The effect of parasympathetic drugs on energy expenditure: relevance to the autonomic hypothesis.
The influence of the parasympathetic nervous system in the control of energy expenditure was investigated in obese and lean rodents during chronic administration of drugs that alter parasympathetic transmission. In the genetically obese ob/ob mice and fa/fa rats and in monosodium glutamate induced hypothalamic obese mice, administration of the parasympathetic inhibitors hyoscine, benztropine, and mecamylamine either had no effect on energy balance or caused losses in body weight that could entirely be accounted for by a reduction in food intake; 24-h oxygen consumption in drug-treated animals was no different from that of the nontreated controls. In the lean animals, both the parasympathetic inhibitors (hyoscine, benztropine, and mecamylamine) and stimulators (bethanecol and neostigmine) had no influence on energy balance nor on body composition. These studies refute the concept that an overactive parasympathetic tone underlies the elevated energetic efficiency of obese models and suggests that the parasympathetic nervous system is unlikely to play an important role in the long-term control of energy expenditure.
D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001835:Body Weight / Q000187:drug effects; D004435:Eating / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects*; D051379:Mice; D008815:Mice, Inbred Strains; D008959:Models, Neurological; D009765:Obesity / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D010276:Parasympatholytics / Q000494:pharmacology*; D010277:Parasympathomimetics / Q000494:pharmacology*; D051381:Rats; D011924:Rats, Zucker; D012970:Sodium Glutamate
D010276:Parasympatholytics; D010277:Parasympathomimetics; D012970:Sodium Glutamate