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Pulsatile insulin release from islets isolated from three subjects with type 2 diabetes
Jian-Man Lin1, Marta E Fabregat, Ramon Gomis
1Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
Diabetes
|March 28, 2002
Summary
Type 2 diabetes alters insulin release patterns, with islets from affected individuals showing impaired glucose response. This suggests potential metabolic defects in insulin secretion, impacting blood sugar control.
Area of Science:
- Endocrinology
- Metabolic Disorders
- Cellular Physiology
Background:
- Plasma insulin exhibits regular oscillations crucial for glucose regulation in healthy individuals.
- Altered insulin secretion patterns are observed in type 2 diabetes, potentially contributing to insulin resistance and hyperglycemia.
- Derangements in pancreatic islet secretory patterns are suspected causes for altered insulin dynamics in type 2 diabetes.
Purpose of the Study:
- To investigate the dynamics of insulin release from individual pancreatic islets in subjects with type 2 diabetes.
- To compare insulin secretion patterns between type 2 diabetic and normal subjects under varying glucose and tolbutamide conditions.
Main Methods:
- Isolation and perifusion of individual islets from three type 2 diabetic and four normal subjects.
- Measurement of insulin release rates and pulsatility at basal (3 mmol/l) and high (11 mmol/l) glucose concentrations.
- Assessment of insulin release in response to tolbutamide stimulation.
Main Results:
- Islets from type 2 diabetic subjects released insulin in pulses, similar to normal subjects, but showed impaired responses to elevated glucose.
- In one type 2 diabetic subject, high glucose increased insulin pulse amplitude but not frequency; tolbutamide had no effect.
- Islets from other type 2 diabetic subjects showed no significant glucose-stimulated insulin release, with tolbutamide showing a transient effect in one.
- Normal islets demonstrated increased insulin release at high glucose, with further enhancement by tolbutamide in some cases.
Conclusions:
- Pancreatic islets in type 2 diabetes do release insulin in pulses.
- The impaired insulin secretory response to glucose in type 2 diabetes may stem from defects in glucose metabolism prior to mitochondrial processing.
- These findings highlight potential cellular mechanisms contributing to dysregulated insulin secretion in type 2 diabetes.