Hostname: page-component-cd9895bd7-lnqnp Total loading time: 0 Render date: 2024-12-22T23:57:01.000Z Has data issue: false hasContentIssue false

Influence of low- and high-protein diets on glucose homeostasis in the rat

Published online by Cambridge University Press:  09 March 2007

W. Okitolonda
Affiliation:
Unité de Diabétologie et Nutrition, University of Louvain Faculty of Medicine, UCL 54.74, B-1200 Brussels, Belgium
S. M. Brichard
Affiliation:
Unité de Diabétologie et Nutrition, University of Louvain Faculty of Medicine, UCL 54.74, B-1200 Brussels, Belgium
A. M. Pottier
Affiliation:
Unité de Diabétologie et Nutrition, University of Louvain Faculty of Medicine, UCL 54.74, B-1200 Brussels, Belgium
J. C. Henquin
Affiliation:
Unité de Diabétologie et Nutrition, University of Louvain Faculty of Medicine, UCL 54.74, B-1200 Brussels, Belgium
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. The influence of the protein content of the diet on glucose homeostasis was studied in the rat. Rats of 28 d of age received ad lib. a control diet containing (g/kg) 150 protein (P15), or a diet containing 50 protein (P5) or 450 protein (P45). Since P5 rats spontaneously reduced their food intake, a fourth group of rats (P25) received the same amount of energy as P5 rats and the same amount of protein as P15 rats.

2. After 12–13 weeks on these diets, plasma glucose and insulin levels were similar in fed P45, P25 and control P15 rats, but were lower in P5 rats. In fasted animals, plasma glucose and insulin levels were also decreased in P5 rats, whereas plasma glucose levels were increased in both P45 and P25 animals.

3. During an oral glucose tolerance test, the glucose rise was only slightly larger in P5 than in P15 rats in spite of a considerably smaller increase in insulin levels. P45 rats displayed a normal tolerance to glucose with a normal insulin response, whereas tolerance to glucose was slightly poorer in P25 rats in spite of a normal insulin response.

4. Pancreatic insulin stores were lower in P5 than in control P15 rats, not only because of the smaller size of their pancreas, but also because of a decrease in the insulin concentration in the gland. A much smaller decrease was also observed in P25 rats, whereas insulin reserves were not altered in P45 rats.

5. It is concluded that the changes in glucose homeostasis observed in protein-energy malnutrition (P5 rats) are due to protein deprivation rather than to energy deprivation. A high-protein diet has little influence on glucose homeostasis in the rat.

Type
Other Studies Relevant to Human Nutrition
Copyright
Copyright © The Nutrition Society 1988

References

Abu-Bakare, A., Gill, G. V., Taylor, R. & Alberti, K. G. M. M. (1986) Lancet i, 11351138.CrossRefGoogle Scholar
Becker, D. J. (1983) Annual Reviews of Nutrition 3, 187212.CrossRefGoogle Scholar
Bhutani, V., Kumar, V. & Misra, U. K. (1985) Nutrition Reports International 32, 14131420.Google Scholar
Blazquez, E. & Lopez Quijada, C. (1970) Journal of Endocrinology 46, 445451.CrossRefGoogle Scholar
Dollet, J. M., Beck, B., Villaume, C., Max, J. P. & Debry, G. (1985) Journal of Nutrition 115, 15811588.CrossRefGoogle Scholar
Edozien, J. C. (1978). In Handbook Series in Nutrition and Food, sect. E, Vol. 3, pp. 285312 [M. Rechcigl, editor]. West Palm Beach: CRC Press.Google Scholar
Eisenstein, A. B. & Strack, I. (1971) Diabetes 20, 577585.CrossRefGoogle Scholar
Eisenstein, A. B. & Strack, I. (1976) Diabetes 25, 5155.CrossRefGoogle Scholar
Eizirik, D. L. & Migliorini, R. H. (1984) Diabetes 33, 383388.CrossRefGoogle Scholar
Heard, C. R. C. (1978) World Review of Nutrition and Dietetics 30, 107147.CrossRefGoogle Scholar
Heard, C. R. C., Platt, B. S. & Stewart, R. J. C. (1958) Proceedings of the Nutrition Society 17, 4142.Google Scholar
Hell, N. S., Costa, De, Oliveira, L. B., Dolkinoff, M. S., Scivoletto, S. & Timo-Iaria, C. (1980) Physiology and Behaviour 24, 473477.CrossRefGoogle Scholar
Imai, K., Ohnaka, M. & Nijama, J. (1986) Journal of Nutritional Science and Vitaminology 32, 513525.CrossRefGoogle Scholar
Kettelhut, I. C., Foss, M. C. & Migliorini, R. H. (1980) American Journal of Physiology 239, R437R444.Google Scholar
Levine, L. S., Wright, P. G. & Marcos, F. (1983) Acta Endocrinologica 102, 240245.Google Scholar
Mohan, P. F. & Narasinga Rao, B. S. (1983) Journal of Nutrition 113, 7985.CrossRefGoogle Scholar
Mohan, V., Ramachadran, A. & Viswanathan, M. (1985). In The Diabetes Annual I, pp. 8292 [Alberti, K.G. M. M. and Krall, L. P., editors]. Amsterdam: Elsevier.Google Scholar
Okitolonda, W., Brichard, S. M. & Henquin, J. C. (1987) Diabetologia 30, 946951.CrossRefGoogle Scholar
Peret, J., Foustock, S., Chanez, M., Bois-Joyeux, B. & Assan, R. (1981) Journal of Nutrition 111, 11731184.CrossRefGoogle Scholar
Phillips, L. S. (1981). In Endocrine Control of Growth, pp. 121173 [Daughaday, W. H. editor]. New York: Elsevier.Google Scholar
Rao, R. H. (1984) Diabetes Care 6, 595601.CrossRefGoogle Scholar
Sokal, R. R. & Rohlf, F. J. (1969). Biometry. The Principles and Practice of Statistics in Biological Research. San Francisco: W. H. Freeman and Co.Google Scholar
Swenne, I., Crace, C. J. & Milner, D. G. (1987) Diabetes 36, 454458.CrossRefGoogle Scholar
Usami, M., Seino, S., Takemura, J., Nakahara, H., Ikeda, M. & Imura, H. (1982) Journal of Nutrition 112, 681685.CrossRefGoogle Scholar
Weinkove, C., Weinkove, E. A. & Pimstone, B. L. (1976) Clinical Science and Molecular Medicine 50, 153163.Google Scholar
Weinkove, C., Weinkove, E. A., Timme, A. & Pimstone, B. L. (1977) Archives of Pathology and Laboratory Medicine 101, 266269.Google Scholar
Younoszai, R. & Dixit, P. K. (1980) Proceedings of the Society for Experimental Biology and Medicine 164, 317321.CrossRefGoogle Scholar