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

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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


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.

Original languageEnglish
Article number111779
JournalExperimental Gerontology
Publication statusPublished - 2022 Jun 15


  • NF-κB
  • Non-obese older adults
  • Sirt1
  • Type 2 diabetes

ASJC Scopus subject areas

  • Biochemistry
  • Ageing
  • Molecular Biology
  • Genetics
  • Endocrinology
  • Cell Biology


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