GENERAL CLINICAL RESEARCH CENTER

  • Shamoon, Harry (PI)
  • Karen, Gil (PI)
  • Cohen, Burton (PI)
  • Lynn, Robert (PI)
  • Nitowsky, H. (PI)
  • Bash, R. (PI)
  • Barth, R. (PI)
  • Deming, Quentin (PI)
  • Halbreich, U. (PI)
  • Hein, Karen (PI)
  • Saenger, Paul (PI)
  • Sherwood, L. (PI)
  • Kaplan, Barry (PI)
  • Portenoy, R. (PI)
  • Dutcher, J. (PI)
  • Rubinstein, Ayre (PI)
  • Billett, H. (PI)
  • Shim, C. (PI)
  • Vogl, Steven (PI)
  • Asnis, Gregory (PI)
  • Eder, Howard (PI)
  • Mitchell, Yale (PI)
  • Ferraru, Elaine (PI)
  • Crystal, H. (PI)
  • Engel, S. (PI)
  • Wolfson, L. (PI)
  • Wolfson, Leslie (PI)
  • Gilbert, Harriet (PI)
  • Thal, Leon (PI)
  • Stein, H. David (PI)
  • Romney, Seymour (PI)
  • Nagel, Ronald (PI)
  • Wylie-Rosett, Judy (PI)
  • Blechman, Elaine (PI)
  • Nagel, R. (PI)
  • Nieberger, R. (PI)
  • Appel, D. (PI)
  • Aronson, M. (PI)
  • Simon, Douglas (PI)
  • Freeman, Ruth (PI)
  • Wiernik, Peter (PI)
  • Fleischer, Norman (PI)
  • Scheinberg, I. Herbert (PI)
  • Brown, Serena-Lynn (PI)
  • Soeiro, R.U.Y. (PI)
  • Rubinstein, Arye (PI)
  • Mazze, Roger (PI)
  • Edelmann, Chester (PI)
  • Romney, S. (PI)
  • Keefe, D. (PI)
  • Rubin, David (PI)
  • Bornstein, Murray (PI)
  • Fotino, S. (PI)
  • Purpura, Dominick (PI)
  • Nitowsky, H. (PI)
  • Bash, R. (PI)
  • Barth, R. (PI)
  • Halbreich, U. (PI)
  • Sherwood, L. (PI)
  • Portenoy, R. (PI)
  • Dutcher, J. (PI)
  • Billett, H. (PI)
  • Shim, C. (PI)
  • Crystal, H. (PI)
  • Engel, S. (PI)
  • Wolfson, L. (PI)
  • Stein, H. David (PI)
  • Nagel, R. (PI)
  • Nieberger, R. (PI)
  • Appel, D. (PI)
  • Aronson, M. (PI)
  • Scheinberg, I. Herbert (PI)
  • Soeiro, R.U.Y. (PI)
  • Romney, S. (PI)
  • Keefe, D. (PI)
  • Fotino, S. (PI)

Project: Research project

Description

Dr. Shamoon has shown that, in contrast to the findings in normals, insulin
treated juvenile-onset diabetics exhibited exaggerated hepatic responses to
cortisol and epinephrine. He will now examine whether: (1) alterations in the
hepatic response to cortisol and epinephrine in diabetes are the result of
exaggerated gluconeogenesis induced by these hormones; (2) cortisol sustains
glucose production induced by epinephrine in normal man by enhancing it
gluconeogenic effects; and (3) whether altered sensitivity to epinephrine in
diabetes is due to changes in the response of the liver to Alpha or
Beta-adrenergic stimulation. Infusions of physiologic doses of cortisol and
epinephrine will be carried out in normal and diabetic subjects. Glucose and
gluconeogenic precursor tracers will be infused to quantitate hepatic glucose
production and conversion of substrates into glucose (gluconeogenesis).
Diabetics will be studied during insulin infusion, after normalization of the
plasma glucose, to exclude the effects of insulin deficiency per se. Selective
Alpha and Beta antagonists will be infused in order to determine whether
hypersensitivity to epinephrine is mediated by altered Alpha- or Beta-adrenergic
responsiveness in diabetes. These studies are designed to clarify the
pathogenesis of stress-induced diabetes in normal man and the mechanism
underlying the propensity of even the well-controlled diabetic to develop severe
hyperglycemia during minor illness.
StatusFinished
Effective start/end date10/1/753/31/91

Funding

  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health

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Epinephrine
Hydrocortisone
Glucose
Gluconeogenesis
Insulin
Liver
Feasibility Studies
Diabetes Complications
Propranolol
Adrenergic Agents
Blood Vessels
Renal Dialysis
Randomized Controlled Trials
Hormones
Exercise
Type 1 Diabetes Mellitus

ASJC

  • Medicine(all)