Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital

The acute effects of low-dose TNF-α on glucose metabolism and β-cell function in humans

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review


  1. Circulating Inflammatory Markers Are Inversely Associated with Heart Rate Variability Measures in Type 1 Diabetes

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Genetic Ablation of Soluble TNF Does Not Affect Lesion Size and Functional Recovery after Moderate Spinal Cord Injury in Mice

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Obesity and low-grade inflammation increase plasma follistatin-like 3 in humans

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

Type 2 diabetes is characterized by increased insulin resistance and impaired insulin secretion. Type 2 diabetes is also associated with low-grade inflammation and increased levels of proinflammatory cytokines such as TNF-α. TNF-α has been shown to impair peripheral insulin signaling in vitro and in vivo. However, it is unclear whether TNF-α may also affect endogenous glucose production (EGP) during fasting and glucose-stimulated insulin secretion (GSIS) in vivo. We hypothesized that low-dose TNF- α would increase EGP and attenuate GSIS. Recombinant human TNF-α or placebo was infused in healthy, nondiabetic young men (n = 10) during a 4-hour basal period followed by an intravenous glucose tolerance test (IVGTT). TNF-α lowered insulin levels by 12% during the basal period (P < 0.05). In response to the IVGTT, insulin levels increased markedly in both trials, but there was no difference between trials. Compared to placebo, TNF-α did not affect EGP during the basal period. Our results indicate that TNF-α acutely lowers basal plasma insulin levels but does not impair GSIS. The mechanisms behind this are unknown but we suggest that it may be due to TNF-α increasing clearance of insulin from plasma without impairing beta-cell function or hepatic insulin sensitivity.

TidsskriftMediators of Inflammation
Sider (fra-til)295478
StatusUdgivet - 16 feb. 2014

ID: 45021359