Summary The prevalence of diabetes in China has increased rapidly from 0.67% in 1980 to 10.4% in 2013, with the aging of the population and westernization of lifestyle. Since its foundation in 1991, the Chinese Diabetes Society (CDS) has been dedicated to improving academic exchange and the academic level of diabetes research in China. From 2003 to 2014, four versions of Chinese diabetes care guidelines have been published. The guidelines have played an important role in standardizing clinical practice and improving the status quo of diabetes prevention and control in China. Since September 2016, the CDS has invited experts in cardiovascular diseases, psychiatric diseases, nutrition, and traditional Chinese medicine to work with endocrinologists from the CDS to review the new clinical research evidence related to diabetes over the previous 4 years. Over a year of careful revision, this has resulted in the present, new version of guidelines for prevention and care of type 2 diabetes in China. The main contents include epidemiology of type 2 diabetes in China; diagnosis and classification of diabetes; primary, secondary, and tertiary diabetes prevention; diabetes education and management support; blood glucose monitoring; integrated control targets for type 2 diabetes and treatments for hyperglycaemia; medical nutrition therapy; exercise therapy for type 2 diabetes; smoking cessation; pharmacologic therapy for hyperglycaemia; metabolic surgery for type 2 diabetes; prevention and treatment of cardiovascular and cerebrovascular diseases in patients with type 2 diabetes; hypoglycaemia; chronic diabetic complications; special types of diabetes; metabolic syndrome; and diabetes and traditional Chinese medicine.

No abstract

Cancer cells present sustained de novo fatty acid (FA) synthesis with increased production of saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs). This change in FA metabolism is associated with overexpression of stearoyl-CoA desaturase 1 (SCD1), which catalyses the transformation of SFAs into MUFAs (e.g., oleic acid). In this study, we provide new evidence that SCD1 inhibition leads to the anti-proliferation effect of breast cancer cells through induction of apoptosis, cell cycle arrest and migration prevention. However, the antitumor effect of the SCD1 inhibitor can be reversed by exogenous oleic acid. We hypothesize that, in addition to de novo synthesis, cancer cells may uptake exogenous FAs actively. CD36, also known as FA translocase (FAT), that functions as a transmembrane protein and mediates the uptake of FAs, is observed to be highly expressed in breast cancer tissues. Furthermore, the anti-proliferation effect caused by the SCD1 inhibitor can not be reversed by exogenous oleic acid supplementation in CD36 knockdown breast cancer cells. Our study revealed that the lipid metabolism of breast cancer is regulated not only by de novo lipogenesis but also by the availability of lipids outside cancer cells. Consistent with FA synthesis, FA uptake and transport will be another important target pathway for anticancer therapy, and the FA channel protein CD36 may provide a promising therapeutic target. Lipogenesis combined with FA transport will be a new orientation for antitumor therapy.

No abstract

Objective. Parkinson's disease (PD) is a severe neurological disease and its risk factors remain largely unknown. A meta-analysis was carried out to investigate the relationship of overweight and obesity with PD. Methods. We used PubMed, EMBASE, and the Chinese National Knowledge Infrastructure (CNKI) databases to identify studies of associations between overweight/obesity and PD. Overweight, obesity, and PD were used as keywords, and published works were retrieved until September 30, 2013. The extracted data were classified (BMI ≥ 30, 25 ≤ BMI < 30, and BMI < 25) according to BMI values and analyzed using RevMan5.2 and Stata11.0. Results. Four cohort studies and three case-control studies were used to evaluate the association between overweight/obesity and PD, including 2857 PD patients and 5, 683, 939 cases of non-PD controls. There was a statistically significant difference between 25 ≤ BMI < 30  and BMI < 25 in the cohort study (RR = 1.17, 95% CI, 1.03–1.32,  P = 0.03), but there was no difference between BMI ≥ 30  and BMI < 25 or BMI ≥ 30  and 25 ≤ BMI < 30, where the respective RR was 1.16 and 0.84; the respective 95% CI was 0.67–2.01 and 0.61–1.15, respectively, and the P values were 0.60 and 0.28, respectively. Case-control studies showed that there was no statistical difference between any two groups. Conclusion. Meta-analysis showed that overweight might be a potential risk factor of PD. Demonstration of a causal role of overweight/obesity in PD development could have important therapeutic implications.