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Pancreatic function in the essential fatty acid deficient rat.
L Hjelte1, B Ahrén, A Andrén-Sandberg
1Department of Pediatrics, Karolinska Institutet, Huddinge Hospital, Stockholm, Sweden.
Metabolism: Clinical and Experimental
|August 1, 1990
Summary
Essential fatty acid deficiency in rats leads to basal hyperinsulinemia and hypoglycemia. Pancreatic endocrine and exocrine functions remain operational despite exaggerated insulin response to glucose.
Area of Science:
- Endocrinology
- Nutritional Science
- Pancreatic Physiology
Background:
- Essential fatty acid (EFA) deficiency can impact metabolic processes.
- The effects of EFA deficiency on pancreatic function require further elucidation.
Purpose of the Study:
- To investigate the influence of essential fatty acid (EFA) deficiency on pancreatic endocrine and exocrine function in rats.
- To assess insulin and glucagon responses to glucose and arginine challenges.
- To evaluate exocrine pancreatic function and islet cell morphology.
Main Methods:
- Studied 120-day-old rats with induced essential fatty acid deficiency (EFAD).
- Measured plasma insulin and glucagon responses to glucose and arginine.
- Assessed pancreatic amylase secretion in isolated acinar cells.
- Examined islet peptides using immunocytochemistry.
Main Results:
- EFAD rats exhibited higher basal insulin and lower basal glucose levels.
- An exaggerated plasma insulin response to glucose was observed in EFAD rats.
- Arginine-stimulated insulin and glucagon responses were normal.
- Exocrine pancreatic function (amylase secretion) was largely unaffected.
- No significant morphological changes were observed in pancreatic islet cells.
Conclusions:
- Pancreatic endocrine and exocrine secretory functions are operational in essential fatty acid deficiency.
- EFA deficiency is associated with basal hyperinsulinemia, hypoglycemia, and an exaggerated insulin response to glucose.
- The pathophysiology underlying these metabolic alterations warrants further investigation.