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Interleukin-1 induced increases in glucose utilization are insulin mediated
1Department of Physiology, Louisiana State University Medical Center, New Orleans.
Life Sciences
|January 1, 1989
Summary
Interleukin-1 (IL-1) enhances glucose uptake in various tissues, including the lungs and skeletal muscle. This effect is mediated by insulin, as demonstrated in studies with rats.
Area of Science:
- Immunology
- Metabolic Research
- Endocrinology
Background:
- Interleukin-1 (IL-1) plays a role in the body's acute-phase response to infection.
- Infection often leads to increased whole-body glucose utilization during the hypermetabolic phase.
Purpose of the Study:
- To investigate whether Interleukin-1 (IL-1) can increase glucose uptake.
- To determine if IL-1-induced glucose uptake is dependent on elevated plasma insulin levels.
Main Methods:
- Utilized the 2-deoxyglucose tracer technique in vivo to measure tissue glucose utilization (Rg) in conscious rats.
- Administered human purified IL-1 and somatostatin (SRIF) to manipulate insulin levels.
- Examined IL-1 effects in streptozotocin-induced diabetic rats.
Main Results:
- IL-1 administration increased plasma insulin levels and tissue glucose utilization (Rg) in macrophage-rich tissues (lung, spleen, liver, skin) and skeletal muscle.
- Somatostatin (SRIF) infusion prevented the IL-1-induced increase in insulin and tissue glucose utilization.
- IL-1 did not increase glucose utilization in diabetic rats.
Conclusions:
- Interleukin-1 (IL-1) administration increases organ glucose utilization.
- This increase in glucose utilization is dependent on insulin.
- IL-1's role in infection response may involve insulin-mediated glucose uptake regulation.