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Pregnancy damps thermoregulatory rhythms across timescales through neural estrogen signaling in mice

ABSTRACT: Pregnancy is accompanied by reductions in core body temperature (Tc) and its circadian amplitude, changes that are thought to provide fetal thermal stability. In the associated manuscript, we show that pregnancy profoundly reshapes thermoregulatory dynamics across diurnal and ultradian timescales, and identify estrogen receptor alpha (ERα) signaling in the preoptic area (POA) as a central mediator of these effects. During pregnancy, ERα-expressing in neurons of the medial POA (MPO) show enhanced estrogen signaling and hormone-responsive gene expression changes. Silencing ERα neurons or selectively deleting ERα in the POA attenuates pregnancy-induced decreases in Tc and its rhythmicity, leading to alterations in gestational length and/or birth weight. Together, these findings demonstrate that ERα signaling within the POA coordinates adaptive remodeling of thermoregulatory rhythms during pregnancy, with direct consequences on fetal outcomes. Here, we share transcriptomic data from ERα-expressing neurons in the MPO from non-pregnant and late pregnant mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE346233 | GEO | 2026/09/04

REPOSITORIES: GEO

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Project description:Maternal obesity is linked with increased adverse outcomes for mother and fetus. However, the metabolic impact of excessive fat accumulation within the altered hormonal context of pregnancy is not well understood. We used a murine model of obesity, the high fat diet-fed C57BL/6J mouse to determine adipose tissue-mediated molecular mechanisms driving metabolic dysfunction throughout pregnancy. Remarkably, obese mice exhibited a normalization of visceral fat accumulation at late-stage pregnancy (-53%, P<0.001 E18.5) to achieve levels comparable in mass (per gram of body weight) to that of non pregnant, control diet fed mice. Moreover, whilst obese pregnant mice showed a marked glucose intolerance and apparent insulin resistance at mid-stage pregnancy (E14.5), glucose homeostasis converged with that of lean pregnant mice at late-stage pregnancy, suggesting an unexpected amelioration of the worsening metabolic dysfunction in obese pregnant mice. Transcriptomic analysis of the late-stage visceral fat indicated reduced de novo lipogenic drive (Me1, Fasn, Scd1, Dgat2), retinol metabolism (Rdh11, Rbp4) and inflammation (Mcp1, Tnfα) in obese pregnant mice that was confirmed functionally by their lower adipose proinflammatory macrophage density. Elevated expression of estrogen receptor a (ERα) in visceral adipose tissue was identified as potential unifying mechanism for the transcriptional changes and reduced adiposity of late stage obese pregnancy. Support for a role for ERα was provided by experiments showing that the ERα selective agonist PPT suppressed lipogenesis in primary mouse adipocytes and suppressed Me1, Fasn, SCD1 and Dgat2 mRNA levels in mature female human ChubS7 clonal fat cells. Our data reveal a novel role for elevated visceral adipocyte estrogen signaling as a protective mechanism against visceral fat hypertrophy and inflammation in late pregnancy. Pregnant high fat, pregnant control fat, non pregnant high fat, non pregnant control fat. Five biologial replictes each (20 samples).

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Pregnancy damps thermoregulatory rhythms across timescales through neural estrogen signaling in mice

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