Obesity causes aberrant uterine embryo distribution and macrosomia at term

BAZZANO MARÍA VICTORIA; ELIA EVELIN MARIEL; PAZ DANTE AGUSTÍN

Buenos Aires

Jornada; XVIII Jornadas Anuales Multidisciplinarias de la Sociedad Argentina de Biología; 2016

Sociedad Argentina de Biología

The prevalence of obesity is increasing worldwide.It is related toseveral reproductive disorders but the molecular mechanisms linking them remainunclear. Using cafeteria diet-induced obesity as animal model, we found that obesitycauses aberrant uterine fetal distribution and macrosomia at term (gestationday (gd) 18.5) when compared to controls. To elucidate whether this alteration is consequence offetal re absorptions or due to alterations in the foregoing embryo spacing, weanalyzed embryo distribution just after implantation time (on gd 5.5). We alsofound asymmetric uterine embryo distribution on gd5.5, indicating that obesity alters the uterineembryo distribution prior to implantation. Then, to analyze embryo distributionjust before implantation, uterus from rats at gd 4.5 were flushed and embryoswere collected. The total number of embryos detected in obese rats was lowerthan in controls (p<0.001). When each uterine horn was analyzed separately,it was found that this reduction was due to a lower number of embryos presentin one of the horns (p<0.01), while the number of embryos in the other hornwas similar to controls. Since adrenergic receptor beta 2 (b2AR) is involved inthe uterine embryo distribution, we analyzed its gene expression by qPCR. We foundthat the b2AR expression was up regulated (p <0.01) in uterus from obeserats at gd 4.5 when compared to controls. When we evaluated the b2AR expressionin the pre-conception period we found that its gene and protein expression was downregulated (p <0.01) in obese uteri when compare to controls. Thesealterations may be one of the mechanisms underlying the aberrant uterine embryodistribution