DECREASED SERUM 1,5-ANHYDROGLUCITOL IN NONDIABETIC SUBJECTS WITH A FAMILY HISTORY OF NIDDM

Citation
S. Tsukui et al., DECREASED SERUM 1,5-ANHYDROGLUCITOL IN NONDIABETIC SUBJECTS WITH A FAMILY HISTORY OF NIDDM, Diabetes care, 19(9), 1996, pp. 940-944
Citations number
27
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
Journal title
ISSN journal
01495992
Volume
19
Issue
9
Year of publication
1996
Pages
940 - 944
Database
ISI
SICI code
0149-5992(1996)19:9<940:DS1INS>2.0.ZU;2-T
Abstract
OBJECTIVE - To investigate the effect of a family history of NIDDM on HbA(1c) and serum 1,5-anhydroglucitol (AG) in nondiabetic subjects. RE SEARCH DESIGN AND METHODS - A 75-g oral glucose tolerance test was per formed: 258 subjects with normal glucose tolerance and 106 subjects wi th impaired glucose tolerance (IGT) were selected. HbA(1c) and serum A G were compared between subjects with and without a family history of NIDDM. The relationships between age, BMI, HbA(1c), serum AG, Fasting and 2-h plasma glucose, and urinary glucose were also examined using p rincipal component analysis with a varimax rotation. RESULTS - In the normal group, only serum AG was lower in subjects with a positive fami ly history than in those with no family history. On the other hand, in the IGT group, subjects with a positive Family history were younger a nd had a higher 2-h plasma glucose, a higher urinary glucose, and a lo wer serum AG than those with no family history, whereas there was no d ifference in HbA(1c). Principal component analysis identified three fa ctors. The first factor, a linear combination of HbA(1c) and fasting p lasma glucose, was labeled an average glycemic factor. The second Fact or, which included serum AG, 2-h plasma glucose, and urinary glucose, was labeled an oscillatory glycemic factor. The third factor, which co ntrasted age against BMI, was labeled an environmental factor. CONCLUS IONS - Serum AG is related to glycosuria even among nondiabetic subjec ts, and its concentrations are decreased in those with a family histor y of NIDDM. Our results suggest that serum AG rather than HbA(1c) refl ects early metabolic abnormalities in these subjects.