ArticleVeterinary research communications2026
Heat stress during pregnancy and its relationship with IGFR1/insulin signaling expression in ovarian follicles of dairy cow adult offspring.
Article in Veterinary research communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Heat stress during pregnancy can affect the intrauterine development and modify the expression of key molecules involved in reproductive function in offspring adulthood. This study aimed to evaluate changes in the expression of insulin-like growth factor receptor 1 (IGFR1), insulin receptor (IR) and their downstream signaling pathways in dominant ovarian follicles of Holstein cows born to dams naturally exposed to different temperature-humidity index (THI) conditions during gestation. Cows (n = 26) were evaluated according to their exposure to a THI ≥ 72 during gestation, determined using their birth date or effective service date of their dam. Gestation was divided, based on key events in ovarian development, into two periods (P1 = days 0-150; P2 = day 151 to calving) and three trimesters (T1 = days 0-90; T2 = days 91-180; T3 = day 181 to calving), and the exposure to THI ≥ 72 was calculated in each. Total and phosphorylated expression levels of IGFR1, IR, IRS, PI3K, and AKT were assessed in the dominant follicles of adult offspring. Variables related to prenatal heat stress in P1, T1 and T2 were positively associated with IGFR1 and pIGFR1 expression (P < 0.05). Instead, variables related to prenatal heat stress in P2 were negatively associated with IGFR1 and pIGFR1 expression (P < 0.05). Signaling components such as IRS, pIRS, and pAKT were positively associated with variables related to prenatal heat stress in T2 in ovarian cells of adult offspring. However, PI3K expression in adulthood was negatively associated with variables related to prenatal heat stress in T1 (P < 0.05). These findings indicate that heat stress during pregnancy is associated with persistent alterations in key components of the IGF1/insulin signaling pathway in dominant follicles of adult offspring.
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