Sexual function was studied in 175 diabetic male outpatients randomly selected. Data collected included medical and sexual histories, physical examination, complete blood count, urinalysis, T4, 12 channel chemistry screening profile and plasma testosterone determination. Eighty-five of the 175 men were impotent (49 per cent), four reported premature ejaculation (2 per cent) and two subjects had retrograde ejaculation (1 per cent). In the group with impotence, the mean age of the subjects and duration of diabetes were respectively fifty-three and six years. In patients without impotence, the comparable values were fortyfive and five years. Typically, the onset of impotence was gradual, usually progressing over a period of six months to a year with an interval during which firmness of erection was decreased. Levels of sexual interest were sustained in almost all subjects. Over 90 per cent of the males studied gave a pattern of impotence compatible with an organic rather than a psychologic etiology. Occurrence of impotence'was not definitely correlated with duration of diabetes or with insulin or oral agents. Incidence of peripheral neuropathy was increased in the group with sexual dysfunction. Plasma testosterone levels were within normal limits in impotent diabetics or in the group without impotence, respectively (mean ± S.E.M.) 627 ±15 and 637 ± 14 ng per cent. It is apparent from these findings that androgen deficiency was not an etiologic factor in this group of diabetic men with impotence.
Current physiologic knowledge about glucose-insulin homeostasis in liver, brain, pancreas, kidney, peripheral tissues, and central vascular organs has been synthesized to form a whole-system mathematical model of glucose metabolism in normal, ideal man. In addition to data of other workers, results from more than 100 intravenous glucose tolerance tests, including variable dosage, variable duration of infusion, and double pulse studies, were used to determine model structure and parameters. Model and clinical testing have focused particularly on the fast phase of insulin response to vascular glucose. The model incorporates blood circulation and equilibration of substances between vascular and interstitial spaces, and it assumes constant fractional clearance of insulin by liver and kidney. Studies using a double pulse of glucose suggest that the time derivative of glucose level is not the sole or predominant influence on fast phase insulin release, but that preinfusion glucose level and/or previous glucose exposure of the pancreas are also important. Variable dosage glucose studies suggest that the amount of insulin released during the fast phase rather than the insulin release rate is regulated by the glucose level. A two-pool, heterogeneous threshold mechanism for beta cell response to glucose is presented that is compatible with the clinical results.
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