Abstract
The chronically elevated heat production of lactating Norway rats makes them vulnerable to acute hyperthermia during pup contact and thereby limits the duration of such interactions. High lactational levels of progesterone and corticosterone may act in concert to increase maternal heat load. Specifically, progesterone appears to increase maternal thermal set point and corticosterone is necessary for the increase in maternal heat production. Thyroid hormones and brown adipose tissue do not seem to contribute to the chronic increase in maternal heat production. While mammary tissue does contribute to maternal heat load, it is no more hypermetabolic than other maternal tissues.
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