Modifications of gastric inhibitory polypeptide ( XXXX ) secretion in man by a @entity1386 .

@entity8242 @entity413 @entity1386
1. Five healthy volunteers (usual fat intake 103 (SE 9) g/d and energy intake 9855 (SE 937) kJ/d were given on two separate occasions (a) 100 g oral @entity413 and (b) sufficient intravenous (IV) @entity413 to obtain similar arterialized plasma @entity413 levels to those after oral @entity413 . 2. Subjects increased their fat intake by 68 (SE 9.6)% for 28 d by supplementing their diet with 146 ml double cream/d (fat intake on @entity1386 ( @entity1386 ) 170 (SE 8) g/d; energy intake 12347 (SE 770)). 3. The 100 g oral @entity413 load was repeated and IV @entity413 again given in quantities sufficient to obtain similar arterialized blood @entity413 levels. Immunoreactive plasma insulin, C-peptide and gastric inhibitory polypeptide ( @entity8242 ) were measured. 4. Plasma @entity8242 levels were higher following oral @entity413 after the @entity1386 (area under plasma @entity8242 curve 0-180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and @entity1386 respectively; P less than 0.05). Both insulin and C-peptide levels were significantly higher after oral than after IV @entity413 (P less than 0.01) but neither were affected by the @entity1386 . @entity413 levels were lower following the @entity1386 after both oral and IV @entity413 (area under plasma @entity413 curve 0-180 min, following oral @entity413 6.7 (SE 0.3) mmol/l.h for control and 4.2 (SE 0.6) mmol/l.h for @entity1386 ; P less than 0.01). 5. @entity413 -stimulated @entity8242 secretion was thus enhanced by the @entity1386 . Insulin secretion in response to oral @entity413 was unchanged, in spite of an improvement in @entity413 tolerance. 6. The improvement in @entity413 tolerance post- @entity1386 could possibly be due to a @entity8242 -mediated inhibition of hepatic glycogenolysis, or a decreased rate of @entity413 uptake from the small intestine.
