were determined. A logistic regression analysis was performed to evaluate the association of serum hepcidin and ferritin concentrations with T2D. A linear regression analysis was used to test for associations between serum hepcidin and ferritin concentrations and a number of clinical, demographic and diabetes-associated variables. We found that serum hepcidin concentrations correlated with Hb and serum ferritin concentrations. No differences in hepcidin concentrations were found between the group with diabetes and the control group. Hepcidin concentrations were not significantly correlated with T2D risk factors. We also found that serum ferritin concentrations were elevated in individuals with diabetes and were positively correlated with both Hb concentrations and T2D risk factors. The present findings suggest that serum ferritin concentrations correlate with T2D risk factors, while serum hepcidin concentrations are positively associated with Hb and serum ferritin concentrations, but do not correlate with T2D.
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