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Title: Role of Insulinopenia in Cystic Fibrosis-Related Diabetes

URL: http://www.blackwell-synergy.com/servlet/useragent?func=synergy&
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Diabetic Medicine 19 (3), 221-226. "Cystic fibrosis-related diabetes: the role of peripheral insulin resistance and beta-cell dysfunction"
04/09/2002 08:56:00 AM
By David Ball

Insulinopenia could be a major factor in developing glucose intolerance, and subsequently cystic fibrosis-related diabetes (CFRD), in adults with cystic fibrosis (CF) who have no previous history of glycaemic disturbances. A study by investigators at the Royal Brompton and Harefield NHS Trust and Chelsea and Westminster Hospital, London, England, suggests that peripheral insulin resistance (IR) is not significant in the pathogenesis of CFRD. They found little difference in peripheral IR between 68 CF patients and 46 normal healthy controls measured by the homeostasis model assessment for insulin resistance (HOMA-IR). However, pancreatic-cell function, already subnormal in CF patients with normal glucose tolerance status as defined by two hour oral glucose tolerance tests (OGTTs), was found to deteriorate further with worsening glycaemic status. A subset of 30 CF patients and 16 controls were also measured for pancreatic ß-cell function, and glucose-induced insulin response was determined in 24 CF patients and eight controls. Glucose tolerances were seen to be normal in 41 of the CF patients, impaired in 18 and diabetic in nine. No significant differences were found in the mean HOMA-IR values (mU/mmol) in patients compared with controls. Glycaemic status had no impact on HOMA-IR (mU/mmol) in the CF patients as a whole. Compared with the healthy control group, ß-cell function (mU/mmol) was significantly lower in the whole CF group as well as in CF patients with normal glucose tolerance. In general, mean plasma glucose concentrations were higher in the CF group compared to controls, while mean plasma insulin concentrations were lower. Worsening glycaemic status among the CF patients led to a progressive decline in glucose-induced insulin release.

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