Major: Biological Sciences
Home City: Ventura
Faculty Mentor: Professor Rudy Ortiz
Pablo Juarez is a fourth year undergraduate student majoring in Molecular/Cell Biology at the University of California, Merced. Pablo’s undergraduate research experience began last summer when he joined the CAMP program and will continue through this summer and beyond as a MARC scholar. Pablo’s research is composed of elucidating some of the robust mechanisms by which northern elephant seal pups are naturally able to go on prolonged fasting periods while simultaneously remaining metabolically active by using their lipid reserves as energy sources. Aside from having research experience, Pablo believes that it is fundamental to volunteer and give back to the community in a capacity that will not only benefit himself but those around him. He expects to graduate in the spring of 2018 and aspires to one day attend a graduate school in hopes of completing an MD/PhD program. Pablo’s ultimate desire is to enter the health care industry and provide help to underserved communities which are in most need of it. Outside of academics, Pablo enjoys playing sports with friends, traveling and spending time with family. As a first generation college student, Pablo hopes to serve as a remodel and facilitate the path for younger students who one day aspire to not only attend a university, but move on to a graduate program.
Glucocorticoid Receptor-Mediated Lipolysis Increases Following Chronic Adrenocorticotropin Infusion in Northern Elephant Seal Pups
Pablo Juarez1, Jose Pablo Vasquez-Medina PhD1, Debby Lee1, Daniel E. Crocker, PhD2 and Rudy M. Ortiz, PhD1, School of Natural Sciences; University of California, Merced, Merced, CA; Department of Biology, Sonoma State University, Rohnert Park, CA2
Northern elephant seal (NES) pups experience prolonged fasting, relying on the oxidation of fatty acids to satisfy energetic needs. Fasting is characterized by an increase in cortisol, non-esterified fatty acids (NEFA), and heat shock protein 90 (HSP90), which is necessary for glucocorticoid-mediated lipolysis. The functional relevance of increased cortisol via the GR is not well defined. We hypothesized that ACTH infusion increases lipolysis in NES via HSP90-mediated mechanism. The contributions of cortisol and its receptor (GR) were assessed by exogenous infusion of ACTH in the presence or absence of a GR blocker in the following groups (n=6): (1) control, (2) ACTH (40 units), (3) GR blocker (GRb; 400mg mifepristone), and (4) ACTH+GRb (Combo). Plasma and adipose biopsy samples were collected at days 0 (T0; immediately prior to infusion) and 6 (T6). Mean plasma cortisol concentrations decreased 41±5% in ACTH and 21±3% in Combo, but remained constant in the control and GRb groups suggestive of adrenal exhaustion. Mean plasma aldosterone increased 135%± 4 in ACTH suggesting that the adrenal gland is differentially responsive. Mean NEFA and HSP90 expression levels increased 38%±4% and 119%±1% , respectively, in the ACTH suggesting that the GR-mediated increase in lipolysis is regulated by HSP90. Mean HSP90 expression increased 31%±3% in GRb and 192%±4% in Combo compared to control suggesting that blockade of the GR has no residual effect on the binding of HSP90 to the GRE. The data suggest that the fasting-associated increase in cortisol contributes to the increase in lipolysis through a HSP90-GR-mediated pathway.