Validation of an enzyme immunoassay and comparison of fecal cortisol metabolite levels in black and gold howler monkeys (Alouatta caraya) inhabiting fragmented and continuous areas of the humid Chaco region, Argentina. Contrary to our initial prediction, no significant differences in Alouatta caraya fecal cortisol metabolite levels were detected; cortisol metabolites were significantly higher in females. Probably, animals adjusted their diet to cope with feeding in degraded habitats, but with new leaves and buds.

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 were 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±64.0mm3 vs ghrelin=663.3±102.8mm3 and control=512.3±116.4mm3; 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.

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