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,
HILDA REBAGLIAT
,
MARVIN GLASSER
and
J. M. B. BLOODWORTH||
Department of Medicine, Diabetes and Metabolism Division, and Department of Community and Preventive Medicine, Information Processing Center, New York Medical College, New York, New York 10029; and the Department of Pathology, University of Wisconsin-Medical School Madison, Wisconsin 53706
Address requests for reprints to: Dr. Rafael A. Camerini-Davalos, Professor of Medicine, Director, Diabetes and Metabolism Division, New York Medical College, 1249 Fifth Avenue, New York, New York 10029.
Muscle capillary basement membrane width (MCBMW) was determined in 30 offspring with normal glucose tolerance of proven conjugal maturity-onset diabetic parents [genetic prediabetics (GPs)] and in 40 control subjects. For the GPs, the follow-up period with normal oral glucose tolerance testing ranged from 11-98 months, with an average of 22 months before and 18 months after the muscle biopsy and an average of five oral glucose tolerance tests before and four after.
MCBMW for GPs was 1396 Å ± 56 (SE) compared to 1153 Å ± 40 for controls (P < 0.01). There was a positive relationship between age and MCBMW for both the GPs and controls, with a slope of 8.65 and 3.40 Å/yr, respectively (P < 0.20). MCBMW adjusted for age by means of an analysis of covariance shows even greater differences between the means of the two groups (P < 0.001). On the basis of age-adjusted 95% tolerance limits derived from our controls, seven GP (23%) and two controls (5%) had diffuse basement membrane thickening (BMT).
Mean SDS of individual basement membrane measurements were higher in GPs (531 Å) than controls (423 Å P < 0.005). Eight GPs (27%) and two controls (5%) had larger SDS than the tolerance limits.
Based on the theoretical considerations of Kilo et al. (Diabetes 21: 881,1972) that diffuse BMT will be characterized by a relatively uniform thickening and that increase in the SD will be the statistical expression of nondiffuse BMT, 10 GP, (33%) were found with BMT.
It is concluded that in some subjects highly predisposed to diabetes on a genetic basis, changes may occur in the microvessels before detectable hyperglycemia. (J Clin Endocrinol Metab 48: 251, 1979)
* The work was supported in part by General Research Support Grant RR-05398 from the General Research Support Branch, Division of Research Resources, NIH; Health Research Council of the City of New York; NIH Training Grant AM05617-05; Diabetes Research Fund (New York, NY); Hope for Diabetics Foundation (New York, NY); Veterans Research Fund (J.M.B.B.); and The Upjohn Co. (Kalamazoo, MI).
Present address: Assistant Professor of Medicine, Diabetes and Metabolism Division, New York Medical College New York, New York 10029
Present address: Research Associate: Medicine, Diabetes and Metabolism Division, New York Medical College New York, New York 10029
Present address: Associate Professor, Department of Community and Preventive Medicine, Director of Statistical Services, Information Processing Center, New York Medical College New York, New York 10029
|| Present address: Professor of Pathology, University of Wisconsin Medical School, Chief, Laboratory Service, Middleton Memorial Veterans Hospital, 470 North Charter Street Madison, Wisconsin 53706
Received June 9, 1978.
This article has been cited by other articles:
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  A. S. Reddi and R. A. Camerini-Davalos Diabetic Nephropathy: An Update Arch Intern Med, January 1, 1990; 150(1): 31 - 43. [Abstract] [PDF]
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