Association of vitamins B1 and B2 intake with early-onset sarcopenia in the general adult population of the US: a cross-sectional study of NHANES data from 2011 to 2018.

Background: Early-onset sarcopenia refers to the progressive loss of muscle mass and function that occurs at an early age. This condition perpetuates the vicious cycle of muscle loss and is associated with adverse outcomes. It is important to identify the contributing factors for early intervention and prevention. While diet is known to impact muscle mass, the association of B vitamins with early-onset sarcopenia remains unexplored. Objectives: To investigate the association of B vitamins intake with early-onset sarcopenia risk in a cross-sectional study. Methods: We conducted data analysis on a total of 8,711 participants aged between 20 and 59 years who took part in the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018. Early-onset sarcopenia was defined as a SMI measured by DXA that was one standard deviation below the sex-specific mean of the reference population. B vitamins intake (B1, B2, B3, B6, B9, and B12) was assessed by 24-h dietary recall. We used weighted multiple logistic regression and RCS models to estimate the OR and 95% CI of sarcopenia by B vitamins intake, adjusting for demographic, physical, lifestyle, comorbidities, and nutritional covariates. Results: Higher intake of vitamin B1 was associated with a 22% lower sarcopenia risk (OR = 0.78, CI = 0.63-0.97, p = 0.022), and higher intake of vitamin B2 with a 16% lower risk (OR = 0.84, CI = 0.74-0.97, p = 0.012) in both genders. Gender-specific analyses showed a 28% reduction in sarcopenia risk among males with each additional mg of vitamin B1 intake (OR = 0.72, CI = 0.52-0.97, p = 0.038), and a 26% decrease among females with each additional mg of vitamin B2 intake (OR = 0.74, CI = 0.57-0.96, p = 0.021). No significant differences were found between vitamin B2 and males, or between vitamin B1 and females. The RCS model suggested a nonlinear relationship between vitamin B2 intake and sarcopenia risk (POverall = 0.001, PNonlinear = 0.033), with a plateau effect above 3 mg/d. Conclusion: Higher intake of vitamin B1 and B2 may lower the risk of early-onset sarcopenia, with gender differences. This suggests the potential of nutritional intervention by increasing these vitamins intake through diet and supplements. Further research is warranted to elucidate the mechanisms and design targeted interventions.

Single-cell analysis reveals that Jinwu Gutong capsule attenuates the inflammatory activity of synovial cells in osteoarthritis by inhibiting AKR1C3.

Jinwu Gutong capsule (JGC) is a traditional Chinese medicine formula for the treatment of osteoarthritis (OA). Synovitis is a typical pathological change in OA and promotes disease progression. Elucidating the therapeutic mechanism of JGC is crucial for the precise treatment of OA synovitis. In this study, we demonstrate that JGC effectively inhibits hyperproliferation, attenuates inflammation, and promotes apoptosis of synovial cells. Through scRNA-seq data analysis of OA synovitis, we dissected two distinct cell fates that influence disease progression (one fate led to recovery while the other fate resulted in deterioration), which illustrates the principles of fate determination. By intersecting JGC targets with synovitis hub genes and then mimicking picomolar affinity interactions between bioactive compounds and binding pockets, we found that the quercetin-AKR1C3 pair exhibited the best affinity, indicating that this pair constitutes the most promising molecular mechanism. In vitro experiments confirmed that the expression of AKR1C3 in synovial cells was reduced after JGC addition. Further overexpression of AKR1C3 significantly attenuated the therapeutic efficacy of JGC. Thus, we revealed that JGC effectively treats OA synovitis by inhibiting AKR1C3 expression.

Vitamin D deficiency affects the immunity against Mycobacterium tuberculosis infection in mice.

The aim of the study is to investigate the immunological changes after stimulation with bacillus Calmette-Guerin (BCG) in mice with vitamin D deficiency. After weaning, mice were divided into the vitamin D-deficient group (-D group), the normal group (N group), and the vitamin D-supplemented group (+D group). Twelve-week-old mice were intraperitoneally injected with 0.5 mg/ml BCG (≥1.0 × 10(6) CFU/mg) and maintained for 6 weeks. Spleen lymphocytes were isolated, and the percentages of CD4(+) and CD8(+) lymphocytes were determined by flow cytometry. IFN-γ levels, IL-10 levels, and the TB-PPD-specific antibody titer were determined by ELISA. The inter-group difference was analyzed using one-way ANOVA, and multiple comparisons were analyzed using the LSD test. The percentage of CD4(+) cells was 27.1 ± 0.6 in the -D group, 23.62 ± 0.42 in the N group, and 19.46 ± 0.32 in the +D group (P < 0.05). The percentage of CD8(+) lymphocytes was 12.15 ± 0.61 in the -D group, 8.7 ± 0.64 in the N group, and 7.12 ± 0.48 in the +D group (P < 0.05). The CD4(+)/CD8(+) ratio was 2.23 ± 0.15 in the -D group, 2.71 ± 0.21 in the N group, and 2.73 ± 0.31 in the +D group (P < 0.05). The plasma IFN-γ levels were 416.42 ± 16.42 pg/ml in the -D group, 325.41 ± 11.16 pg/ml in the N group, and 276.26 ± 25.32 pg/ml in the +D group (P < 0.005). The plasma IL-10 levels were 16.45 ± 1.58 pg/ml in the -D group, 24.31 ± 2.16 pg/ml in the N group, and 26.28 ± 0.42 pg/ml in the +D group (P < 0.005). The serum TB-PPD-specific antibody level was significantly higher in the -D group than in the N and +D groups. Vitamin D deficiency affects the immunity against Mycobacterium tuberculosis infection in mice.