Weight loss in rats following lateral hypothalamic or thalamic lesions

Abstract

It has been reported frequently that rats sustaining lateral hypothalamic (LH) lesions lose more body weight than can be accounted for by their failure to eat and drink. This phenomenon was investigated in two experiments. The results indicated a tendency for rats sustaining LH lesions to lose more body weight than deprived, unoperated controls on some postoperative days. However, rats sustaining control lesions of the thalamus and also deprived generally lost about the same amount of weight as those sustaining LH lesions. The rats with LH lesions excreted more urine and displayed depressed locomotor activity compared with either lesion or unoperated controls. Fecal output and the retractive index of the urine did not differ among groups. It is suggested that excessive weight loss following LH lesions is not specific to LH lesions. The importance of these findings to current hypotheses of metabolic disruptions produced by LH lesions is discussed.It is well established that rats with bilateral, lateral hypothalamic (LH) damage display a period of aphagia and adipsia lasting several days and thus lose weight (Teitelbaum & Epstein, 1962). Previous researchers have reported that, during this period, rats with LH lesions lose more weight than foodand water-deprived unoperated or sham-operated controls (Glick & Greenstein, 1972;Lindholm, Shumway, Grijalva, Schallert, & Ruppel, 1975;Montemurro & Stevenson, 1957;Morgane, 1961;Morrison, 1968;Stevenson & Montemurro, 1963). The excessive weight loss ("excessive" weight loss will be used consistently in this report to denote weight loss greater than can be accounted for by the total absence of food and water intake), when found, has been used as evidence to support claims of abnormally high metabolic rates (Morgane, 1961;Morrison, 1968;Stevenson & Montemurro, 1963), excessive urinary excretion (Crow, 1962; Dorn & Rothballer, 1968; O'Kelley & Hatton, 1969), and locomotor hyperactivity (Epstein, 1971;Morrison, 1968).However, the experimental literature is not consistent on any of these important points. There is evidence that endocrine and metabolic functions are not grossly abnormal in rats with LH lesions (Gladfelter & Brobeck, 1962 Concerning locomotor hyperactivity, Balagura, Wilcox, and Coscina (1969), Campbell and Baez (1974), Gladfelter and Brobeck (1962) and Harrell et al. (1975) reported that locomotor hyPeractivity was either not present or was not present in sufficient amounts during the first few days to account for excessive weight loss in rats with LH lesions.Even more importantly, the excessive weight loss itself may not be a reliable aspect of the LH syndrome. Levine and Schwartzbaum (1973) and Morrison and Mayer (1957) failed to find excessive weight loss in rats with LH lesions compared with deprived unoperated or sham-operated controls. Moreover, only two experiments investigating excessive weight loss have compared the effects of LH lesions with the effects of control lesions rather than unoperated controls or sham-operated controls. These two experiments...