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Ketoacidosis in pancreatectomized man
The New England Journal of Medicine
|June 2, 1977
Summary
Glucagon is not essential for developing diabetic ketoacidosis. However, this study shows it can accelerate the onset of high ketone and glucose levels during insulin deficiency.
Area of Science:
- Endocrinology
- Metabolic Disorders
- Diabetes Research
Background:
- Diabetic ketoacidosis (DKA) is a serious complication of diabetes.
- The role of glucagon in DKA development has been debated.
- Previous hypotheses suggested glucagon is essential for DKA.
Purpose of the Study:
- To investigate the necessity of glucagon in the development of diabetic ketoacidosis.
- To determine if glucagon is essential or merely contributory to DKA.
- To clarify the hormonal interplay in insulin deficiency-induced metabolic decompensation.
Main Methods:
- Withholding insulin from patients with juvenile-type diabetes and pancreatectomized subjects.
- Monitoring plasma glucagon, blood ketone, and blood glucose concentrations.
- Controlled study involving fasting patients previously maintained on intravenous insulin.
Main Results:
- In diabetic patients, insulin withdrawal led to sharp increases in plasma glucagon, blood ketones (4.1+/-0.7 mmol/L), and blood glucose (12.5+/-1.8 mmol/L).
- In pancreatectomized patients lacking measurable glucagon, blood ketones rose by 1.8+/-0.8 mmol/L and blood glucose by 7.7+/-1.5 mmol/L.
- These findings indicate glucagon is not indispensable for DKA development.
Conclusions:
- Glucagon is not essential for the development of diabetic ketoacidosis.
- Glucagon may accelerate the onset of ketonemia and hyperglycemia in insulin deficiency.
- The study refutes the essentiality of glucagon in DKA pathogenesis but highlights its accelerating role.