The Pregnancy Heat Shield
The regulation of body temperature during pregnancy is a precise process, as heat stress can pose a risk to the developing fetus. To ensure healthy fetal development, the maternal body undergoes extensive hormonal and metabolic adaptations throughout pregnancy. One of the key hormones involved in this process is thyroid hormone, which is also a central regulator of thermogenesis: as under normal conditions, thyroid hormone increases peripheral heat production and raises core body temperature.
A recent study by López-Alcántara and colleagues shows that pregnancy can override these temperature-raising effects. In a mouse model of maternal hyperthyroidism, elevated thyroid hormone levels increased body temperature only during early pregnancy. In later stages, however, the maternal body became resistant to these effects. Tissues such as brown adipose tissue and skeletal muscle showed little response, and instead of generating heat, energy appears to be redirected in favor of fetal needs.
The study thus reveals a previously unknown protective mechanism by which the maternal organism shields the fetus from overheating, even under conditions of thyroid hormone excess.
López-Alcántara N, Adam L, Resch J, Keipert S, Mittag J, Oelkrug R. (2026) Pregnancy negates thyroid hormone-induced pyrexia, Am J Physiol Endocrinol Metab 330:E796-E809. doi: 10.1152/ajpendo.00569.2025.
Hepatocyte clock as potential therapeutic target in liver disease
De Assis and colleagues investigated how disruption of the hepatocyte circadian clock influences progression of metabolic dysfunction-associated steatohepatitis (MASH). Using hepatocyte-specific Bmal1 knockout mice, they found accelerated disease progression characterized by increased hepatic cholesterol accumulation, inflammation, and fibrosis. Transcriptomic and lipidomic analyses revealed disrupted cholesterol metabolism and altered expression of key cholesterol-regulating genes, with Chrebp identified as a possible co-regulator.Complementary in-vitro experiments showed that Bmal1 specifically controlled cholesterol accumulation independent of Chrebp. Human patient data further supported altered circadian timing in MASH, highlighting the hepatocyte clock as an important regulator and potential therapeutic target in liver disease.
Hepatocyte Circadian Clocks Control Cholesterol Metabolism and Protect From Metabolic Dysfunction-Associated Steatohepatitis (MASH). Monteiro de Assis LV, Jegodzinski L, Inderhees J, Wowro SJ, Affonso JM, Heyde I, Fischer EL, von Schönfels W, Schenk A, Roßner F, Schupp M, Marquardt JU, Demir M, Oster H. Cell Mol Gastroenterol Hepatol. 2026 May
