Context Branched-chain amino acids (BCAA) are substrates for protein synthesis. Although their intake may contribute to an increase in skeletal muscle mass, elevated serum BCAA levels have been reported to be associated with insulin resistance, potentially resulting in decreased skeletal muscle mass. Objective This study aimed to explore the association between elevated serum BCAA levels and longitudinal skeletal muscle loss. Design and Setting A cohort analysis was conducted, in which serum amino acids were analyzed in healthy individuals who underwent a medical health checkup at Kameoka Municipal Hospital (HOZUGAWA study), Japan. Patients Seventy-one participants (37 men and 34 women) underwent follow-up checkups after the baseline visit. The follow-up duration was 1.2 ± .4 years. Main Outcome Measures The relationship between fasting baseline serum BCAA levels and lifestyle factors, body composition, blood test results, dietary history, and changes in skeletal muscle mass was evaluated. Results In both men and women, serum BCAA levels were positively correlated with body weight, body mass index, skeletal muscle mass index (SMI), and serum triglycerides but inversely correlated with serum high-density lipoprotein cholesterol. In men, fasting serum BCAA levels were inversely associated with the rate of change in SMI (adjusted β = −.529, P = .006), and elevated BCAA levels were independently associated with a longitudinal decrease in skeletal muscle mass (odds ratio: 1.740; 95% confidence interval: 1.023-2.960 per 50 nmol/mL serum BCAAs increase). Conclusion Increased circulating BCAAs could be an indicator of skeletal muscle loss in men.

This study reports the use of single-cell RNA sequencing to evaluate B cells in the peripheral blood mononuclear cells (PBMCs) and intrathyroidal blood mononuclear cells of patients with Graves’ disease (GD) undergoing thyroidectomy. These cells were stimulated with overlapping peptides of thyroid autoantigens, including thyroid-stimulating hormone receptor (TSHR), thyroglobulin (Tg), and thyroid peroxidase (TPO). In PBMCs, naive B cells are characterized by IL6 and CXCR5, whereas memory B cells express IGHG1, IGHG2, and CD74. HLA-DMA, HLA-DRB1, IGHG, IGHM, CD74, CD79A, and MS4A1 expression increased in peptide-stimulated naive and memory B cells compared to those in the controls. Thyroid naive B cells are characterized by CD40 and TNFRSF13C, whereas memory B cells express IGHM, CD79A, and MS4A1. Thyroid B cells showed higher DUSP1, DUSP2, CD69, FOSB, RGS1, and immunoglobulin gene expression than control PBMCs and thyroid cells. B-cell receptor analysis revealed frequent IGHV3-23 and IGHV4-34 usage in controls, whereas IGHV4-34/IGHJ4 expression was increased in TSHR-stimulated groups. We concluded that B-cell responses to TSHR, Tg, and TPO differed and that changes in B-cell reactivity also occurred in PBMCs and the thyroid. Additionally, IGHV3-23 and IGHV4-34 may be associated with autoantibody production in GD.

High-fat diets are closely implicated in the pathogenesis of chronic conditions, including obesity and hepatic steatosis. Recently, coconut oil, which is rich in medium-chain fatty acids, has attracted significant attention for its potential anti-obesity and anti-inflammatory properties. This study aimed to evaluate the effects of medium-chain fatty acids derived from coconut oil on metabolic disorders, particularly fatty liver, using a mouse model established by a high-fat diet. C57BL/6J mice were assigned to either the lard diet group or the coconut oil diet group and fed for 12 weeks. Glucose tolerance was assessed, and biochemical parameters, liver histology, and gene expression in the liver were analysed. Additionally, the concentrations of medium-chain fatty acids within the liver were determined through gas chromatography-mass spectrometry analysis. Mice fed a coconut oil diet exhibited suppressed weight gain and improved glucose tolerance compared to mice fed a lard diet. Furthermore, the coconut oil diet resulted in reduced hepatic fat accumulation, decreased expression levels of genes implicated in inflammation and lipid metabolism within the liver, and higher concentrations of medium-chain fatty acids in the liver. Coconut oil may contribute to the suppression of hepatic fat accumulation in the liver and the prevention of non-alcoholic fatty liver disease/metabolic dysfunction-associated steatotic liver disease by increasing the levels of medium-chain fatty acids in the liver and suppressing the expression of genes implicated in inflammation and lipid metabolism.

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.

Takahiro Tsujikawa and Shigeru Hirano were not included as authors in the original publication