The role of intragestational ghrelin on postnatal development and reproductive programming in mice

Autor:	Torres PJ; Secretaría de Ciencia y Tecnología de la Universidad Nacional de Córdoba (SECyT-UNC), Córdoba, Argentina., Luque EM; Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina., Ponzio MF; Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina.; Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET), INICSA (CONICET-FCM), Córdoba, Argentina., Cantarelli V; Fondo Nacional de Ciencia y Tecnología (FONCyT), Córdoba, Argentina., Diez M; Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina., Figueroa S; Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina., Vincenti LM; Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina., Carlini VP; Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina.; Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET), INICSA (CONICET-FCM), Córdoba, Argentina., Martini AC; Instituto de Fisiología, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina.; Consejo Nacional de Investigaciones Científicas y Tecnológicas (CONICET), INICSA (CONICET-FCM), Córdoba, Argentina.
Jazyk:	angličtina
Zdroj:	Reproduction (Cambridge, England) [Reproduction] 2018 Oct 01; Vol. 156 (4), pp. 331-341. Date of Electronic Publication: 2018 Oct 01.
DOI:	10.1530/REP-18-0192
Abstrakt:	The purpose of this study was to evaluate the intragestational role of ghrelin in offspring development and reproductive programming in a mouse model of ghrelin imbalance during pregnancy. Female mice were injected with ghrelin (supraphysiological levels: 4 nmol/animal/day), antagonist (endogenous ghrelin inhibition with (D-Lys3)GHRP-6, 6 nmol/animal/day) or vehicle (control = normal ghrelin levels) throughout the pregnancy. Parameters evaluated in litters were growth, physical, neurobiological and sexual development and, at adulthood, reproductive function. Litter size and initial weight did not vary between treatments. Male pups from dams treated with ghrelin showed higher body weight increase until adulthood (31.7 ± 0.8 vs control = 29.7 ± 0.7, n = 11–14 litters/treatment; P < 0.05). Postnatal physical and neurobiological development was not modified by treatments. The antagonist accelerated male puberty onset, evidenced as earlier testis descent and increased relative testicular weight (antagonist = 0.5 ± 0.0% vs ghrelin = 0.4 ± 0.0% and control = 0.4 ± 0.0%, n = 5–10 litters/treatment; P < 0.05). At adulthood, these males exhibited lower relative testicular weight and reduced sperm motility (63.9 ± 3.6% vs control = 70.9 ± 3.3 and ghrelin = 75.6 ± 3.0, n = 13–15 animals; P < 0.05), without changes in plasma testosterone or fertility. Female pups intragestationally exposed to the antagonist showed earlier vaginal opening (statistically significant only at Day 25) and higher ovarian volume (antagonist = 1085.7 ± 64.0 mm3 vs ghrelin = 663.3 ± 102.8 mm3 and control = 512.3 ± 116.4 mm3; n = 4–6 animals/treatment; P < 0.05), indicating earlier sexual maturation. At adulthood, these females and those exposed to ghrelin showed a tendency to higher percentages of embryo loss and/or foetal atrophy. In conclusion, ghrelin participates in reproductive foetal programming: alterations in ghrelin activity during pregnancy modified body weight increase and anticipated puberty onset, exerting (or tending to) negative effects on adult reproductive function. (2018 Society for Reproduction and Fertility)
Databáze:	MEDLINE
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