This study explores the impact of royal jelly (RJ) on small intestinal epigenomic changes. RJ, produced by honeybees, is known for its effects on metabolic diseases. The hypothesis is that RJ induces epigenomic modifications in small intestinal epithelial cells, affecting gene expression and contributing to metabolic health. Male db/m and db/db mice were used to examine RJ’s effects through mRNA sequencing and CUT&Tag methods. This study focused on histone modifications and gene expression changes, with statistical significance set at p < 0.05. RJ administration improved insulin sensitivity and lipid metabolism without affecting body weight. GO and KEGG pathway analyses showed significant enrichment in metabolic processes, cellular components, and molecular functions. RJ altered histone modifications, increasing H3K27me3 and decreasing H3K23Ac in genes associated with the G2M checkpoint. These genes, including Smc2, Mcm3, Ccnd1, Rasal2, Mcm6, and Mad2l1, are linked to cancer progression and metabolic regulation. RJ induces beneficial epigenomic changes in small intestinal epithelial cells, improving metabolic health and reducing cancer-associated gene expression. These findings highlight RJ’s potential as a therapeutic agent for metabolic disorders. Further research is needed to fully understand the mechanisms behind these effects and their implications for human health.

Objectives: We investigated the relationship between bone metabolic markers or bone mineral density (BMD) and sarcopenia in patients with type 2 diabetes mellitus (T2DM). Methods: In this cross-sectional study involving 119 subjects (76 women and 43 men), bone metabolic markers were evaluated by bone alkaline phosphatase and bone tartrate-resistant acid phosphatase (TRACP-5b). BMD was measured using the dual-energy X-ray absorptiometry method, and sarcopenia was diagnosed using skeletal muscle mass index (SMI), evaluated by body composition measurement and handgrip strength. Results: Significant correlation was observed between handgrip strength or SMI and TRACP-5b in both sexes (correlation coefficients were −0.50 in handgrip strength and −0.41 in SMI in men; −0.25 in handgrip strength and −0.21 in SMI in women). Furthermore, significant correlation was observed between handgrip strength or SMI and BMD of the femoral neck in both sexes (correlation coefficients were 0.33 in handgrip strength and 0.44 in SMI in men; 0.34 in handgrip strength and 0.47 in SMI in women). The concentrations of TRACP-5b with sarcopenia were significantly higher than those without (643.8 ± 261.9 vs. 455.7 ± 165.6 mU/dL), and BMD of femoral neck with sarcopenia was significantly lower than those without (0.54 ± 0.12 vs. 0.66 ± 0.16 g/cm²). TRACP-5b (odds ratio 1.05, 95% confidence interval 1.01–1.10) and femoral neck BMD (odds ratio 0.30, 95% confidence interval 0.14–0.68) were associated with the presence of sarcopenia after adjustment for confounders. Conclusions: TRACP-5b and BMD of the femoral neck were associated with sarcopenia in patients with T2DM.

Background/Objectives: Medium-chain fatty acids (MCFAs), abundant in coconut oil, have attracted considerable attention in recent years owing to their potential impact on muscle atrophy. However, the mechanisms underlying their effects remain inadequately understood. This study aimed to examine the impact of coconut-oil-derived MCFAs on skeletal muscle in a mouse model administered a high-fat diet. Methods: C57BL/6J mice were assigned to a normal diet, lard diet, or coconut oil diet and maintained for a duration of 12 weeks. A glucose tolerance test was conducted, and biochemical parameters, muscle histological analysis, and gene expression in muscle tissue were assessed. MCFA concentrations in serum and muscle were quantified utilizing gas chromatography–mass spectrometry. An in vitro experiment was conducted by treating mouse C2C12 myotube cells with lauric acid and palmitic acid, followed by a gene expression evaluation. Results: Mice fed a coconut-oil-based diet exhibited reduced body weight gain and lower blood glucose and total cholesterol levels compared to those fed a lard-based diet. The coconut-oil-fed group showed increased concentrations of MCFAs in both serum and muscle tissue, along with an improvement in relative grip strength. The expression levels of proteins and genes associated with muscle atrophy were reduced in muscle tissue. These findings were corroborated in vitro using C2C12 myotube cells. Conclusions: Coconut oil may preserve muscle strength by increasing MCFA concentrations in serum and muscle tissue, while suppressing the expression of muscle-atrophy-related proteins and genes. These findings suggest that coconut oil may be beneficial in preventing muscle atrophy induced by long-chain fatty acids.