Increased body fat due to elevated energetic efficiency following chronic administration of inhibitors of sympathetic nervous system activity.
The effects on energy balance of drugs known to inhibit the sympathetic nervous system at different sites and with various modes of action were studied in lean mice of the CFLP strain. Metabolizable energy intake was monitored continuously over seven-week experimental periods and energy expenditure was determined by the comparative carcass method as well as by measurements of 24-hour oxygen consumption. Administration of either propranolol, phenoxybenzamine, clonidine, or mecamylamine had no influence on energy balance nor on body composition. On the other hand, administration of alpha-methyl para tyrosine, reserpine, and bethanidine, ie, drugs capable of reducing the levels of noradrenaline at sympathetic terminals, resulted in significant increases in body fat by 38%, 24%, and 46% respectively: this effect was brought about by a reduction in the metabolic rate of these drug-treated groups and the efficiency of energy utilization (both gross and net) was increased by three to nine times. These studies indicate that chronic administration of drugs that act at the receptor level to inhibit sympathetic activity fail to influence metabolic rate, thereby suggesting that thermogenesis under noradrenaline control may involve mechanisms other than the alpha and beta classification of adrenergic receptors. Nonetheless, the ability of some drugs which both reduce noradrenaline levels and decrease metabolic rate would support the concept of an important role of the sympathetic nervous system in the overall control of thermogenesis and in energy balance regulation.
D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001833:Body Temperature Regulation / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D008297:Male; D051379:Mice; D009638:Norepinephrine / Q000037:antagonists & inhibitors / Q000502:physiology; D010101:Oxygen Consumption / Q000187:drug effects; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*; D013565:Sympatholytics / Q000494:pharmacology*; D009435:Synaptic Transmission / Q000187:drug effects
D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D013565:Sympatholytics; D009638:Norepinephrine