Background and AimsMaintenance of muscle mass is important for sarcopenia prevention. However, the effect of eating speed, especially fast, normal, or slow speed, on muscle mass changes remains unclear. Therefore, the purpose of this prospective study was to investigate the effect of eating speed on muscle mass changes in patients with type 2 diabetes (T2DM).MethodsThis study included 284 patients with T2DM. Based on a self–reported questionnaire, participants were classified into three groups: fast–, normal–, and slow–speed eating. Muscle mass was assessed using a multifrequency impedance body composition analyzer, and skeletal muscle mass (SMI) decrease (kg/m2/year) was defined as [baseline SMI (kg/m2)–follow–up SMI (kg/m2)] ÷ follow–up duration (year). The rate of SMI decrease (%) was defined as [SMI decrease (kg/m2/year) ÷ baseline SMI (kg/m2)] × 100.ResultsThe proportions of patients with fast–, normal–, and slow–speed eating were, respectively, 50.5%, 42.9%, and 6.6% among those aged <65 years and 40.4%, 38.3%, and 21.3% among those aged ≥65 years. In patients aged ≥65 years, the rate of SMI decrease in the normal (0.85 [95% confidence interval, CI: −0.66 to 2.35]) and slow (0.93 [95% CI −0.61 to 2.46]) speed eating groups was higher than that in the fast speed eating group (−1.08 [95% CI −2.52 to 0.36]). On the contrary, there was no difference in the rate of SMI decrease among the groups in patients aged <65 years. Compared with slow speed eating, the adjusted odds ratios of incident muscle loss [defined as rate of SMI decrease (%) ≥0.5%] due to fast– and normal–speed eating were 0.42 (95% CI 0.18 to 0.98) and 0.82 (95% CI 0.36 to 2.03), respectively.ConclusionSlow–speed eating is associated with a higher risk of muscle mass loss in older patients with T2DM.

Low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and LDL/HDL ratio have been associated with new-onset diabetes; however, their cut-off levels have not been determined. We clarified the association between dyslipidemia and the incidence of diabetes. People who underwent a health checkup under a program conducted by Panasonic Corporation from 2008 to 2018 were included. In total, 87,570 participants were included, of whom 5,110 developed type 2 diabetes. Cox regression analyses and time-dependent receiver operating characteristic (ROC) curves were used to evaluate the association between LDL cholesterol, HDL cholesterol, or LDL/HDL ratio and incident diabetes and to identify the cut-off values for incident diabetes. Multivariate analysis showed that LDL cholesterol, HDL cholesterol, and LDL/HDL ratio were significantly associated with the risk of incident type 2 diabetes. Further, the area under the ROC curve and optimized cut-off values for LDL cholesterol, HDL cholesterol, and LDL/HDL ratio for incident type 2 diabetes at 10 years were 0.613 and 124 mg/dl, 0.640 and 54 mg/dl, and 0.662 and 2.4 mg/dl, respectively. The LDL/HDL ratio with a cut-off value of 2.4 was a better predictor of incident diabetes within 10 years than LDL and HDL cholesterol.

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Royal jelly (RJ) is a naturally occurring substance synthesized by honeybees and has various health benefits. Herein, we focused on the medium-chain fatty acids (MCFAs) unique to RJ and evaluated their therapeutic efficacy in treating non-alcoholic fatty liver disease (NAFLD). We examined db/m mice that were exclusively fed a normal diet, db/db mice exclusively fed a normal diet, and db/db mice fed varying RJ quantities (0.2, 1, and 5%). RJ improved NAFLD activity scores and decreased gene expression related to fatty acid metabolism, fibrosis, and inflammation in the liver. RJ regulated innate immunity-related inflammatory responses in the small intestine and decreased the expression of genes associated with inflammation and nutrient absorption transporters. RJ increased the number of operational taxonomic units, the abundance of Bacteroides, and seven taxa, including bacteria that produce short-chain fatty acids. RJ increased the concentrations of RJ-related MCFAs (10-hidroxy-2-decenoic acid, 10-hydroxydecanoic acid, 2-decenedioic acid, and sebacic acid) in the serum and liver. These RJ-related MCFAs decreased saturated fatty acid deposition in HepG2 cells and decreased the gene expression associated with fibrosis and fatty acid metabolism. RJ and RJ-related MCFAs improved dysbiosis and regulated the expression of inflammation-, fibrosis-, and nutrient absorption transporter-related genes, thereby preventing NAFLD.