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Aggregation of insulin by chlorpromazine
1Protein Chemistry Laboratory, Department of Chemistry, Bose Institute, 93/1 Acharyya Prafulla Chandra Road, 700 009, Calcutta, India. bhattacharyyaj@health.missouri.edu
Biochemical Pharmacology
|November 14, 2001
Summary
Chlorpromazine (CPZ) causes high blood sugar by inactivating insulin. This drug may lead to insulin aggregation through disulphide bond reduction, impacting glucose levels in normal and diabetic individuals.
Area of Science:
- Biochemistry
- Pharmacology
- Endocrinology
Background:
- Chlorpromazine (CPZ) is recognized for inducing hyperglycemia.
- CPZ can inhibit insulin secretion in individuals with and without latent diabetes mellitus.
Purpose of the Study:
- To investigate the mechanism underlying CPZ-induced hyperglycemia.
- To explore the potential role of insulin aggregation in CPZ's hyperglycemic effects.
Main Methods:
- The study focused on determining the probable mechanism of CPZ-induced hyperglycemia.
- Investigated the potential for CPZ to cause insulin aggregation.
Main Results:
- CPZ may cause insulin aggregation by reducing disulphide bonds.
- This aggregation potentially inactivates insulin, leading to hyperglycemia.
Conclusions:
- CPZ-induced hyperglycemia may result from the inactivation of insulin.
- Disulphide bond reduction leading to insulin aggregation is a probable mechanism.