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The characteristics of genetically obese mutants

  • Chapter
Animal Models of Obesity

Summary

A number of characteristics are common to the differing forms of rodent obesity. An increased efficiency of energy utilisation is accompanied by, but not dependent upon, hyperphagia and hypoactivity. An impairment in thermogenic processes may be responsible for the increase in efficiency in a number of the obese models. The developmental sequence of the obesity varies between the differing models, recessively inherited obesities being associated with early pre-weaning excess fat deposition, whereas obesity in other forms of rodent obesity develops at a later age and is of a more moderate type. The rodent models also differ in the type of adipose tissue expansion between hypertrophic and hypertrophic-hyperplastic growth. The hyperinsulinaemia characteristic of all obesities is together with the hyperphagia the major stimulus for the enhanced hepatic and adipose tissue lipogenesis. The obese-hyperinsulinaemic state produces secondary effects which include changes in pancreatic morphology, insulin resistance, enhanced gluconeogenesis, increased basal lipolysis and loss of responsiveness to lipolytic hormones. Hyperadrenocortism and sterility observed in the recessively inherited obesities may result from hypothalamic dysfunction. The possible metabolic basis of the obesities is discussed.

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Authors and Affiliations

  1. Department of Nutrition, School of Biochemical and Physiological Sciences, University of Southampton, Southampton, UK

    David A. York

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  1. David A. York
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Editors and Affiliations

  1. Medical Research Council Laboratory Animals Centre, Carshalton, Surrey, UK

    Michael F. W. Festing B.Sc., M.Sc., Ph.D., M.I.S., M.I.Biol.

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© 1979 The Medical Research Council

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York, D.A. (1979). The characteristics of genetically obese mutants. In: Festing, M.F.W. (eds) Animal Models of Obesity. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-04201-2_3

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