Related Experiment Videos
Hyperglycemic effect of neurotensin.
The Tohoku Journal of Experimental Medicine
|June 1, 1984
Summary
Neurotensin causes hyperglycemia through glucagon and catecholamines, not directly on the liver. Hypotension-induced baroceptor stimulation contributes to this effect.
Area of Science:
- Endocrinology
- Neuroscience
- Gastroenterology
Background:
- Neurotensin is a peptide hormone involved in various physiological processes.
- Its role in glucose homeostasis and potential hyperglycemic effects require further elucidation.
Purpose of the Study:
- To investigate the mechanisms underlying neurotensin-induced hyperglycemia in anesthetized dogs.
- To determine the involvement of glucagon, insulin, catecholamines, and baroceptor reflexes.
Main Methods:
- Intravenous and intraportal administration of neurotensin in anesthetized dogs.
- Measurement of blood glucose, glucagon, and insulin levels.
- Pharmacological interventions including somatostatin, alpha-adrenoceptor blockade, and baroceptor denervation.
Main Results:
- Neurotensin administration caused a decrease in blood pressure and increased blood glucose, glucagon, and insulin levels.
- Somatostatin inhibited glucagon and insulin responses but not hyperglycemia.
- Alpha-adrenoceptor blockade or baroceptor denervation suppressed the hyperglycemic response.
- Neurotensin did not directly stimulate the liver or anterior pituitary hormones.
Conclusions:
- Neurotensin-induced hyperglycemia involves both glucagon and catecholamines.
- Catecholamine release is likely mediated by baroceptor stimulation due to hypotension.
- Neurotensin does not act directly on the liver to induce hyperglycemia.