Abstract
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-TNF-has been shown to impair peripheral insulin signaling in vitro and in vivo. However, it is unclear whether TNF-may also affect endogenous glucose production (EGP) during fasting and glucose-stimulated insulin secretion (GSIS) in vivo. We hypothesized that low-dose TNF-would increase EGP and attenuate GSIS. Recombinant human TNF-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-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-did not affect EGP during the basal period. Our results indicate that TNF-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-increasing clearance of insulin from plasma without impairing beta-cell function or hepatic insulin sensitivity.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 295478 |
| Tidsskrift | Mediators of Inflammation |
| Vol/bind | 2014 |
| Sider (fra-til) | 1-7 |
| Antal sider | 7 |
| ISSN | 0962-9351 |
| DOI | |
| Status | Udgivet - 2014 |
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