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Gluconeogenesis in perfused livers from dexamethasone-treated chickens
T Kobayashi1, H Iwai, R Uchimoto
1Department of Veterinary Physiology, College of Agriculture, University of Osaka Prefecture, Japan.
The American Journal of Physiology
|April 1, 1989
Summary
Dexamethasone treatment in chickens significantly impacts glucose metabolism, increasing plasma glucose and liver glycogen. It also alters gluconeogenesis from lactate and fructose, highlighting the role of mitochondrial alanine aminotransferase in regulating hepatic glucose production.
Area of Science:
- Biochemistry
- Endocrinology
- Animal Physiology
Background:
- Dexamethasone sulfate is a synthetic glucocorticoid known to influence carbohydrate metabolism.
- Understanding the regulation of gluconeogenesis is crucial for metabolic research.
Purpose of the Study:
- To investigate the effects of dexamethasone sulfate on hepatic gluconeogenesis in chickens.
- To elucidate the role of specific enzymes in dexamethasone-induced metabolic changes.
Main Methods:
- Hemoglobin-free perfused chicken livers were utilized.
- Chickens received daily dexamethasone sulfate injections for 5 days.
- Gluconeogenesis rates were measured using various substrates (lactate, fructose, pyruvate) and inhibitors (quinolinate, NH4Cl, aminooxyacetate).
Main Results:
- Dexamethasone increased plasma glucose by ~160% and hepatic glycogen content twofold in fed chickens.
- In starved chickens, glucose production from lactate decreased by ~30% post-dexamethasone.
- Mitochondrial alanine aminotransferase activity was implicated in regulating hepatic gluconeogenesis in dexamethasone-treated chickens.
Conclusions:
- Dexamethasone significantly alters hepatic glucose production pathways in chickens.
- Mitochondrial alanine aminotransferase plays a key regulatory role in dexamethasone-influenced gluconeogenesis.