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Somatostatin and epinephrine decrease insulin messenger ribonucleic acid in HIT cells through a pertussis

H J Zhang¹, J B Redmon, J M Andresen

¹Department of Medicine, University of Minnesota Medical School, Minneapolis 55455.

|November 1, 1991

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Somatostatin and epinephrine reduce insulin secretion and also decrease insulin mRNA and content in beta-cells. These hormones act before the exocytotic pathway, suggesting a novel, long-term regulation of insulin synthesis.

Area of Science:

Endocrinology
Molecular Biology
Cell Biology

Background:

Somatostatin and epinephrine are known to inhibit insulin secretion.
Their mechanism of action was previously thought to be solely within the exocytotic pathway.

Purpose of the Study:

To investigate potential non-exocytotic effects of somatostatin and epinephrine on insulin synthesis.
To explore the role of these hormones in regulating insulin messenger RNA (mRNA) levels.

Main Methods:

Utilized HIT cells, a clonal beta-cell line.
Measured insulin secretion, insulin mRNA levels, and insulin content.
Investigated the effect of pertussis toxin preincubation.

Main Results:

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Both somatostatin and epinephrine significantly inhibited insulin secretion.

These hormones also decreased insulin mRNA levels and insulin content in HIT cells.

These non-exocytotic effects were observed within 24 hours, maximal by 48 hours, and blocked by pertussis toxin.

Conclusions:

Somatostatin and epinephrine negatively modulate insulin availability through a guanine nucleotide binding protein-mediated pathway.
This action occurs during insulin synthesis, preceding the exocytotic pathway.
These findings suggest a role for somatostatin and epinephrine as long-term regulators of insulin synthesis and availability.