Gluttony. 2. Thermogenesis in overeating man.
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Adult↗
Biomedical subjects
M J Stock
Publications and source records attributed to M J Stock.
Effects of epinephrine on thermoregulatory behavior in lean and obese Zucker rats in the cold.
This series of experiments examined whether epinephrine (EPI) produces the same thermoregulatory effects in the cold that have been reported for norepinephrine and isoproterenol. Lean and obese Zucker rats were trained to press a lever to activate infrared heat lamps in a cold (-8 degrees C) environment. Operant thermoregulatory behavior increased dose-dependently following EPI (0-100 micrograms/kg), but posttest colonic temperature (Tc) fell. Thermal balance calculations showed a substantial increase in net heat loss, more so in obese than lean animals. EPI is therefore thermolytic--i.e., disrupts thermal balance. A low dose (100 micrograms/kg) of the alpha-antagonist phentolamine produced a marked improvement in operant behavior, Tc, and thermal balance, whereas a comparable dose of the beta-antagonist propranolol had no beneficial effect. Increasing the dose of phentolamine worsened the responses with respect to the 100-micrograms/kg dose. The selective alpha 1-antagonist prazosin ameliorated the decrease in Tc induced by EPI but had little effect on operant behavior or thermal balance; the selective alpha 2-antagonist yohimbine had no effect on any parameter compared to EPI alone. These results suggest that the paradoxical effects of EPI in the cold are mediated by alpha-adrenoceptors, but definitive identification of the subclass of receptor involved cannot be determined.
Adipose Tissue, Brown↗
Temperature-dependent effects of alpha-adrenergic agonists and antagonists in the cold.
This series of experiments examined whether temperature-dependent effects of the alpha-antagonists prazosin and yohimbine compromised their use as blockers of alpha-adrenergic agonist responses in cold-exposed rats. An operant leverpressing task was used to measure the demand for heat in a cold environment. The alpha 1-antagonist prazosin had modest effects, but the alpha 2-antagonist yohimbine was thermolytic in that it dose dependently increased operant responding but decreased posttest colonic temperature (Tc). These potent effects of the alpha 2-antagonist led to tests of the alpha 2-agonist clonidine. Clonidine increased operant responding for heat to an extraordinary degree, resulting in significant increases in posttest Tc. However, clonidine was found to be a hypothermic agent when tested in rats at 5 degrees C but denied the opportunity to increase body temperature by operant lever pressing, suggesting a central effect on the control of thermal balance. Measurement of changes in metabolic rate at 5 and 23 degrees C showed that yohimbine increased metabolism at 23 degrees C but decreased it in the cold. Prazosin had little effect on metabolism or Tc at either temperature. Prazosin inhibited the decrease in Tc induced by norepinephrine (NE), but had little effect on the lever-pressing response. Yohimbine had no significant antagonistic effect on NE-induced changes in lever-pressing behavior or posttest Tc, but neither did the thermolytic effects of yohimbine exacerbate those of NE. These results show that alpha-antagonist interactions with agonists can be complicated by temperature-dependent effects of each.
Adrenergic alpha-Agonists↗
Effects of alpha 1-adrenoceptor and Ca2+ channel inhibition on norepinephrine-induced thermoregulatory behavior in the cold.
This experiment examined whether paradoxical temperature-dependent effects of norepinephrine (NE) can be blocked by the alpha 1-adrenoceptor antagonist WB 4101 (WB) and the Ca(2+)-channel blocker nifedipine. An operant lever-pressing task was used to measure the demand for heat in a cold environment. As noted previously, NE alone (250 micrograms/kg) produced a substantial and significant increase in the demand for heat, and yet post-test colonic temperature (Tc) fell. When tested alone, WB and nifedipine also increased the demand for heat, but this was sufficient to maintain Tc. When combined with NE, WB and nifedipine reduced the demand for heat and the fall in Tc such that there were no differences between the effects of the blockers given alone or with NE. These results indicate that paradoxical thermoregulatory effects of NE in the cold can be antagonized effectively by either an alpha 1-adrenoceptor antagonist or a Ca(2+)-channel blocker.
Adrenergic alpha-Antagonists↗