Kisspeptin Restores Placental mTOR Signaling and Improves Glucose Homeostasis Mediators Disrupted by Maternal Hypothyroidism in Rats.

Santos BR, Dos Anjos Cordeiro JM, Santos LC, Oliveira CS, Alvarez MCPS, Rodrigues NP, Lopez-Tello J, Sferruzzi-Perri AN, Serakides R, Silva JF

Acta physiologica (Oxford, England)1 Apr 2026Cited by 1 (Europe PMC)

PMID41782211PMCIDPMC12960837DOI10.1111/apha.70188PepBankPUB-41782211

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Summary

AimReduced 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.MethodsMaternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.ResultsMaternal 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.ConclusionThese 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.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

5 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In hypothyroid pregnant rats, kisspeptin‑10 treatment did not improve maternal glucose homeostasis.
In plain wordsIn pregnant rats with low thyroid function, kisspeptin‑10 did not improve blood sugar control.
Peptide
Kisspeptin-10
Outcome
No significant changeMaternal glucose homeostasis
Study
ratn: not reported in source
Pregnant rats with propylthiouracil-induced hypothyroidism
Outcome group
Glycemic control · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
Although kisspeptin-10 treatment did not improve maternal glucose homeostasis
1 context sentence(design, population, supporting numbers)
Summary · context
Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.
Show in the study text Report a problemFND-4178221101
02AnimalAnimal study (in vivo)Efficacy outcome
In hypothyroid pregnant rats, kisspeptin‑10 treatment did not prevent feto-placental growth restriction.
In plain wordsIn pregnant rats with low thyroid function, kisspeptin‑10 did not prevent poor growth of the fetus and placenta.
Peptide
Kisspeptin-10
Outcome
No significant changeFeto-placental growth restriction
Study
ratn: not reported in source
Pregnant rats with propylthiouracil-induced hypothyroidism
Outcome group
Body weight · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
Although kisspeptin-10 treatment did not improve maternal glucose homeostasis or prevent feto-placental growth restriction
1 context sentence(design, population, supporting numbers)
Summary · context
Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.
Show in the study text Report a problemFND-4178221102
03AnimalAnimal study (in vivo)Mechanism
In hypothyroid pregnant rats, kisspeptin‑10 attenuated the maternal hypothyroidism-induced placental Glut1 dysregulation (Glut1 was downregulated by hypothyroidism).
In plain wordsIn pregnant rats with low thyroid function, kisspeptin‑10 reduced the drop in a placental glucose transporter, Glut1.
Peptide
Kisspeptin-10
Outcome
IncreasePlacental Glut1
Study
ratn: not reported in source
Pregnant rats with propylthiouracil-induced hypothyroidism
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
it attenuated maternal hypothyroidism-induced placental Glut1 dysregulation
2 context sentences(design, population, supporting numbers)
Summary · context
downregulating placental p-mTOR/mTOR and Glut1
Summary · context
Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.
Show in the study text Report a problemFND-4178221103
04AnimalAnimal study (in vivo)Mechanism
In hypothyroid pregnant rats, kisspeptin‑10 treatment upregulated the placental IGF1/IGF1R axis.
In plain wordsIn pregnant rats with low thyroid function, kisspeptin‑10 raised a placental growth-signal pathway, IGF1/IGF1R.
Peptide
Kisspeptin-10
Outcome
IncreasePlacental IGF1/IGF1R axis
Study
ratn: not reported in source
Pregnant rats with propylthiouracil-induced hypothyroidism
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
upregulated the IGF1/IGF1R axis
1 context sentence(design, population, supporting numbers)
Summary · context
Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.
Show in the study text Report a problemFND-4178221104
05AnimalAnimal study (in vivo)Mechanism
In hypothyroid pregnant rats, kisspeptin‑10 treatment restored placental AKT/mTOR expression, which hypothyroidism had altered.
In plain wordsIn pregnant rats with low thyroid function, kisspeptin‑10 restored placental AKT and mTOR levels that thyroid deficiency had changed.
Peptide
Kisspeptin-10
Outcome
MixedPlacental AKT/mTOR expression
Study
ratn: not reported in source
Pregnant rats with propylthiouracil-induced hypothyroidism
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated
Source sentences
Summary
restored placental AKT/mTOR expression
2 context sentences(design, population, supporting numbers)
Summary · context
It also increased INSRβ and AKT, while downregulating placental p-mTOR/mTOR and Glut1.
Summary · context
Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.
Show in the study text Report a problemFND-4178221105

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Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 09:43 UTC
Study results updated
Version 1
9 Oct 2026, 03:04 UTC
First added · source update from Europe PMC

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