Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

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

Research output: Contribution to journalJournal articleResearchpeer-review

DOI

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

    Research output: Contribution to journalJournal articleResearchpeer-review

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

    Research output: Contribution to journalJournal articleResearchpeer-review

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

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. Altered brown fat thermoregulation and enhanced cold-induced thermogenesis in young, healthy, winter-swimming men

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Blocking endogenous IL-6 impairs mobilization of free fatty acids during rest and exercise in lean and obese men

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Neprilysin inhibition increases glucagon levels in humans and mice with potential effects on amino acid metabolism

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

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.

Original languageEnglish
JournalMediators of Inflammation
Volume2014
Pages (from-to)295478
ISSN0962-9351
DOIs
Publication statusPublished - 16 Feb 2014

    Research areas

  • Adult, Blood Glucose, Diabetes Mellitus, Type 2, Double-Blind Method, Glucose, Glucose Tolerance Test, Humans, Insulin, Insulin-Secreting Cells, Male, Recombinant Proteins, Signal Transduction, Tumor Necrosis Factor-alpha, Young Adult

ID: 45021359