Hypothalamic Obesity in the Mouse

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Abstract
Hypothalamic obesity was induced in Swiss mice as well as in thin littermates of mice with the hereditary obese-hyperglycemic syndrome. A modification of a previous stereotaxic instrument designed for rats (Krieg) which permits the placing of reproducible lesions in the mouse''s brain is described. Coordinates of successful lesions are given. Successful lesions involved both ventromedial nuclei. Besides obesity, ovarian atrophy was noted as a result of these lesions. In Swiss mice with hypothalamic obesity the positive energy balance is the result of both marked hyperphagia and very low spontaneous activity. O2 consumption appears to follow the "surface" law. Blood glucose, resistance to growth hormone and sensitivity to insulin are normal following induction of hypothalamic obesity in Swiss mice as well as in "non-obese" littermates of hereditarily obese mice successfully operated. Weight gain was greatest in high fat diets and minimal in high protein diets. The fact that genetic, hypothalamic and goldthioglucose obesity can be either found or produced in littermate animals offers a useful tool for the study of experimental obesity. Comparisons of 3 obese types of obese mice which differ in the relative importance of various factors in the establishment of a positive energy balance, emphasize the multiplicity of mechanisms leading to obesity.