Hostname: page-component-cd9895bd7-fscjk Total loading time: 0 Render date: 2024-12-25T02:26:46.896Z Has data issue: false hasContentIssue false
  • English
  • Français

Dietary components and plasma insulin responses to fasting and refeeding in genetically obese hyperglycaemic (ob/ob) mice

Published online by Cambridge University Press:  09 March 2007

Peter R. Flatt  and
Clifford J. Bailey
Peter R. Flatt
Affiliation:
Division of Nutrition and Food Science, Department of Biochemistry, University of Surrey, Guildford, Surrey GU2 5XH
Clifford J. Bailey
Affiliation:
Department of Biological Sciences, University of Aston in Birmingham, Birmingham B4 7ET
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. To investigate the role of dietary components in the hyperinsulinaemia of the obese hyperglycaemic (ob/ob) syndrome, plasma insulin responses to fasting and refeeding were examined in Aston ob/ob mice supplied with standard diet, non-digestible-carbohydrate test food, and isoenergetic test foods from which either carbohydrate, protein or fat was omitted.

2. During fasting, plasma insulin concentrations fell more rapidly and to a greater extent than plasma glucose. Refeeding the standard diet raised insulin concentrations above normal, associated with a 25% compensatory increase in food intake over 24 h.

3. Test foods supplied to previously fed or fasted mice produced glucose responses consistent with the available carbohydrate content. Carbohydrate-free food (protein and fat) provided a small insulinotropic stimulus; the effect of protein-free food (carbohydrate and fat) was greater; and the combination of carbohydrate with protein (fat-free food) evoked a marked insulin response. In contrast, insulin concentrations declined in mice given the non-digestible-carbohydrate food.

4. Consumption of the standard diet was increased after 24 h feeding non-digestible-carbohydrate food, but was unaffected by a 30 h fast initiated 54 h previously.

5. These results demonstrate that hyperinsulinaemia in ob/ob mice is not merely triggered by the ingestion of bulk, but depends on the type of nutrient ingested. Dietary carbohydrate appears to be the major stimulus to the hyperinsulinaemia, with an important augmentation in the presence of protein. Since direct glucose stimulation of insulin release is defective in ob/ob mice, the hyperinsulinaemia must be mediated by increased activity of the enteroinsular axis.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 51 , Issue 3 , May 1984 , pp. 403 - 413
Copyright
Copyright © The Nutrition Society 1984

References

REFERENCES

Assimacopoulos-Jeannet, F. & Jeanrenaud, B. (1976). Clinics in Endocrinology and Metabolism 5, 337–365.CrossRefGoogle Scholar
Bailey, C. J., Atkins, T. W., Conner, M. J., Manley, G. G. & Matty, A. J. (1975). Hormone Research 6, 380–386.CrossRefGoogle Scholar
Bailey, C. J., Flatt, P. R. & Atkins, T. W. (1982). International Journal of Obesity 6, 11–21.Google Scholar
Bray, G. A. & York, D. A. (1979). Physiological Reviews 59, 719–809.CrossRefGoogle Scholar
Chlouverakis, C. (1971). Diabetologia 7, 373–378.CrossRefGoogle Scholar
Creutzfeldt, W. (1979). Diabetologia 16, 75–85.CrossRefGoogle Scholar
Cuendet, G. S., Loten, E. G., Cameron, D. P., Renold, A. E. & Marliss, E. B. (1975). American Journal of Physiology 228, 276–283.CrossRefGoogle Scholar
Dubuc, P. U. (1976). Metabolism 25, 1567–1574.CrossRefGoogle Scholar
Ebert, R. & Creutzfeldt, W. (1982). Endocrinology 111, 1601–1606.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1981 a). Diabetologia 20, 573–577.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1981 b). Hormone and Metabolic Research 13, 556–560.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1981 c). Biochemical Society Transactions 9, 220–221.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1982 a). Journal of Nutrition 112, 2212–2216.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1982 b). Biochemical Society Transactions 10, 29–30.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1982 c). Hormone and Metabolic Research 14, 127–130.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1983 a). Metabolism 32, 504–509.CrossRefGoogle Scholar
Flatt, P. R. & Bailey, C. J. (1983 b). In Lessons from Animal Diabetes [Shafrir, I., Renold, E.A., editors]. London: John Libbey and Co. Ltd.Google Scholar
Flatt, P. R., Bailey, C. J. & Buchanan, K. D. (1982). Journal of Endocrinology 95, 215–227.CrossRefGoogle Scholar
Flatt, P. R., Bailey, C. J., Kwasowski, P., Swanston-Flatt, S. K. & Marks, V. (1983 a). Diabetes 32, 433–435.CrossRefGoogle ScholarPubMed
Flatt, P. R., Bailey, C. J. & Swanston-Flatt, S. K. (1983 b). Hormone and Metabolic Research 15, 308–309.CrossRefGoogle Scholar
Flatt, P. R., Bailey, C. J., Swanston-Flatt, S. K., Best, L., Kwasowski, P., Buchanan, K. D. & Marks, V. (1983 c). In Lessons from Animal Diabetes [Shafrir, I., Renold, A.E., editors]. London: John Libbey and Co. Ltd.Google Scholar
Fuller, J. L. & Jacoby, G. A. (1955). American Journal of Physiology 183, 279–283.CrossRefGoogle Scholar
Genuth, S. M. (1976). Diabetologia 12, 155–159.CrossRefGoogle Scholar
Herberg, L. & Coleman, D. L. (1977). Metabolism 26, 59–99.CrossRefGoogle Scholar
Hunt, J. N. & Knox, M. J. (1968). In Handbook of Physiology, Section 6, Alimentary Canal Vol. 4, pp. 1917–1935 [Code, C.F., editor]. Washington, DC: American Physiological Society.Google Scholar
Lemonnier, D., Winand, J., Furnelle, J. & Christophe, J. (1971). Diabetologia 7, 328–338.CrossRefGoogle Scholar
Parsons, W., Camp, J. L. & Crispell, K. R. (1954). Metabolism 3, 351–356.Google Scholar
Ramirez, I. & Sprott, R. L. (1978). Physiology and Behaviour 20, 257–264.CrossRefGoogle Scholar
Stevens, J. F. (1971). Clinica Chimica Acta 32, 199–201.CrossRefGoogle Scholar