No abstract

Recently, it was reported that reduction in serum adiponectin levels is correlated with the incidence of breast cancer. As an effort to explain this, we screened various human breast cancer cell lines to identify those in which proliferation is directly controlled by adiponectin. Among the five tested cell lines, proliferation of MDA-MB-231 cancer cell was significantly suppressed by adiponectin within the range of physiological concentration. Furthermore, prolonged adiponectin treatment caused cell growth arrest and even apoptosis of MDA-MB-231. This result is the first to show that adiponectin can directly control cancer cell growth and provides a rationale for the theory that reduction in plasma adiponectin levels could be a risk factor for breast cancer.

ObjectiveWe conducted a systematic review and meta-analysis of studies to quantify the association between body mass index (BMI) and the risks of all-cause and cardiovascular mortality in patients with type 2 diabetes.MethodsWe included studies assessing the impact of BMI on all-cause and cardiovascular mortality in patients with type 2 diabetes. Data were combined using a random-effects dose-response model.ResultsSixteen cohort studies on all-cause mortality (n = 445,125) and two studies on cardiovascular mortality (n = 92,841) were evaluated in the meta-analysis. A non-linear association was observed between BMI and all-cause mortality among patients with type 2 diabetes. With a BMI nadir of 28–30 kg/m2, the risk of all-cause mortality displayed a U-shaped increase. With a BMI nadir of 29–31 kg/m2, the risk of cardiovascular mortality exhibited a gradual non-linear increase for BMI > 31 kg/m2. Subgroup analyses suggested that study location, diabetes duration, and smoking history may have contributed to heterogeneity among the studies.ConclusionsAn obesity paradox exists for patients with type 2 diabetes with respect to all-cause and cardiovascular mortality. Study location, diabetes duration, and smoking history might contribute to heterogeneity among obesity paradox studies of patients with type 2 diabetes.

Background: Obese people have a higher prevalence of cardiovascular disease, but the mechanism of this result remains obscure. The purpose of this study was to prove heart rate variability (HRV) response at rest and during stimuli in these persons.Methods: The subjects were 41 healthy persons (19 men, 22 women) ranging in age from 20 to 65 years. HRV was measured at rest and at given stresses with noise and standing.Results: Higher levels of fat mass, percentage fat content, and waist/hip ratio were significantly associated with lower low frequency (LF) (r ‫؍‬ ؊0.34, r ‫؍‬ ؊0.43; P < .01, r ‫؍‬ ؊0.33, P < .05), and lower root mean square differences of successive NN intervals (RMS standard deviation) (r ‫؍‬ ؊0.33, r ‫؍‬ ؊0.35, r ‫؍‬ ؊0.38, P < .05). During rest, noise, and standing, the change amount of the standard deviation of NN interval (SDNN) and low frequency/high frequency ratio were not different between normal and obese groups (P > .05).Conclusion: Although there was no significant HRV response to stimuli, root mean square of successive differences (which reflects parasympathetic acivity) and low frequency (which mainly reflects sympathetic activity) were negatively correlated with fat mass, fat percentage, and waist-to-hip ratio at rest in obese persons. These results mean obesity can change cardiac autonomic nervous response, meaning that the mechanism by which obesity increases cardiac mortality would be explained, at least partially.