Responses of plasma immunoreactive gastric inhibitory polypep-tide (IRGIP) to oral triglycéride or galactose were compared in normal and mildly diabetic (non-insulin-dependent) subjects. After triglyceride the responses of IRGIP were similar, but after galactose those of the diabetics were slightly exaggerated. Both stimuli evoked increments of plasma immunoreactive glucagon (IRG) in diabetics but not in normal subjects. Plasma immunoreactive insulin (IRI) did not change.

In normal subjects given oral triglyceride or galactose followed by intravenous (I.V.) glucose the early-phase response of plasma IRI was enhanced and glucose tolerance improved. In the diabet-ics, oral triglyceride did not affect insulin release or glucose tolerance after I. V. glucose; oral galactose elicited a slight increase of insulin release without improving glucose tolerance. In the diabetics the rise in plasma IRG after ingestion of triglyceride or galactose was maintained after I. V. glucose.

It is concluded that endogenous GIP is insulinotropic and that there is partial resistance to this action in diabetes. The results were compatible with feedback inhibition of GIP secretion by insulin and with the suggestion that the rise of plasma IRG associated with secretion of GIP in diabetics may be due to the glucagono-tropic action of this peptide.

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