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Abstract
Rats with bilateral electrolytic lesions in the general region of the ventromedial
hypothalamic (VMH) nucleus develop hyperinsulinemia, excessive food intake and obesity.
Monosodium glutamate (MSG) destroys neurons of the arcuate hypothalamic (AH) nucleus
and produces hyperinsulinemic but hypophagic obesity. Bipiperidyl mustard (BPM) primarily
destroys VMH neurons, but has produced only a slight obesity even when rats were maintained
on high-fat diets. In the present study, rats treated with MSG (AH lesion) were hyperinsulinemic,
moderately obese and hypophagic; BPM rats (primarily VMH lesion) were not different
from controls when fed standard chow diets. However, MSG/BPM rats (AH + VMH lesion)
were hyperinsulinemic, massively obese and hyperphagic. Thus, two components of the
electrolytic lesion syndrome previously attributed to VMH damage (hyperinsulinemia
and obesity) were reproduced simply by MSG treatment alone. The third component (hyperphagia)
occurred only when both AH and VMH were lesioned, suggesting that neurons in both
nuclei may perform a satiety function and may be able to substitute for one another
in this respect. Since MSG treatment is required for all components of both obesity
syndromes described here, this underscores the importance of MSG-sensitive neurons
in mechanisms of obesity. The combined treatment approach also represents the first
rat model of hyperinsulinemic, hyperphagic obesity that can be entirely produced by
systemic administration of neurotoxins.