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Defective glucose utilization in patients with functioning beta-cell tumors persists after tumor excision
G S McGee1, M M Kulaylat, N N Abumrad
1Department of Surgery, Vanderbilt University, School of Medicine, Nashville, Tennessee.
Annals of Surgery
|October 1, 1987
Summary
Chronic hyperinsulinemia, often from tumors, impairs glucose utilization in humans. This defect in glucose metabolism improves after tumor removal but may not fully resolve.
Area of Science:
- Endocrinology
- Metabolic Research
Background:
- Insulin-secreting tumors cause endogenous hyperinsulinemia.
- The impact of chronic hyperinsulinemia on human glucose utilization is not fully understood.
Purpose of the Study:
- To assess glucose utilization in patients with insulin-secreting tumors before and after surgery.
- To compare glucose utilization in patients with controls experiencing acute or chronic hyperinsulinemia.
Main Methods:
- Euglycemic clamp technique was used to measure glucose utilization.
- Patients with insulinomas and matched control groups with induced hyperinsulinemia were studied.
Main Results:
- Postoperative patients and chronic hyperinsulinemia controls showed impaired glucose utilization compared to acute controls.
- A patient with a proinsulin-producing tumor also exhibited defective glucose utilization, which partially improved after tumor excision.
Conclusions:
- Chronic endogenous hyperinsulinemia in humans is linked to impaired peripheral glucose utilization.
- This metabolic defect shows only partial resolution even two years after tumor removal.