VMH obesity reduced but not reserved by scopolamine methyl nitrate

The role of hyperinsulinema and the vagus nerve in hypothalamic hyperphagia reexamined

“…The findings of our experiments along with those of Carpenter et al [7] seriously challenge the view that vagally-mediated insulin secretion is critical for the expression of the VMH hyperphagia and obesity. The results do not exclude the possibility that nonvagal or non-cholinergic visceral responses are essential to the hyperphagia syndrome, but certainly scopolamine or atropine-sensitive responses do not appear to be involved.…”

“…If vagally-mediated hyperinsulinemia is a primary cause of hypothalamic hyperphagia, then pharmacological blockade of this neuroendocrine response should prevent the overeating and obesity of VMH rats. In independent tests of this prediction, Carpenter et al [7] and Sclafani et al ([28], in preparation) treated VMH hyperphagic rats with peripherally acting anticholinergic drugs based on the findings that such drugs prevent the insulin response to oral stimulation with food and to electrical stimulation of the vagus nerve [12,16]. Carpenter et al chronically administered high doses of scopolamine methyl nitrate to VMH lesioned and control rats and observed that the treatment reduced but did not reverse static phase obesity, and did not prevent VMH electrolytic lesions from increasing food intake and body weight.…”

Atropine fails to block the overconsumption of sugar solutions by hypothalamic hyperphagic rats.

“…A second purpose of this experiment was to assess the effects of atropine treatment on water intake. Previous studies have found that atropine increases the water intake oi rats (Carpenter et al, 1979;Soulairac, 1969). although this does not occur under all conditions (Gerald & Maickel, 1969;Stein, 1963).…”

“…Therefore, if the vagal release of insulin is an essential component of VMH hyperphagia, then blocking this neuroendocrine response with anticholinergic drugs should inhibit the overeating of VMH-damaged animals. In a recent test of this prediction, Carpenter, Stamoutsos, Dalton, Frohman, and Grossman (1979) reported that chronic treatment with scopolamine methyl nitrate did not prevent VMH lesions from increasing the food intake of rats, although the duration of the hyperphagia was reduced. They also observed that scopolamine treatment did not reverse the established obesity of static phase VMH rats, although their body weights were reduced and their hyperphagia was completely eliminated.…”

“…In a series of experiments, the effects of acute injections of atropine methyl nitrite on the sugar-solution intake of VMH and normal rats was investigated. This test paradigm was used because (a) the sweet taste of sugar is a particularly potent stimulus for the vagal release of insulin (Berthroud et al, 1980;Louis-Sylvestre, 1976; (b) fluid intake is less disrupted by the effects of anticholinergic drugs on salivation and gastrointestinal motility than is solid food intake (Burks & Fisher, 1970;Carpenter et al, 1979;Stein, 1963); and (c) VMH hyperphagic rats consistently overconsume concentrated sugar solutions during brief daily tests (Sclafani, Koopmans, Vasselli, & Reichman, 1978;Sclafani & Xenakis, Note 1).…”