Disproportionate hyperproinsulinemia is one manifestation of the B-cell dysfunction observed in non-insulin-dependent diabetes mellitus (NIDDM), but it is unclear when this abnormality develops and whether it predicts the development of NIDDM. At baseline, measurements of proinsulin (PI) and immunoreactive insulin (IRI) levels were made in 87 second-generation Japanese-American men, a population at high risk for the subsequent development of NIDDM, and, by using World Health Organization criteria, subjects were categorized as having normal glucose tolerance (NGT; n = 49) or impaired glucose tolerance (IGT; n = 38). After a 5-year follow-up period, they were recategorized as NGT, IGT, or NIDDM using the same criteria. After 5 years, 16 subjects had developed NTODM, while 71 had NGT or IGT. Individuals who developed NIDDM were more obese at baseline, measured as intra-abdominal fat (IAF) area on computed tomography (P = 0.046) but did not differ in age from those who continued to have NGT or IGT. At baseline, subjects who subsequently developed NIDDM had higher fasting glucose (P = 0.0042), 2-h glucose (P = 0.0002), fasting C-peptide (P = 0.0011), and fasting PI levels (P = 0.0033) and disproportionate hyperproinsulinemia (P = 0.056) than those who continued to have NGT or IGT after 5 years of follow-up. NIDDM incidence was positively correlated with the absolute fasting PI level (relative odds = 2.35; P = 0.0025), even after adjustment for fasting IRI, IAF, and body mass index (relative odds = 2.17; P = 0.013). Because 12 of the 16 subjects who developed NTODM had IGT at baseline, the 38 IGT subjects were also examined separately. In this cohort, the same risk factors (fasting and 2-h glucose, fasting C-peptide, and fasting PI levels) were predictive for the development of NIDDM. We conclude that Japanese-American men who subsequently develop NIDDM have more IAF and increased glucose, C-peptide, and PI levels. These data suggest that alterations in PI may be a new marker for the subsequent development of NTODM.
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Original Articles|
February 01 1995
Proinsulin as a Marker for the Development of NIDDM in Japanese-American Men
Steven E Kahn;
Steven E Kahn
University of Washington and Veterans Affairs Medical Center
Seattle, Washington
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Donna L Leonetti;
Donna L Leonetti
Department of Anthropology
Seattle, Washington
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Ronald L Prigeon;
Ronald L Prigeon
University of Washington and Veterans Affairs Medical Center
Seattle, Washington
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Edward J Boyko;
Edward J Boyko
Department of Medicine, Division of Metabolism, Endocrinology, and Nutrition and the Division of General Internal Medicine
Seattle, Washington
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Richard W Bergstrom;
Richard W Bergstrom
University of Washington and Veterans Affairs Medical Center
Seattle, Washington
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Wilfred Y Fujimoto
Wilfred Y Fujimoto
University of Washington and Veterans Affairs Medical Center
Seattle, Washington
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Address correspondence to Dr. Steven E. Kahn, VA Medical Center (151L), 1660 S. Columbian Way, Seattle, WA 98108.
Diabetes 1995;44(2):173–179
Article history
Received:
August 08 1994
Revision Received:
October 20 1994
Accepted:
October 20 1994
PubMed:
7859937
Citation
Steven E Kahn, Donna L Leonetti, Ronald L Prigeon, Edward J Boyko, Richard W Bergstrom, Wilfred Y Fujimoto; Proinsulin as a Marker for the Development of NIDDM in Japanese-American Men. Diabetes 1 February 1995; 44 (2): 173–179. https://doi.org/10.2337/diab.44.2.173
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