Fatty acid metabolism during norepinephrine-induced thermogenesis in the cold-acclimatized rat

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Abstract
Intravenous infusion of cold-acclimatized rats with l-norepinephrine (2 µg/min) caused a marked increase in metabolic rate and rectal temperature and a sustained reduction of the respiratory quotient. Prior to infusion the blood and liver concentrations of nonesterified fatty acids (NEFA) were greater in cold-acclimatized than in control rats. Upon infusion blood NEFA levels were markedly increased, but reached the same ultimate concentration in both groups. In vitro studies showed that liver tissue from cold-acclimatized rats had a significantly higher capacity for NEFA (palmitate) oxidation than liver tissue from controls. In vitro studies also showed that epididymal fat tissue from cold-acclimatized rats was considerably more sensitive to NEFA-mobilizing action of norepinephrine than similar tissue from controls. Continuous measurements of respiratory gas exchange during acute cold exposure (5 and –15 C) or cold-acclimatized rats caused reduction of the RQ, limited to the transition stage from a lower to higher metabolic steady state. We conclude that: a) norepinephrine-calorigenesis is primarily supported by oxidation of NEFA; b) greater calorigenic response to norepinephrine in cold-acclimatized animals is due to improved capacity to form and oxidize NEFA; c) norepinephrine is not the sole mediator of nonshivering thermogenesis. We suggest that the calorigenic action of this hormone is either limited to periods of acute cold stress or exerted in conjunction with other neurohumoral agents during chronic exposure.

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