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Updated: Aug 8, 2026
Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine
Published on: February 26, 2019
Functional and morphological effects of interleukin-1 beta on the perfused rat pancreas
L D Wogensen1, V Kolb-Bachofen, P Christensen
1Steno Memorial Hospital, Hagedorn Research Laboratory, Gentofte, Denmark.
Insights
Interleukin-1 beta enhances insulin and glucagon secretion from pancreatic B cells, with its effect on insulin release being dose-dependent and potentially priming B-cell function.
Area of Science:
- Endocrinology
- Immunology
- Cell Biology
Background:
- Recombinant human interleukin-1 beta (IL-1β) has shown a potentiating effect on glucose-stimulated insulin release.
- The precise modulation of IL-1β's stimulatory effect on B cells requires further investigation.
Purpose of the Study:
- To determine how varying concentrations and exposure times of IL-1β affect B-cell function.
- To elucidate the mechanism of action of IL-1β on pancreatic endocrine cells.
- To examine the influence of IL-1β on pancreatic B-cell morphology.
Main Methods:
- Perfusion of isolated rat pancreas with recombinant human IL-1β under varying glucose concentrations (5, 11, 20 mmol/l).
- Dose-response experiments with IL-1β concentrations ranging from 0.1 x 10(-3) to 100 ng/ml.
- Measurement of insulin, glucagon, and prostaglandin E2 release.
- Morphological examination of endocrine pancreas post-cytokine exposure.
Main Results:
- IL-1β stimulated insulin secretion at 11 and 20 mmol/l D-glucose, potentiating both first and second phases in a dose-dependent manner.
- The potentiating effect on insulin release decreased at higher IL-1β concentrations.
- IL-1β stimulated glucagon secretion independently of glucose and insulin levels.
- The effect of IL-1β on insulin secretion persisted after perfusion cessation, indicating a priming effect.
Conclusions:
- Interleukin-1 beta modulates pancreatic B-cell function by stimulating insulin and glucagon secretion.
- The cytokine exhibits a dose-dependent effect on insulin release, with potential priming of B-cell function.
- IL-1β's influence on pancreatic endocrine cells warrants further study for understanding metabolic regulation.
Abstract:
We recently reported a potentiating effect of recombinant human interleukin-1 beta on glucose-stimulated insulin release from the isolated perfused pancreas. With the aim of determining whether the stimulatory effect of recombinant interleukin-1 beta on the B cell in the intact gland was modulated by varying the concentration, time of exposure to recombinant interleukin-1 beta or B-cell activity, and to elucidate a possible mechanism of action, we measured in the perfused rat pancreas the release of insulin, glucagon and/or prostaglandin E2 according to the following three different protocols: (1) perfusion with 20 ng/ml of recombinant interleukin-1 beta for 92 min at 5 and 20 mmol/l D-glucose (2) perfusion with varying concentrations of recombinant interleukin-1 beta ranging from 0.1 x 10(-3) ng/ml to 100 ng/ml at 5 and 20 mmol/l D-glucose (3) perfusion with 20 ng/ml of recombinant interleukin-1 beta at 5, 11 or 20 mmol/l D-glucose. Furthermore, in a separate set of experiments we examined the influence of the cytokine on the morphology of the endocrine pancreas. Interleukin-1 beta stimulated insulin secretion at 11 and 20 mmol/l D-glucose and potentiated first as well as second phase insulin release in a dose-dependent fashion, with decreasing effect at higher concentrations. Glucagon secretion was also stimulated by recombinant interleukin-1 beta, irrespective of increasing glucose (5, 11, 20 mmol/l) and insulin concentrations. The potentiating effect of recombinant interleukin-1 beta on insulin secretion was evident even after discontinued perfusion with the cytokine, suggesting a priming effect on B-cell function.(ABSTRACT TRUNCATED AT 250 WORDS)
