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Research Article Free access | 10.1172/JCI106434
Evans Division of Clinical Research, Boston University Hospital, Boston, Massachusetts 02118
Boston University Medical Service, Boston City Hospital, Boston, Massachusetts 02118
Department of Internal Medicine, The University of Texas, Southwestern Medical School, Dallas, Texas 75235
Find articles by Merimee, T. in: JCI | PubMed | Google Scholar
Evans Division of Clinical Research, Boston University Hospital, Boston, Massachusetts 02118
Boston University Medical Service, Boston City Hospital, Boston, Massachusetts 02118
Department of Internal Medicine, The University of Texas, Southwestern Medical School, Dallas, Texas 75235
Find articles by Siperstein, M. in: JCI | PubMed | Google Scholar
Evans Division of Clinical Research, Boston University Hospital, Boston, Massachusetts 02118
Boston University Medical Service, Boston City Hospital, Boston, Massachusetts 02118
Department of Internal Medicine, The University of Texas, Southwestern Medical School, Dallas, Texas 75235
Find articles by Hall, J. in: JCI | PubMed | Google Scholar
Evans Division of Clinical Research, Boston University Hospital, Boston, Massachusetts 02118
Boston University Medical Service, Boston City Hospital, Boston, Massachusetts 02118
Department of Internal Medicine, The University of Texas, Southwestern Medical School, Dallas, Texas 75235
Find articles by Fineberg, S. in: JCI | PubMed | Google Scholar
Published December 1, 1970 - More info
A group of 32 sexual ateliotic dwarfs with an isolated deficiency of human growth hormone (HGH) were shown previously to resemble subjects with genetic diabetes mellitus in terms of hyperlipemia, carbohydrate intolerance, and patterns of insulin secretion. 11 of these dwarfs had needle biopsies of the quadriceps femoris carried out and tissue fixed for electron microscopy. Capillary basement membrane thickness was measured and compared with measurements previously obtained in diabetics and normal controls. Measurements were similar in controls and dwarfs (1080 ±27 A and 1086 ±90 A, respectively) and significantly less than in diabetics (2403 ±119 A). Placed in juxtaposition with the absence of retinopathy in dwarfs and the high incidence in the diabetic group (41%), the data support the thesis that these anatomical abnormalities are largely independent of serum lipid and carbohydrate abnormalities. The data are consistent with a supportive, if not causative role of growth hormone in the pathogenesis of these lesions.
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