Study on the inhibitory control system of nonshivering thermogenesis by gene signal analysis.

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Brown adipose tissue (BAT) is the major site of nonshivering thermogenesis (NST) during cold acclimation. It is well established that the thermogenic activity of BAT is mainly regulated by sympathetic noradrenaline (NA) and pancreatic glucagon, but little is known about the factor concerning inhibitory control of BAT.Therefore, the present research was undertaken to evaluate the possibility of inhibitory role of prolactin (PRL) on BAT activity.In male rats cold-exposure for 1 hr or 1 day decreased plasma PRL levels, but after cold-acclimation the plasma levels returned to the warm-acclimated control levels. Saline injection elevated the plasma PRL level and this elevation was blocked by noradrenaline (NA). In repeatedly-immobilized rats the elevation of plasma PRL level during immobilization stress was blocked. The resting plasma PRL level of genetically heat-tolerant FOK rats was lower as compared with those of other strains. In female animals haloperidol-treatment, causing hyper-prolactinemia, suppressed, while bromocriptine-treatment, causing hypo-prolactinemia, enhanced the in vitro responsiveness of BAT to glucagon, but not to NA.Dopamine mimicked the responses of BAT to bromocriptine. These results strongly suggest that PRL inhibits NST,especially by modifying the thermogenic action of glucagon in BAT.However, visible mRNA for PRL receptor was not detected in BAT.Further study on the subtypes of PRL receptor-mRNA is needed to clarify the role of PRL on BAT activity.