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Dr. Raymond Pederson, Dr. Jill Dryburgh and I commenced work on GIP in 1968, when, with the generous help of Professor Viktor Mutt and Professor Erik Jorpes of the Karolinska Inst,itute, Stockholm, we were able to establish that there existed an inhibitory material for acid secretion in cholecystokinin-pancreozymin prepara tions. Once the physiological evidence for the inhibitor was established it seemed appropriate to seek help in its isolation. Dr. J. Dryburgh and Dr. R. Pederson were left to bioassay fractions in Vancouver whilst I enjoyed the company of Professor Mutt at the Karolinska for one year, as a Medical Research Council of Canada Visiting Scientist. Purification of the inhibitory factor proceeded rapidly due, in no small measure, to Professor Mutt's untirmg efforts on my behalf. Later that year, Dr. Dryburgh joined us in Stockholm to begin the sequence work on GIP. This was completed late in 1970 in Vancouver. In Stockholm in June 1970, I met a fellow Canadian Dr. John Dupre (McGill University) at a cocktail party who kept commenting about the possibility of GIP being an insulinotropic hormone, the "incretin" of earlier days. At that time, gastrointestinal physiologist as I was, I did not recognize the importance of his comment. This became apparent two or three years later when Dr. Dupre demonstrated that GIP was insulinotropic in man. In 1972, Maryanne Kuzio and Dr.
Sommario
A. Introduction.- I. Enterogastrone Concept.- II. Incretin Concept.- III. Evidence for the Existence of GIP.- B. Chemistry.- I. Isolation and Purification.- II. Amino Acid Sequence.- III. Correction to Sequence.- IV. Synthesis.- C. Physiological Actions of Exogenous GIP.- I. Gastrointestinal Effects.- II. Metabolic Effects.- D. Radioimmunoassay.- I. Development.- II. Immunordactive GIP (IR-GIP).- III. Inhibition of IR-GIP Release.- IV. Nature of IR-GIP.- E. Localization.- I. Cellular Localization.- II. Release Studies.- F. Pathophysiology.- I. Diabetes Mellitus.- II. Pancreatitis.- III. Other Gastrointestinal Disorders.- IV. Obesity.- V. Uraemia.- VI. Other Clinical Situations.- G. Summary and Conclusions.- I. Physiological Role.- II. Pathophysiological Role.- References.- Acknowledgements.
