Influence of Thyrotrophin‐Releasing Hormone on Thermoregulatory Adaptation after Birth in Near‐Term Lambs Delivered by Caesarean Section

Abstract

We investigated the hypothesis that exogenous stimulation with thyrotrophin-releasing hormone (TRH) immediately prior to umbilical cord clamping can improve thermoregulatory adaptation after birth in near-term lambs delivered by Caesarean section. Lambs received an umbilical vein injection of saline +/- TRH (8 microg) prior to cord clamping. The rate of change in colonic temperature and oxygen consumption after birth were not influenced by TRH, but TRH-treated lambs exhibited a greater incidence of shivering compared with controls over the first hour of neonatal life. Two and a half hours after birth, TRH-treated lambs possessed brown adipose tissue (BAT) with a higher thermogenic activity (i.e. GDP binding to mitochondrial protein), but their BAT had a reduced DNA content and they had less hepatic glycogen than control lambs. TRH administration had no effect on iodothyronine 5' deiodinase activity in BAT and liver, or on plasma concentrations of total triiodothyronine, thyroxine, cortisol or free fatty acids. Three TRH-treated but no control lambs, failed to establish continuous breathing, so tissues from these treated lambs together with time-matched controls were sampled 25 min after birth. These 'non-surviving' TRH-treated lambs had very high plasma catecholamine concentrations, but their lung weights were similar to controls. 'Surviving' TRH-treated lambs possessed lungs with less DNA than non-surviving TRH-treated lambs. It is concluded that umbilical vein injection of TRH prior to umbilical cord clamping increases the recruitment of both shivering and non-shivering thermogenesis after birth.

Effects of intravenous thyrotropin-releasing hormone on 18F-fluorodeoxyglucose uptake in human brown adipose tissue: a randomized controlled trial

“…In the hypothalamus-pituitarythyroid axis, the cold-induced increase in TRH stimulates TSH secretion by the pituitary, which in turn stimulates thyroid hormone release from the thyroid (11). Research in various species showed that both core body temperature (32,33) and BAT-specific temperature (13) are increased by central or peripheral administration of TRH. Intracerebroventricular infusion of TRH in rodents was found to activate BAT via sympathetic neurons, an effect that could be blocked by pre-treatment with TRHreceptor type 1 antibodies and attenuated by sympathetic denervation of BAT depots (13,14).…”

“…Indeed, TRHknockout mice show cold intolerance (12). Interestingly, both central and peripheral administration of TRH was found to increase BAT thermogenesis in several mammals (13,14). Whether peripheral administration of TRH has similar effects in humans is unknown.…”