Association between Triglyceride-glucose index and sarcopenia in China: A nationally representative cohort study.

BACKGROUND: The relationship between sarcopenia and insulin resistance (IR) has seldom been reported. Triglyceride-glucose (TyG) index, a new IR indicator, has gained traction as a prognostic tool for many diseases. We aimed to investigate whether the level of TyG index was related to the incidence of sarcopenia. METHOD: A total of 1819 participants above 60 without sarcopenia at baseline were included from the China Health and Retirement Longitudinal Study (CHARLS). Cox models were applied to evaluate the association between TyG and incident sarcopenia. Mediation analyses were performed to evaluate the contribution of the level of BMI to observed associations. RESULTS: During a median follow-up of 4.0 years, 217 (11.9 %) participants developed sarcopenia. The multivariable-adjusted hazard ratios of total sarcopenia in higher quartiles of TyG index versus the lowest quartiles were 0.59, 0.61, and 0.46, respectively. There were significant trends toward a decreasing risk of sarcopenia across the quartiles of TyG index before adjusting for BMI, but no significant association was observed after accounting for BMI. The area under the ROC curve was 0.6281 (0.597-0.660). In subgroup analysis, there was an inverse significant association between TyG index and sarcopenia among male participants. In mediation analyses, BMI explained 88.7 % of the association of TyG index and sarcopenia. CONCLUSIONS: Our findings indicated that TyG index was negatively associated with incident sarcopenia in older Chinese without considering BMI adjustment. The association was not more significant after adjusting for BMI. BMI mediated the relationship between sarcopenia and TyG index among older Chinese population. Future study should validate our findings in a larger population.

Changes in Expression of the Membrane Receptors CD14, MHC-II, SR-A, and TLR4 in Tissue-Specific Monocytes/Macrophages Following Porphyromonas gingivalis-LPS Stimulation.

The aim of the study was to provide a theoretical foundation for understanding the relationship between periodontal diseases and systemic diseases by examining the inflammatory effect of Porphyromonas gingivalis lipopolysaccharide (LPS) on monocytes/macrophages isolated from tissues distinct from the oral cavity in normal and hyperlipidemic New Zealand white rabbits. Macrophages were isolated from four separate tissues (mononuclear cells from blood, alveolar macrophages, peritoneal macrophages, and Kupffer cells) from both normal and hyperlipidemic New Zealand white rabbits. Cells were either stimulated for 24 h in vitro with P. gingivalis-LPS or Escherichia coli-LPS, or were pre-treated with IL-10 before P. gingivalis-LPS treatment. RNA was isolated and the expression of SR-A, TLR4, CD14, and MHC-II measured by RT-PCR. For MHC-II, the suppression effects of P. gingivalis-LPS were similar to the effects of E. coli-LPS in all macrophages examined. In general, the magnitude of the effects of P. gingivalis-LPS on gene expression was lower than that of E. coli-LPS, and there were differences in the relative membrane receptors between the two, implying that the two LPSs stimulate different responses. IL-10 increased the expression of the defensive receptor SR-A and decreased the expression of CD14, TLR4, and the antigen-presenting molecule MHC-II in all types of macrophages examined, regardless of hyperlipidemic state. These data are consistent with an anti-inflammatory effect of IL-10. P. gingivalis-LPS is an activator of gene expression in macrophages isolated from tissues distinct from the oral cavity.