Gestational hypothermia in mice is not proportional to foetal mass or affected by maternal thermal environment, but pups grow faster at temperatures below thermoneutrality

During mammalian pregnancy, maternal thermal physiology and the associated thermoregulatory control systems undergo various changes. As the foetus grows, it produces an increasing amount of metabolic heat. That heat is dissipated either via feto-maternal exchange in the placental circulation (~85%), or via heat conductance pathways through the foetal skin, amniotic fluid and across the uterine wall (~15%). As gestation progresses, maternal core body temperature (Tcore) decreases (gestational hypothermia). There are several theories concerning why gestational hypothermia occurs. The aim of this study was to confirm that gestational hypothermia occurs in mice. It was predicted that the amount of heat generated by foetal mass in utero would be proportional to the gestational decrease in maternal Tcore.

It was also predicted that a change in maternal thermal balance by means of altered ambient temperature (Ta), may affect the extent of gestational hypothermia. Maternal intraperitoneal Tcore was measured during gestation in mice assigned to two ambient temperature groups, thermoneutral (29ºC, T29, n=8) and standard animal housing (22ºC, T22, n=7). Thermoneutral and below thermoneutral environments were used to alter the maternal thermal balance by changing the thermal gradient between the animal and her surroundings. A cosinor analysis was applied to the temperature data to obtain the mesor, amplitude and acrophase of the fitted cosine wave at several defined stages of pregnancy. Food intake and maternal body mass were measured throughout pregnancy, and pups were weighed immediately after birth and during lactation.

The mesor of Tcore decreased during gestation (P<0.001) by ~1ºC from premating levels, between the middle of trimester 1, reaching a nadir one day prepartum and increasing significantly (P = 0.001) by 0.6°C on the day of birth and a further 0.4°C by day two of lactation (P<0.001). The decrease in maternal Tcore was the same at the two housing temperatures. The extent of gestational hypothermia was not correlated with the foetal mass, the number of pups in the litter, or the proportion of maternal body mass made up by foetal mass at term. There was no difference in the litter mass or litter size at parturition between the treatment groups. However, pups grew faster in the T22 group than the T29 group during the first two days (by 0.2 g/day/pup, P=0.003), and from days four to six (by 0.1 g/day/pup, P=0.03) of lactation, but there was no difference in maternal body mass or maternal food intake between T22 and T29 at any stage of gestation or lactation.

The present study found that mice do exhibit gestational hypothermia as shown previously in rats, sheep, rabbits, dogs and goats. Gestational hypothermia is unaffected by housing temperature and is not correlated with the foetal parameters that influence feto-maternal heat exchange. This indicates that foetal temperature is not the regulated variable and some other mechanism or signalling pathway is causing the occurrence of gestational hypothermia. Pup growth during lactation appears to be more successful at sub thermoneutral temperatures, but is not associated with a difference in maternal mass or food intake between the two temperature groups. It is thought that maternal heat dissipation occurs at a faster rate at T22, thus reducing the heat burden on those mothers, allowing them to process more food into milk.