Electrolytic lesions of the ventromedial hypothalamus produce an obesity syndrome in experimental animals characterized by behavioural and metabolic disturbances. Historically, theories of VMH obesity have considered a single disturbance, either behavioural or metabolic, to be the primary effect of the lesion, which in turn causes other components of the syndrome. An alternative view suggests that VMH lesions simultaneously disturb both behavioural and metabolic mechanisms due to the anatomical proximity of these mechanisms in the hypothalamus. Therefore, more discrete lesions in the VMH may produce some syndrome components but not others. This thesis presents a series of experiments that test this "dissociative" perspective of the VMH obesity syndrome.
First, rats having different hypothalamic ablations were compared on: caloric intakes on a series of test diets, body weight changes, and body fat. Bilateral parafornical hypothalamic knife cuts (PFKC) that spared the ventromedial hypothalamic nucleus (VMN), produced overeating and weight gain characteristic of VMH lesions. However, measurement of percentage body fat (i.e. level of obesity) indicated that PFKC rats were less obese than VMH rats, even though PFKC lesions produced a greater hyperphagia and weight gain than VMH lesions. In contrast, lesions restricted to VMN produced obesity, but did not produce hyperphagia or weight gain.
Since parafornical knife cuts produced a greater hyperphagia than VMH lesions, it is possible that VMN damage actually reduces caloric intake in VMH rats. To test this hypothesis, the effects of VMH, PFKC, and combined PFKC/VMN lesions on caloric intake and body weight were compared. PFKC and VMH lesions produced hyperphagia and weight gain. However, knife cuts were not significantly more effective than VMH lesions for producing these disturbances in this experiment. Therefore, PFKC lesions do not invariably produce a greater hyperphagia than VMH lesions. Furthermore, VMN lesions had no effect on the level of overeating or weight gain in rats bearing PFKC lesions. Therefore, damage to VMN does not reduce the hyperphagia produced by PFKC lesions.
Finally, the effects of these different hypothalamic manipulations on metabolic measures were determined. To eliminate the confound of hyperphagia on metabolic variables, all lesion rats were fed a daily food ration sufficient to maintain their body weight at the level of controls. VMH and PFKC lesions resulted in elevated parasympathetic tone, indicated by elevated basal gastric acid secretion. VMN lesions did not affect gastric acid secretion. In contrast, only VMH and VMN lesions produced obesity when overeating was prevented. PFKC rats did not become obese.
These experiments demonstrate that separate hypothalamic mechanisms underly the hyperphagia and obesity characteristic of VMH lesions. Furthermore, different mechanisms underly obesity and elevated parasympathetic tone following VMH lesions. Therefore, these observations support a dissociative model of the VMH obesity syndrome. / Thesis / Doctor of Philosophy (PhD)
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/29606 |
| Date | 07 1900 |
| Creators | Parkinson, William Lloyd |
| Contributors | Weingarten, Harvey, Psychology |
| Source Sets | McMaster University |
| Language | English |
| Detected Language | English |
| Type | Thesis |
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