Gerold Grodsky, PhD

Professor (Emeritus, Active)
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Honors:

Rumbaugh Award of the Juvenile Diabetes Research Foundation International; R.H Williams/R. Levine Award of the Western Metabolism Club; Merit Award of the National Institutes of Public Health

Designated the Herbert Rosenthal Lecturer (New York), the Helen Martin Lecturer (Los Angeles) and the First Somogyi Lecturer (St. Louis).

Dr. Grodsky served as Research Chairman of the Advisory Board for Diabetes to the Secretary of Health and on the editorial boards of numerous journals.  He is Founding Advisory Editor of the journal, Diabetes Science and Technology.

Since 1994, the Juvenile Diabetes Research Foundation gives an Annual Gerold Grodsky Award for basic research in diabetes. Also, In 2004, the Western Regional Islet Study Group created the Gerold Grodsky Lectureship to be presented annually.

Training:

  • 1947 B.S. University of Illinois, Urbana, Chemistry
  • 1948 M.S. University of Illinois, Urbana, Biochemistry
  • 1955 PhD University of California, Berkeley, Biochemistry
  • 1956 Postdoctoral Fellow, Cambridge University, Biochemistry

Dr. Grodsky no longer manages his own laboratory, but is a consultant to laboratories in the Diabetes Center.  He was the developer of the first precipitating radio immunoassay (insulin).

His group published over 200 papers on the mechanisms involved in the synthesis, storage and secretion of insulin, with emphasis on the kinetics and quantitative relationships of these mechanisms. From these studies came the description of the fast and slow phases of insulin release and the hypothesis that insulin is stored in compartments of differing availability for release. The rapid phase of insulin release was shown to be vital in the maintenance of glucose homeostasis and is being utilized in the design of the closed-loop artificial pancreas, faster acting beta-cell secretagogues, and fast absorbing insulin preparations.

Other areas of research activity includes the demonstration of insulin-induced auto antibodies and their contribution to beta-cell destruction.