Activation of inflammatory pathways in PBMCs linking type 2 diabetes in older adults without obesity

Hao Chien Cheng, Shun Hsi Tsai, Hung Wen Liu*

*此作品的通信作者

研究成果: 雜誌貢獻期刊論文同行評審

2 引文 斯高帕斯(Scopus)

摘要

The mechanism that underlies the dysregulation of glucose metabolism in older adults without obesity has yet to be thoroughly understood. This study investigated the risk of developing Type 2 diabetes (T2D) in older adults without obesity (BMI: 18.5 to <25 kg/m2). Data on glucose levels (measured by an oral glucose tolerance test), body composition, physical activity level, lipid profile, inflammatory cytokines, and nuclear factor kappa B (NF-κB) and Sirtuin 1 (SIRT1) signaling pathways in peripheral blood mononuclear cells (PBMCs) in older adults with normal glucose tolerance (NGT, n = 17) and those with prediabetes (n = 20) or T2D (n = 8) were gathered. As expected, participants with T2D exhibited higher insulin resistance; β-cell dysfunction; and higher levels of triglycerides and tumor necrosis factor-α (TNF-α) than those with NGT. No differences in physical activity, lean mass, body fat, or cholesterol were observed between the NGT, prediabetes, and T2D groups. Downregulation of SIRT1 and activation of NF-κB signaling in PBMCs were observed in the T2D group. Increased phosphorylation of NF-κB and low SIRT1 protein expression in PBMCs were associated with insulin resistance and β-cell dysfunction. NF-κB and its upstream inhibitor IκBα were positively and inversely correlated with TNF-α, respectively. SIRT1 expression was positively correlated with IL-10. Activation of NF-κB signaling pathways and downregulation of SIRT1 in PBMCs were associated with the inflammatory milieu in older adults without obesity.

原文英語
文章編號111779
期刊Experimental Gerontology
163
DOIs
出版狀態已發佈 - 2022 6月 15

ASJC Scopus subject areas

  • 生物化學
  • 老化
  • 分子生物學
  • 遺傳學
  • 內分泌
  • 細胞生物學

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