2016-2018 MARC Cohort

 

 

 

 

 

Maximizing Access to Research Careers: Summer 2016-2018 Cohort

 

Pablo Juarez

Major: Biological Sciences

Home City: Ventura

Contact: pjuarez@ucmerced.edu

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.

Kenny Veliz

Major: Biological Sciences

Home City: Riverbank

Contact: kveliz@ucmerced.edu

Faculty Mentor: Professor Rudy Ortiz

Kenny is a fourth year Human Biology major at UC Merced expecting to graduate in the spring of 2018. His research interests lie in studying the effect on glucose and lipid metabolism in the presence of activated Renin Angiotensin Aldosterone system in a metabolic syndrome (MetS) model. Kenny's research specifically focuses on examining the effect of an Angiotensin type 1 receptor blockade on hepatic gluconeogenic enzymes and lipid mobilizing proteins in a model of MetS during an acute glucose challenge. In addition, he also takes great pride in being hands on in his community by volunteering in the Emergency Department at Mercy Medical Hospital, helping tutor at the local Boys & Girls Club, and advocating higher education at his alma mater Riverbank High School. At no surprise, Kenny's ultimate goal is to give back and have a positive impact on his community and other vastly underserved communities. He plans on doing so by implementing skills he gained from his time here at UC Merced and in the MARC program towards the health care field as a practitioner/researcher in his community. During his free time, Kenny enjoys playing sports, networking, learning, and watching his former UCM basketball teammates' Saturday nigh basketball games. Kenny aspires to be an exemplar, mentor, and enlighten future first-generation students like himself. 
 
Angiotensin Receptor Blockade Decreases PEPCK Expression Following a High Glucose Challenge in a Model of Metabolic Syndrome 
 
Kenny Veliz, Max Thorwald, Debby Lee, and Rudy Ortiz, PhD; School of Natural Sciences, University of California, Merced
 
The over production of glucose is a key factor in the development of hyperglycemia in diabetes. Angiotensin II (Ang II), increases de novo glucose production by the liver. Blockade of angiotensin II receptor type 1 (AT1) decreases the expression of phosphoenolpyruvate carboxykinase (PEPCK), the rate limiting enzyme in gluconeogenesis, in non-insulin dependent diabetes. However, whether AT1 activation contributes de novo glucose production by the liver in a metabolic syndrome (MetS) setting is not known. To test the hypothesis that activation of AT1 increases the expression of enzymes involved in de novo glucose production by the liver in MetS, hepatic PEPCK protein expression was examined after a 12 hour fast (T0) and 180 and 360 minutes following a glucose challenge (2g/kg) in the following groups of rats (n = 8/group): 1) untreated, lean Long-Evans Tokushima Otsuka (LETO; 2) untreated, obese Otsuka Long- Evans Tokushima fatty (OLETF); and 3) OLETF + angiotensin receptor blocker (ARB; 10 mg/kgd in diet for 8 wk; OLETF ARB). We expect an increase in PEPCK expression in OLETF at T0 and that it will remain elevated following the glucose challenge as compared to LETO. We also expect that AT1blockade will reverse this effect. In conclusion, the activation of AT1 in a MetS setting, contributes to glucose intolerance via an upregulation of gluconeogenesis which may ultimately lead to type II diabetes.