Summary
Various methods of producing reversible obesity in animals are reviewed, and include high-fat feeding, insulin-induced hyperphagia, force-feeding and feeding a mixed and varied diet (the cafeteria system). Of these, the most successful seem to be force-feeding and the cafeteria feeding system, both of which have been utilised to produce obesity from which animals can spontaneously recover when allowed free access to the stock diet alone.
Our own results suggest that the obesity induced by tube-feeding varying proportions of normal daily energy intake, allowing voluntary feeding to continue, results entirely from an increase in metabolic efficiency, since the animals consume the same amount of energy as their free-feeding controls. When tube-feeding is stopped, the weight loss which follows is accompanied by a marked hypophagia, while energy expenditure remains normal. Conversely, animals fed the cafeteria diet become obese entirely as a result of hyperphagia without any changes in resting oxygen consumption. When returned to the stock diet, these obese rats rapidly return to control body weight as a result of a decrease in energy intake and a simultaneous increase in resting oxygen consumption.
It is concluded that these two examples of experimental obesity provide further evidence for the existence of lipostasis in the rat and imply that controls acting on both intake and expenditure operate to maintain energy balance.
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References
Booth, D. A. (1975). Normal metabolic control of hunger. In Hunger: Basic Mechanisms and Clinical Implications (ed. D. Novin, W. Wyrwicka and G. A. Bray ), New York, Raven Press, pp. 127–143
Cohn, C. and Joseph, D. (1959). Changes in body composition with force-feeding. Am. J. Physiol., 196, 965–968
Cohn, C. and Joseph, D. (1960). The effects of feeding frequency in intermediary metabolism. Metabolism, 9, 492–501
Cohn, C. and Joseph, D. (1962). Influence of body weight and body fat on the appetite of normal lean and obese rats. Yale J. Biol. Med., 34, 598–607
Cox, J. E. and Powley, T. L. (1977). Development of obesity in diabetic mice pair-fed with lean siblings. J. Comp. Physiol. PsychoL, 91, 347–358
Djazayery, A., Miller, D. S. and Stock, M. J. (1979). Energy balance in obese mice. Nutr. Metab. (in press)
Fabry, P. (1969). Feeding Patterns and Nutritional Adaptations, Butterworths, London
Hausberger, F. X. and Hausberger, B. C. (1958). Effect of insulin and cortisone in weight gain, protein and fat content of rats. Am. J. Physiol., 193, 455–460
Herberg, L., Doppen, W., Major, E. and Gries, F. A. (1974). Dietary induced hypertrophic hyperplastic obesity in mice. J. Lipid Res., 15, 580–585
Hoebel, B. G. and Teitelbaum, P. (1966). Weight regulation in normal and hypothalamic hyperphagic rats. J. Comp. Physiol. Psychol., 61, 180–193
Kennedy, G. C. (1953). The role of depot fat in the hypothalamic control of food intake in the rat. Proc. R. Soc. (London), B140, 578–592
Le Magnen, J., Devos, M., Gaudilliere, J., Louis-Sylvestre, J. and Tallon, S. (1973). Role of a lipostatic mechanism in regulation by feeding of energy balance in rats. J. Comp. PhysioL Psychol., 81, 1–23
Lemonnier, D. (1972). Effect of age, sex and site on the cellularity of the adipose tissue in mice and rats rendered obese by a high fat diet. J. Clin. Invest., 51, 2907–2915
Macdonald, I. A. (1977). Metabolic effects of variations in total body lipid. PhD thesis, London
Macdonald, I. A., Rothwell, N. J. and Stock, M. J; (1976). Lipolytic and lipogenic activities of adipose tissue during spontaneous fat depletion and repletion. Proc. Nutr. Soc., 35, 129A
Miller, D. S. (1978). Non-genetic models of obesity In laboratory animals. This volume Mozes, S., Kuchar, S. and Bodak, K. (1977). Hypoglycaemia and food intake in rats given graduated doses of insulin. Physiol. Bohemoslov., 26, 159–164
Pace, N. and Rathbun, E. N. (1945). Studies on body composition. III. The body water and chemically combined nitrogen content in relation to fat content. J. Biol. Chem., 158, 689–691
Peckham, S. C., Centerman, H. W. and Carroll, J. (1962). The influence of hypercaloric diet on gross body and adipose tissue composition in the rat. J. Nutr., 77, 187–197
Quatermain, D., Kissileff, H., Shapiro, R. and Miller, N. E. (1971). Suppression of food intake with intragastric loading: relation to the natural feeding cycle. Science, 173, 941–943
Rolls, B. J. and Rowe, E. A. (1977). Dietary obesity: permanent changes in body weight. J. Physiol. (London), 272, 2 P
Rothwell, N. J. and Stock, M. J. (1979a). Mechanisms of weight gain and loss in reversible obesity in the rat. J. Physiol. (London) (in press)
Rothwell, N. J. and Stock, M. J. (1979b). A paradox in the control of energy intake. Nature (in press)
Schemmel, R. and Mickelsen, O. (1973). Influence of diet, strain, age and sex in fat depot mass and body composition of the nutritionally obese rat. In The Regulation of Adipose Tissue Mass(ed. J. Vague and J. Boyer), Excerpta Medica, Amsterdam, pp. 238–253
Sclafani, A. and Springer, D. (1976). Dietary obesity in adult rats: similarities to hypothalamic and human obesity syndromes. Physiol. Behay., 17, 461–471
Stock, M. J. (1975). An automatic, closed-circuit oxygen consumption apparatus for small animals. J. Appl. Physiol., 39, 849–850
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© 1979 The Medical Research Council
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Stock, M.J., Rothwell, N.J. (1979). Energy balance in reversible obesity. In: Festing, M.F.W. (eds) Animal Models of Obesity. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-04201-2_9
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DOI: https://doi.org/10.1007/978-1-349-04201-2_9
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