This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This project was initiated in July 2005 to study the neuroendocrine mechanisms and genetic vulnerability responsible for socially induced anovulation or functional hypothalamic anovulation using a female rhesus monkey model. The first study tested the hypothesis that females homozygous or heterozygous for the short variant allele for the gene that encodes the serotonin reuptake transporter (SERT; n = 20) would show a hypometabolic phenotype compared to females homozygous for the long allele (n = 20). Females with the short allele had significantly lower body weights and body fat mass indices than females with the long allele (weight: 7.89 0.24 vs. 9.08 0.35 kg; BMI: 13.66 0.39 vs. 15.24 0.54). Females with the short allele also show evidence of a hypometabolic condition having lower levels of insulin (34.4 7.3 vs.38.6 7.1 ng/ml), T3 (158.9 11.9 vs. 171.3 6.0 ng/ml), and T4 4.7 0.2 vs. 5.3 .4 ng/ml) and higher levels of ghrelin (10.3 1.3 vs. 8.0 1.0 pg/ml). Furthermore, females with the sort allele showed a higher incidence of anovulation compared to females with the long allele (20% vs. 0%). Upcoming studies will define how social status exacerbates this increased genetic vulnerability to metabolic dysregulation to compromise fertility.
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