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Tumor necrosis factor enhances glucose uptake by peripheral tissues
D A Evans1, D O Jacobs, D W Wilmore
1Department of Surgery, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts 02115.
The American Journal of Physiology
|November 1, 1989
Summary
Tumor necrosis factor (TNF) infusion in dogs caused mild hypoglycemia by increasing glucose uptake and disappearance more than production. This suggests TNF directly impacts glucose metabolism, independent of insulin.
Area of Science:
- Physiology
- Endocrinology
- Biochemistry
Background:
- Tumor necrosis factor (TNF) is a pro-inflammatory cytokine with known systemic effects.
- The precise impact of TNF on glucose metabolism and hormonal regulation requires further elucidation.
Purpose of the Study:
- To investigate the effects of continuous intravenous TNF infusion on glucose kinetics and counterregulatory hormone levels in anesthetized dogs.
Main Methods:
- Anesthetized dogs received a 6-hour constant intravenous infusion of either TNF or saline (control).
- Glucose turnover, hindlimb substrate flux, cardiovascular responses, and hormone concentrations were measured.
- Glucose kinetics were analyzed by tracking glucose production and disappearance rates.
Main Results:
- TNF infusion led to a significant decrease in blood glucose levels, inducing mild hypoglycemia.
- This was accompanied by elevated cortisol, glucagon, and epinephrine.
- Both glucose production and disappearance rates increased, with disappearance and clearance showing a more pronounced rise.
- Hindlimb glucose uptake and clearance significantly increased in TNF-infused dogs, despite a drop in insulin levels.
Conclusions:
- TNF infusion causes hypoglycemia in dogs due to an imbalance between glucose production and disappearance.
- Increased glucose uptake in peripheral tissues, like the hindlimb, appears to be a direct effect of TNF and is insulin-independent.
- These findings highlight TNF's significant role in altering glucose homeostasis.