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Suppressibility of glucagon secretion by glucose in juvenile diabetes
Insights
In diabetic children, glucose does not suppress plasma glucagon without insulin. Insulin therapy restores glucagon suppressibility by glucose, indicating insulin deficiency causes inappropriate glucagon levels.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Diabetes Mellitus Research
Background:
- Children with diabetes exhibit hyperglycemia but similar fasting plasma glucagon to normal children.
- Insulin deficiency is a key factor in the dysregulation of glucagon in diabetic children.
Purpose of the Study:
- To investigate the suppressibility of plasma glucagon by glucose in normal and diabetic children.
- To determine the role of insulin deficiency in the inappropriate hyperglucagonemia observed in diabetic children.
Main Methods:
- Fasting plasma glucagon concentrations were measured in normal and diabetic children.
- Glucose infusions were administered to assess glucagon suppression, with and without prior insulin treatment in diabetic participants.
- Blood glucose and plasma glucagon levels were monitored during glucose infusions and insulin administration.
Main Results:
- Glucose infusion suppressed plasma glucagon in normal children and in diabetic children pretreated with insulin.
- Diabetic children did not show glucagon suppression with glucose alone, despite hyperglycemia.
- Insulin administration in diabetic patients led to a transient rise in glucagon as blood glucose fell.
Conclusions:
- Diabetic children deprived of insulin exhibit relative hyperglucagonemia inappropriate for their blood glucose levels.
- This hyperglucagonemia is secondary to insulin deficiency.
- Insulin therapy can restore the normal suppressibility of glucagon by glucose in diabetic children.
Abstract:
The suppressibility of plasma glucagon concentrations by glucose was investigated in normal and diabetic children. Fasting concentrations of plasma glucagon were similar in normal and in diabetic children despite the hyperglycemia of the latter. Infusion of glucose promptly suppressed glucagon values in the normal as well as in the diabetic children pretreated with half of their usual morning dose of insulin. Glucose alone, however, did not suppress plasma glucagon in diabetic patients, despite the attainment of significant hyperglycemia. Administration of insulin during an ongoing glucose infusion in the diabetic patients lowered their blood glucose concentration; the concentration of glucagon rose transiently when the glucose concentration fell. These data confirm the existence of relative hyperglucagonemia inappropriate for the degree of blood glucose concentration in diabetic children deprived of insulin. The data also suggest that this hyperglucagonemia is secondary to insulin deficiency and suppressibility of glucagon by glucose can be restored by insulin therapy.