Nutrition counseling is associated with less sarcopenia in diabetes: A cross-sectional and retrospective cohort study.

OBJECTIVES: Muscle is crucial for blood glucose regulation. There is a need to prevent and treat sarcopenia in diabetes mellitus (DM). This study aimed to estimate the prevalence of sarcopenia and evaluate the association of nutritional counseling with the development of sarcopenia for people with DM. METHODS: In a cross-sectional and retrospective cohort study, people with type 2 DM were recruited from the Diabetes Shared Care Program of a teaching hospital. Muscle mass, muscle strength, and physical functional performance were evaluated using the Asian Working Group for Sarcopenia criteria. The skeletal muscle mass index was determined by dividing muscle mass by the square of the height. Clinical information, including the nutrition counseling record, was retrospectively obtained from medical records for a 2-y period. RESULTS: The prevalence of low skeletal muscle mass index (presarcopenia) and sarcopenia were, respectively, 20.4% and 9.6% (including 3.1% severe) among 1292 participants. Specifically, 15.3% of participants age ≥ 65 y were categorized as having sarcopenia. With more frequent nutritional counseling, there was a lesser risk of sarcopenia; the adjusted odds ratio (95% confidence interval) was 0.51 (0.27-0.94) for ≥ 3 times/2 y compared to no counseling. DM duration and age, glycemic status and medication, and body mass index and counseling frequency had no joint effects; however, these variables (except HbA1 c) were independent risk factors for low skeletal muscle mass index and sarcopenia. CONCLUSIONS: People with type 2 DM have a high risk of sarcopenia. Increased nutrition counseling in outpatients was associated with less sarcopenia. Education about sarcopenia-associated risk factors should be encouraged early in the onset of DM.

Folic acid inhibits endothelial cell proliferation through activating the cSrc/ERK 2/NF-κB/p53 pathway mediated by folic acid receptor.

Folate is important for normal cell division. Folate deficiency has been implicated in various diseases, including atherosclerosis, neural tube defects, and cancer. However, the effect of folate on angiogenesis was unclear. The aim of this study was to investigate the anti-angiogenic action of folic acid (FA). FA (0-10 µmol/L) concentration-dependently decreased DNA synthesis and proliferation in cultured human umbilical venous endothelial cells (HUVEC). Western blot analyses demonstrated that the levels of p21, p27 and p53 protein in HUVEC were increased by FA. The FA-inhibited [3H]thymidine incorporation was completely blocked when the expressions of p21 and p27 were knocked-down together. Knock-down of p53 prevented the FA-induced increases in p21 and p27 protein level. The levels of phosphorylated Src (p-Src) and p-Src-FA receptor (FR) complex in HUVEC were increased by FA. Knock-down of FR reduced the FA-induced increases of p-Src and p53. The FA-induced increases of p21, p27 and p53 protein levels were abolished when cSrc was knocked-down. FA also increased NF-κB nuclear translocation and binding onto the p53 promoter. The FA-induced up-regulation of the p53 promoter activity was prevented by knocked-down of ERK. Matrigel angiogenesis assay in mice demonstrate the anti-angiogenic effect of FA in vivo. In conclusion, our data indicate that FA bound to FR in HUVEC, subsequently activated the cSrc/ERK 2/NF-κB/p53 signaling pathway, which in turn up-regulated the expression of p21 and p27, and finally resulted in cell cycle arrest at the G0/G1 phase. In the present study, we uncover a completely novel role of FA for anti-angiogenesis.