Hostname: page-component-78c5997874-8bhkd Total loading time: 0 Render date: 2024-11-15T01:52:40.574Z Has data issue: false hasContentIssue false
  • English
  • Français

Modifications of gastric inhibitory polypeptide (GIP) secretion in man by a high-fat diet

Published online by Cambridge University Press:  09 March 2007

L. M. Morgan ,
S. M. Hampton ,
J. A. Tredger ,
R. Cramb  and
V. Marks
L. M. Morgan
Affiliation:
Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH
S. M. Hampton
Affiliation:
Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH
J. A. Tredger
Affiliation:
Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH
R. Cramb
Affiliation:
St Luke's Hospital, Guildford, Surrey
V. Marks
Affiliation:
Department of Biochemistry, University of Surrey, Guildford, Surrey, GU2 5XH
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

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.

Type
Research Article
Information
British Journal of Nutrition , Volume 59 , Issue 3 , May 1988 , pp. 373 - 380
Copyright
Copyright © The Nutrition Society 1988

References

Brown, J. C., Dryburgh, J. R., Ross, S. A. & Dupre, J. (1975). Recent Progress in Hormone Research 31, 487–532.Google Scholar
Collier, G. R., Chisholm, K., Sykes, S., Dryden, P. A. & O'Dea, K. (1985). Journal of Nutrition 115, 1471–1476.CrossRefGoogle Scholar
Ebert, R., Willms, B., Brown, J. C. & Creutzfeldt, W. (1976). Europrun Journul of Clinical Investigurion 6, 327.Google Scholar
Elahi, D., Meneilly, G. S., Hinaker, K. L., Rowe, J. W. & Andersen, D. K. (1986). Proceedings of the 6th lnternational Conference on Gustrointestinal Hormones,Vancouver, BC, p. 18.Google Scholar
Elrick, H., Stimmler, L., Hlad, C. J. & Arai, Y. (1964). Journal uf Clinical Endocrinology und Metabolism 24, 1078–1082.Google Scholar
Flatt, P. R., Bailey, C. J., Kwasowski, P., Swanston-Flatt, S. K. & Marks, V. (1985). Nutrition Reports Internutional 32, 847–854.Google Scholar
Gibby, O. M. & Hales, C. N. (1983). British Medical Journal 286, 921–923.CrossRefGoogle Scholar
Hampton, S. M., Kwasowski, P., Tan, K., Morgan, L. M. & Marks, V. (1983). Diabetologia 24, 278–281.CrossRefGoogle Scholar
Hampton, S. M. & Marks, V. (1979). Diabetologia 17, 24.Google Scholar
Hampton, S. M., Morgan, L. M., Tredger, J. A., Cramb, R. & Marks, V. (1986). Diabetes 35, 612–616.CrossRefGoogle Scholar
Hartmann, H., Ebert, R. & Creutzfeldt, W. (1986). Diabelologiu 29, 112–114.CrossRefGoogle Scholar
Jackson, R. A., Roshania, R. D., Hawa, M. I., Sim, B. M. & Disilvio, L. (1986). Journal of Clinical Endocrinology and Metabolism 63, 541–549.CrossRefGoogle Scholar
McIntyre, N., Holdsworth, C. D. & Turner, D. S. (1964). Lancet ii, 20–21.CrossRefGoogle Scholar
McL. Welch, I., Bruce, C., Hill, S. E. & Read, N. W. (1987). Clinical Science 72, 209–216.CrossRefGoogle Scholar
Morgan, L. M., Morris, B. A. & Marks, V. (1978). Annals of Clinical Biochemistry 15, 172–177.CrossRefGoogle Scholar
Mott, D. M., Lillioja, S. & Bogardus, C. (1986). Metabolism 35, 160–165.CrossRefGoogle Scholar
O'Dorisio, T. M. & Cataland, S. (1981). In Gut Hormones, pp. 269–272 [Bloom, S. R. and Polak, J. M., editors]. Edinburgh: Churchill Livingstone.Google Scholar
Paul, A. A. & Southgate, D. A. T. (1978). McCance and Widdowsons' The Composition of Foods, 4th ed. London: H.M. Stationery Office.Google Scholar
Rizza, R., Mandarino, L. & Gerich, J. (1981). American Journal of Physiology 240, E630.Google Scholar
Stout, R. (1982). International Journal of Obesity 6, 111–115.Google Scholar
Willms, B., Ebert, R. & Creutzfeldt, W. (1978). Diabetologia 14, 379–387.CrossRefGoogle Scholar
Zaragoza, N. & Felber, J. P. (1972). Hormones and Metabolic Research 4, 25–30.CrossRefGoogle Scholar