Bayberry is known to be a rich source of natural flavonoids and has been reported to have various health-promoting abilities. However, its function on regulating skeletal muscle fiber type remains unclear. This study examined whether bayberry extract affects skeletal muscle fiber type by promoting fast myofiber formation, as well as the potential molecular mechanism. After eight weeks, the “Biqi” bayberry extract (BBE) groups mice displayed markedly enhanced grip strength and improved metabolic rate compared to the control group mice. BBE also significantly increased myofibers size, LDH activity, MyHC-IIb (fast-twitch mRNA) expression, and the percentage of fast-twitch myofibers, while decreasing SDH activity, MyHC-I (slow-twitch mRNA) expression, and slow-twitch myofibers percentage in the skeletal muscle of the mice. The effect of BBE on regulating skeletal muscle fiber type remodeling is likely attributed to its activation of the Akt-FoxO1 pathway. Our findings indicated that BBE can effectively regulate the expression and proportion of fast-twitch fibers, making it a potential therapy for improving glucose homeostasis of skeletal muscle.

The impact of volatile organic compounds (VOCs) on type 2 diabetes (T2D) among older adults is unknown. The multiple linear regression model and the multiple binary logistic regression were used to evaluate the relationships between mVOCs and glucose homeostasis/T2D, respectively. Among the 19 mVOCs, the higher levels of urinary N-acetyl-S-(2-hydroxypropyl)-L-cysteine (2HPMA, compound CID:44146439) and N-acetyl-S-(2-hydroxypropyl)-L-cysteine (HPMMA, compound CID:107774684) were significantly associated with higher odds of T2D (OR = 1.16, 95% confidence interval [CI]:1.01–1.34 for 2HPMA; and OR = 1.27, 95% CI:1.04–1.54 for HPMMA). In addition, higher concentrations of multiple mVOCs in urine were significantly correlated with glucose homeostasis biomarkers, including 2HPMA and 2-thioxothiazolidine-4-carboxylic acid (TTCA, compound CID:3034757) with fasting glucose, HPMMA and mandelic acid (MA, compound CID:1292) with HbA1c, phenylglyoxylic acid (PGA, compound CID:11915) with serum insulin, HbA1c and HOMA-IR. Our findings suggested that exposure to VOCs were associated with increased odds of T2D in older adults, which might be mediated by impaired glucose homeostasis. Mitigating VOCs should be a necessary component of public health strategies aimed at reducing the burden of type 2 diabetes.

The EAT-Lancet Commission proposed a planetary health diet in 2019, yet its association with frailty remains unclear. This study aimed to examine the relationships between adherence to the EAT-Lancet diet, metabolomic profiles, and frailty risk among older adults. We included 44,465 participants from the UK Biobank, with a mean age of 55.88 years. Frailty was defined based on five physical criteria. Elastic net regression identified a 20-metabolite signature associated with the EAT-Lancet diet. Cox models showed that higher diet adherence was significantly associated with reduced frailty risk (HR: 0.51, 95% CI: 0.40 to 0.64). Each standard deviation increase in the metabolic signature was also associated with lower frailty risk (HR: 0.69, 95% CI: 0.63 to 0.75). Mediation analysis indicated that metabolites mediated 9.88% of the diet-frailty association. These findings suggest that greater adherence to the EAT-Lancet diet may lower frailty risk, partly mediated through specific metabolic pathways.

To examine the association of air pollution with dementia and brain structural alternations, and further to explore the mediating role of accelerated biological aging and brain atrophy in the air pollution-dementia association. A prospective cohort study. A total of 488,348 UK Biobank participants without dementia were included at baseline. Air pollution, including PM_2.5, PM₁₀, PM_2.5 absorbance, NO_2, and NO_x. Cox proportional hazards regression models were used to evaluate the association between air pollution and incident dementia, while linear regression models were used to assess its associations with global and 80 regional brain structures. The mediating roles of biological aging acceleration (measured by Klemera-Doubal method Biological Age [KDM-BA] and PhenoAge) and brain structures in the air pollution-dementia association were evaluated using structural equation modeling (SEM). Compared to participants with the lowest tertile of air pollution exposure, those in the highest exposure group had higher risks of dementia (HR [95%CI]: 1.14 [1.08, 1.21] for PM_2.5; 1.09 [1.03, 1.16] for PM₁₀; 1.09 [1.03, 1.16] for PM_2.5 absorbance; 1.20 [1.13, 1.28] for NO₂; and 1.14 [1.08, 1.21] for NO_X). Air pollution exposure was inversely associated with global and several regional brain structural alterations. SEM revealed a consistent mediating pathway that integrates biological aging and brain structural alterations in the association between air pollution exposure and the risk of dementia. Our findings support the association between air pollution and dementia, as well as a reduction in global and several regional brain volumes. Notably, biological age acceleration and brain atrophy mediated the air pollution-dementia association.