Declining β-cell function in type 2 diabetes: 5-Year follow-up and immunologic studies of the population of Wadena, MN

Frederick C. Goetz, Joseph Roel, David R Jacobs Jr, Jose Barbosa, Peter J Hannan, Jerry Palmer, William Hagopian

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8 Scopus citations


The aim of the study was to describe 5-year changes in meal-stimulated pancreatic insulin reserve in adults with normal and impaired glucose tolerance (NGT, IGT) and diabetes, with or without islet-related antibodies. This was a 5-year follow-up of 270 residents of Wadena, MN, of northern European origin, with good kidney function, defined as creatinine clearance greater than 60 mL/min/1.73 m2The subjects comprised a population-based sample originally studied in 1986 to 1987. Urine C-peptide (CP), in a 260-minute collection, was the integrated measure of insulin secretion; Ensure-Plus (Ross, Columbus, OH) was the liquid meal. Islet cytoplasmic antibodies (ICA), insulin autoantibodies (IAA), and glutamate decarboxylase antibodies (GAD65ab) were measured. In 182 subjects with NGT, there was no mean within-subject change in urine CP over 5 years (P =. 34). In 41 subjects with impaired GT (IGT), there was a moderate, but nonsignificant, increase in mean CP, and 6 (15%) subjects increased. In 37 type 2 diabetic subjects not taking insulin (type 2-No Ins), who had a mean diabetes duration at the 5-year examination of 9.6 ± 6.3 years, there was a 21% decrease in mean urine CP (P =. 012), attributable mostly to a major drop in 8 of the 37 subjects (22%). Islet-related antibody tests were mostly negative; GAD65ab positivity was related to CP decline only among insulin-taking subjects. In summary, in Wadena adults, meal-stimulated urine CP was stable or increased over 5 years in subjects with NGT and IGT, but CP decreased significantly in about one fifth of type 2-No Ins subjects, with no relation to antibody test results.

Original languageEnglish (US)
Pages (from-to)144-148
Number of pages5
JournalMetabolism: clinical and experimental
Issue number2
StatePublished - 2002

Bibliographical note

Funding Information:
Supported by Grant No. DK 33225 from the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (NIH); Grant No. M01 RR 00400 from the NIH General Clinical Research Center at the University of Minnesota; the Minnesota Medical Foundation; and the Diabetes Trust Fund, Inc, Birmingham, Alabama, Buris R. Boshell, MD, founder. W. H. was supported by an American Diabetes Association Career Development Award and by a Clinical Associate Physician Award of the University of Washington General Clinical Research Center (NIH Grant No. RR 00037).


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