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Endоcrine glаnds secrete their hоrmоnes into the:
Tо chаrаcterize the rоles оf leptin аnd insulin in reproductive hormone modulation and offspring viability in over-conditioned ruminants, addressing key gaps in knowledge relative to undernutrition studies. Objective 1: To evaluate offspring production and viability in over-conditioned female and male ruminants. Hypothesis 1: Over-conditioned ruminants will exhibit reduced offspring viability, with increased miscarriage rates in females and sperm abnormalities in males. Objective 2: To characterize leptin and insulin profiles and their effects on GnRH, LH, and downstream reproductive hormones. Hypothesis 2: Over-conditioning disrupts leptin and insulin regulation, inhibiting GnRH and LH surges, and reducing progesterone, estradiol, and testosterone fluctuations. Objective 3: To assess the effects of feed over-supplementation on leptin and insulin efficiency and subsequent GnRH/LH surges. Hypothesis 3: Feed over-supplementation leads to decreased leptin and insulin efficiency, disrupting kisspeptin signaling and reproductive hormone surges in over-conditioned ruminants. References: Harlow, et al. (2022). The Impact of Undernutrition on KNDy Neurons in Female Lambs. Nestor, et al. (2023). KNDy Neurons as the GnRH Pulse Generator in Ruminants. AIM 11: To investigate the potential of KNDy neurons as key modulators of puberty and GnRH activity in ruminants, addressing their role in neuroendocrine reproductive regulation. Objective 1: To evaluate the impact of neurokinin B absence on puberty onset. Hypothesis 1: Puberty will occur in the absence of neurokinin B, albeit at a delayed rate. Objective 2: To assess the functional consequences of removing specific KNDy neuron components. Hypothesis 2: Neurokinin B function will be significantly impaired in the absence of kisspeptins. Objective 3: To explore the potential of KNDy neurons as natural GnRH agonists or antagonists. Hypothesis 3: Isolated KNDy neurons can function as effective exogenous modulators of GnRH activity.