INICSA   23916
INSTITUTO DE INVESTIGACIONES EN CIENCIAS DE LA SALUD
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Ghrelin modulates fertilization, early embryo development and implantation.
Autor/es:
LUQUE EM; VINCENTI LM; STUTZ G; SANTILLÁN ME; RUIZ RD; FIOL DE CUNEO M ; MATINI AC
Lugar:
Florencia
Reunión:
Congreso; XV Congreso Internacional de Endocrinología y XIV Congreso Europeo de Endocrinología; 2012
Institución organizadora:
Sociedad Europea de Endocrinología
Resumen:
Ghrelin modulates fertilization, early embryo
development and implantation
Luque
EM, Vincenti LM, Stutz G, Santillán ME, Ruiz RD, Fiol de Cuneo M and Martini
AC
Instituto de Fisiología,
Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Argentina.
Contact: acmartini2000@yahoo.com.
Ghrelin (Ghr) acts as a
link between energy balance and reproduction; hence, hyperghrelinemia reduces reproductive
success. In addition, this hormone has an evident physiological role on reproduction,
since Ghr and/or its receptor are synthesized by gametes/embryos and several
reproductive tissues (including decidua/placenta); in addition, Ghr plasma concentration rises during
gestation.
The objectives of our
study were to evaluate the effects of ghrelin administration (4 nmol/animal/day;
sc) or endogenous ghrelin inhibition (by 6 nmol/animal/day of (D-Lys3)GHRP-6;
sc) on mice fertilization, embryo development and implantation. We carried out
three experiments treating female mice with Ghr and/or its antagonist: 1) from one week previous to
12 hours after copula, sacrificing mice at Day 18 of pregnancy; 2) from
ovulation induction to 80 hours after ovulation, when we retrieved embryos from
uterus and 3) from Day 3 to Day 7 of pregnancy (peri-implantation
period), sacrificing mice at Day 18.
Experiment 1: the
antagonist increased the percentage of females with one/more atrophied fetuses (antagonist: 75.0% vs control: 11.1%;
n=8-11 females/group; p<0.0134). Experiment 2: the
antagonist significantly diminished induced ovulation and fertilization and
both, Ghr and the antagonist, delayed embryo development (embryos in blastocyte
stage: Ghr 40.8%, Ghr+antagonist 28.9% and antagonist 36.8% vs control
66.3%; n=76-136 embryos/treatment, p<0.0001).
In experiment 3, Ghr and the antagonist significantly diminished fetuses weight
and dams weight gain during gestation. Moreover, Ghr augmented the percentage
of embryo loss (TM±SEM; Ghr: 17.3±6.58 and Ghr+antagonist: 13.3±3.7 vs control:
3.9±4.8 and antagonist: 6.7±4.0; n=9-12 females/treatment; p=0.045) and again, Ghr and the antagonist
increased fetuses atrophy (Ghr: 71.4%, Ghr+antagonist: 44.4% and antagonist
62.5% vs control: 0%; n=7-10 females/group; p<0.01).
Our results suggest that hyperghrelinemia
and/or endogenous ghrelin inhibition exerted immediate and long lasting effects
on oocyte/embryo quality, implantation and embryo/fetal development, supporting
the hypothesis that ghrelin has modulatory actions on these reproductive processes.