Adels L E, Leon M
Physiol Behav. 1986 Jan;36(1):183-96. doi: 10.1016/0031-9384(86)90094-6.
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.
哺乳期挪威大鼠长期产热升高，使其在与幼崽接触时易患急性体温过高，从而限制了此类互动的持续时间。哺乳期高水平的孕酮和皮质酮可能共同作用，增加母体的热负荷。具体而言，孕酮似乎会提高母体的体温设定点，而皮质酮是母体产热增加所必需的。甲状腺激素和棕色脂肪组织似乎并未促成母体产热的长期增加。虽然乳腺组织确实会增加母体的热负荷，但其代谢率并不比其他母体组织更高。
