caa a22 4500 386322368 CHVBK 20180307111631.0 cr unu---uuuuu 161130e198805 xx s 000 0 eng 10.1079/BJN19880046 doi S0007114588000480 pii (NATIONALLICENCE)cambridge-10.1079/BJN19880046 Modifications of gastric inhibitory polypeptide (GIP) secretion in man by a high-fat diet [Elektronische Daten] 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 glucose and (b) sufficient intravenous (IV) glucose to obtain similar arterialized plasma glucose levels to those after oral glucose. 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 high-fat diet (HFD) 170 (SE 8) g/d; energy intake 12347 (SE 770)). 3. The 100 g oral glucose load was repeated and IV glucose again given in quantities sufficient to obtain similar arterialized blood glucose levels. Immunoreactive plasma insulin, C-peptide and gastric inhibitory polypeptide (GIP) were measured. 4. Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0-180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P < 0·05). Both insulin and C-peptide levels were significantly higher after oral than after IV glucose (P < 0·01) but neither were affected by the HFD. Glucose levels were lower following the HFD after both oral and IV glucose (area under plasma glucose curve 0-180 min, following oral glucose 6·7 (SE 0·3) mmol/l.h for control and 4·2 (SE 0·6) mmol/l.h for HFD; P < 0·01). 5. Glucose-stimulated GIP secretion was thus enhanced by the HFD. Insulin secretion in response to oral glucose was unchanged, in spite of an improvement in glucose tolerance. 6. The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine. Copyright © The Nutrition Society 1988 Morgan L. M. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH Hampton S. M. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH Tredger J. A. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH Cramb R. St Luke's Hospital, Guildford, Surrey Marks V. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH British Journal of Nutrition Cambridge University Press 59/3(1988-05), 373-380 0007-1145 59:3<373 1988 59 BJN https://doi.org/10.1079/BJN19880046 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1079/BJN19880046 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Morgan L. M. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH NATIONALLICENCE 700 1- Hampton S. M. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH NATIONALLICENCE 700 1- Tredger J. A. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH NATIONALLICENCE 700 1- Cramb R. St Luke's Hospital, Guildford, Surrey NATIONALLICENCE 700 1- Marks V. Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH NATIONALLICENCE 773 0- British Journal of Nutrition Cambridge University Press 59/3(1988-05), 373-380 0007-1145 59:3<373 1988 59 BJN CC0 http://creativecommons.org/publicdomain/zero/1.0 nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-cambridge