Cystic fibrosis-related diabetes: the role of peripheral insulin resistance and β-cell dysfunction

• Published in: Diabetic medicine 2002-03, Vol.19 (3), p.221-226
• Main Authors: Yung, B., Noormohamed, F. H., Kemp, M., Hooper, J., Lant, A. F., Hodson, M. E.
• Format: Article
• Language: English
• Subjects: Adult; Area Under Curve; Biological and medical sciences; Blood Glucose - metabolism; cystic fibrosis; Cystic Fibrosis - blood; Cystic Fibrosis - complications; diabetes; Diabetes Mellitus - etiology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Female; Gastroenterology. Liver. Pancreas. Abdomen; Glucose Tolerance Test; HOMA; Homeostasis; Humans; Insulin - blood; Insulin - metabolism; Insulin Resistance; Insulin Secretion; Islets of Langerhans - metabolism; Islets of Langerhans - physiopathology; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Medical sciences; Other diseases. Semiology; Reference Values; β-cell function
• ISSN: 0742-3071; 1464-5491
• DOI: 10.1046/j.1464-5491.2002.00666.x

Aims The goal of this study was to identify the glycaemic status and investigate the roles of peripheral insulin resistance (IR) and pancreatic β‐cell dysfunction in the pathogenesis of cystic fibrosis‐related diabetes (CFRD) in adult cystic fibrosis (CF) patients with no previous history of glycaemic disturbances. Methods The glucose tolerance status of 68 CF patients was determined using 2‐h oral glucose tolerance tests (OGTTs). Peripheral IR was measured using the homeostasis model assessment for insulin resistance (HOMA‐IR) in the CF group and 46 normal healthy control subjects. Pancreatic β‐cell function, calculated as the ratio between the 30‐min increment in plasma insulin and the corresponding 30‐min post‐OGTT plasma glucose concentration, was also measured in a subset of 30 CF patients and 16 normal healthy controls. Extended 180‐min OGTTs, with frequent plasma glucose and insulin sampling, were also undertaken in 24 CF patients and eight normal healthy controls to determine glucose‐induced insulin response. Results Of the 68 CF patients studied, 41, 18 and nine were found to have normal, impaired and diabetic glucose tolerances, respectively. The mean HOMA‐IR values (mU/mmol) in the CF patients, as a whole, were not significantly different compared with the normal healthy controls (CF 2.2 ± 1.1 vs. control 1.8 ± 0.9; NS). Within the CF group, glycaemic status had no impact on HOMA‐IR (mU/mmol): 2.2 ± 1.2 (normal glucose tolerance); 2.0 ± 1.0 (impaired glucose tolerance); and 2.3 ± 1.1 (diabetic glucose tolerance). β‐cell function (mU/mmol) was not only significantly lower in the CF group (CF 1.65 ± 1.8; P