Authors: Jacob Prescott
Mentors: Zoe Thompson
Insitution: Utah Valley University
The pro-opiomelanocortin (Pomc) gene encodes POMC, which is differentially processed to produce adrenocorticotropic hormone (ACTH), beta-endorphin, and three melanocyte-stimulating hormones, among other peptides. POMC neurons are principally located in the arcuate nucleus (Arc) of the hypothalamus, where they are essential in the control of food intake, energy expenditure and body weight. Several different mutations in the POMC gene have been shown to cause early-onset obesity and adrenal cortical insufficiency in humans.
We are working with a mouse model with a hypothalamic-specific POMC deficiency. These mice exhibit hyperphagia, early-onset obesity, and also seem to be infertile. We are interested in examining potential differences in pubertal development, as well as reproductive function. Specifically, we will examine day of vaginal opening, day of first estrus, and estrus cycling in juvenile female POMC-deficient mice.
The estrus cycle has four stages: proestrus, estrus, metestrus and diestrus. Although hormone levels in the blood differ during the four stages, these are difficult and expensive to measure. A less invasive measurement is to take vaginal cell samples each day and examine them under the microscope. Three different types of cells are present in different ratios depending on the stage of the cycle: nucleated epithelial cells, leukocytes, and cornified epithelial cells. We will track estrus cycle changes during pubertal development and after to see if there are differences between wildtype, heterozygous, and homozygous POMC-deficient mice.
Learning more about how POMC-deficiency affects reproductive function may help us understand more about the link between obesity and infertility.