Acta physiologica (Oxford, England) · 2026
Kisspeptin Restores Placental mTOR Signaling and Improves Glucose Homeostasis Mediators Disrupted by Maternal Hypothyroidism in Rats.
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Santos Bianca Reis, Dos Anjos Cordeiro Jeane Martinha, Santos Luciano Cardoso, Oliveira Cleisla Souza, Alvarez Maria Clara Pascoal Santos, Rodrigues Natália Panhoca, Lopez-Tello Jorge, Sferruzzi-Perri Amanda N, Serakides Rogéria, Silva Juneo Freitas
Аннотация
AIM: Reduced placental mTOR signaling is associated with intrauterine growth restriction and impaired maternal and placental metabolism. Since maternal hypothyroidism induces intrauterine growth restriction, and maternal treatment with kisspeptin-10 (Kp10) has been shown to improve feto-placental development in hypothyroid rats, this study aimed to evaluate the effects of maternal hypothyroidism, with and without kisspeptin-10 treatment, on maternal energy homeostasis and placental expression of mTOR and glucose metabolism mediators.
METHODS: Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.
RESULTS: Maternal hypothyroidism caused glucose intolerance, decreased insulin and HDL levels, reduced fetal and placental weights, and thinned the placental interhaemal barrier. It also increased INSRβ and AKT, while downregulating placental p-mTOR/mTOR and Glut1. Although kisspeptin-10 treatment did not improve maternal glucose homeostasis or prevent feto-placental growth restriction, it attenuated maternal hypothyroidism-induced placental Glut1 dysregulation, upregulated the IGF1/IGF1R axis, and restored placental AKT/mTOR expression.
CONCLUSION: These findings suggest that kisspeptin-10 treatment in hypothyroid pregnant rats improves placental mTOR signaling and glucose metabolism mediators, highlighting novel pathways through which kisspeptin may modulate placental physiology.
METHODS: Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.
RESULTS: Maternal hypothyroidism caused glucose intolerance, decreased insulin and HDL levels, reduced fetal and placental weights, and thinned the placental interhaemal barrier. It also increased INSRβ and AKT, while downregulating placental p-mTOR/mTOR and Glut1. Although kisspeptin-10 treatment did not improve maternal glucose homeostasis or prevent feto-placental growth restriction, it attenuated maternal hypothyroidism-induced placental Glut1 dysregulation, upregulated the IGF1/IGF1R axis, and restored placental AKT/mTOR expression.
CONCLUSION: These findings suggest that kisspeptin-10 treatment in hypothyroid pregnant rats improves placental mTOR signaling and glucose metabolism mediators, highlighting novel pathways through which kisspeptin may modulate placental physiology.