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Beta cell function, peripheral sensitivity to insulin and islet cell autoimmunity in cystic fibrosis patients with
D Cucinotta1, S Conti Nibali, T Arrigo
1Institute of Pediatrics, University of Messina, Italy.
Insights
Cystic fibrosis (CF) patients show impaired beta cell function and delayed insulin response, even with normal glucose tolerance. These issues are not linked to insulin sensitivity or autoimmune problems.
Area of Science:
- Endocrinology and Metabolism
- Pediatric Gastroenterology
- Genetics and Genetic Diseases
Background:
- Cystic Fibrosis (CF) is a genetic disorder affecting multiple organs.
- Glucose metabolism and pancreatic function can be compromised in CF.
- Understanding beta cell function in CF is crucial for managing potential diabetes.
Purpose of the Study:
- To investigate beta cell function in young individuals with CF and normal glucose tolerance.
- To assess peripheral insulin sensitivity in CF patients.
- To determine the role of pancreatic autoimmunity in CF-related glucose intolerance.
Main Methods:
- Studied 30 young CF patients meeting normal glucose tolerance criteria.
- Utilized oral glucose tolerance tests and intravenous glucose challenges.
- Assessed insulin sensitivity via euglycemic clamp and insulin receptor analysis on monocytes.
Main Results:
- CF patients exhibited significantly lower glucose tolerance compared to controls.
- Insulin response was preserved but delayed in oral glucose tolerance tests; first-phase insulin secretion was blunted.
- Peripheral insulin sensitivity and insulin receptor numbers were comparable between CF patients and controls; no islet-cell antibodies were detected.
Conclusions:
- Beta cell dysfunction can occur in cystic fibrosis patients even with normal glucose tolerance.
- These beta cell abnormalities are independent of peripheral insulin sensitivity.
- Autoimmune processes do not appear to be the cause of these observed beta cell function disorders in CF.
Abstract:
Beta cell function, peripheral sensitivity to insulin and specific pancreatic autoimmunity were studied in 30 youngsters with cystic fibrosis (CF) accurately selected in order to fulfill the criteria for normal glucose tolerance. With respect to weight-matched controls, patients with CF exhibited a significantly lower glucose tolerance and a globally preserved, although delayed, insulin response to oral glucose tolerance test, while first-phase insulin secretion after i.v. glucose was blunted. Peripheral sensitivity to insulin, assessed in vivo by both the euglycemic clamp technique and the number of insulin receptors, directly measured in circulating monocytes, was superimposable in patients and controls. Serum islet-cell antibodies were not found in any of the patients. In conclusion, disorders of beta cell function may be observed in CF patients even when glucose tolerance is within the normal range. Such abnormalities are not associated with changes in peripheral sensitivity to insulin and do not seem to depend on specific autoimmune events.