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Dynamics of insulin and glucagon release in rats: influence of dietary manganese
Abstract:
The effect of manganese on endocrine pancreatic function was examined in manganese-sufficient (control) and manganese-deficient (Mn-) Sprague-Dawley rats. Pancreatic insulin release was lower (P less than 0.05) in Mn- rats than in controls in response to both a 300 mg/dl and a 100 mg/dl glucose stimulus. The 300 mg/dl glucose stimulus induced the synthesis of 19.4 micrograms insulin/g pancreas in control rats. Additionally, no appreciable intracellular degradation of insulin occurred over an 80-min perfusion period. By contrast, in Mn- rats, there occurred an intracellular insulin degradation amounting to 7.8 micrograms/g pancreas. This enhanced degradation was partially compensated by a net insulin synthesis of only 3.4 micrograms insulin/g pancreas. Initial (min 1-3) insulin release by Mn- rats in response to 10 mM arginine was lower (P less than 0.05) than that observed in controls. Pancreatic glucagon release in response to 10 mM arginine was not affected by manganese deficiency. These findings demonstrate that manganese deficiency results in depressed pancreatic insulin synthesis and enhanced degradation. These factors may be responsible for the abnormal carbohydrate metabolism observed in Mn- animals.
Insights
Manganese deficiency in rats impairs pancreatic insulin release and synthesis. This deficiency also increases insulin degradation, potentially causing abnormal carbohydrate metabolism.
Area of Science:
- Endocrinology
- Nutritional Science
- Metabolic Research
Background:
- Manganese is an essential trace element crucial for various physiological processes.
- Pancreatic islet function plays a vital role in glucose homeostasis.
- The impact of manganese on insulin synthesis and secretion requires further elucidation.
Purpose of the Study:
- To investigate the effects of manganese deficiency on endocrine pancreatic function in Sprague-Dawley rats.
- To assess the influence of manganese on insulin synthesis, release, and degradation.
- To determine the relationship between manganese status and pancreatic glucagon release.
Main Methods:
- Comparative study using manganese-sufficient (control) and manganese-deficient (Mn-) Sprague-Dawley rats.
- In vitro pancreatic perfusion studies to measure insulin and glucagon release in response to glucose and arginine stimuli.
- Quantification of insulin synthesis and intracellular degradation rates.
Main Results:
- Manganese deficiency significantly reduced pancreatic insulin release in response to glucose stimuli (300 mg/dl and 100 mg/dl).
- Mn- rats exhibited significantly lower insulin synthesis (3.4 micrograms/g pancreas) compared to controls (19.4 micrograms/g pancreas).
- Intracellular insulin degradation was markedly enhanced in Mn- rats (7.8 micrograms/g pancreas) compared to controls.
- Arginine-stimulated insulin release was lower in Mn- rats, while glucagon release remained unaffected.
Conclusions:
- Manganese deficiency leads to depressed pancreatic insulin synthesis and increased insulin degradation.
- These pancreatic dysfunctions in manganese deficiency may contribute to abnormal carbohydrate metabolism.
- Maintaining adequate manganese levels is crucial for normal endocrine pancreatic function and glucose regulation.