John Cupit Butler University
Faculty Sponsor(s): Mark Macbeth Butler UniversityThis past summer I was chosen by the Elmquist Lab at UT Southwestern to assist in unraveling this biological tapestry through the use of Endocannabinoids, endogenous lipid-derived ligands that bind with respective CB1R receptors. These receptors have been characterized as a class of G-proteins within the natural human and animal body. It has been shown that deletion of the cannabinoid 1 receptor (CB1R KO) have improved glucose tolerance in mice when healthy and when fed a healthy food diet. However, selective reactivation of the CB1R in the VMH of similar mice (CB1R SF1-RA) counter acts some of the improvements in glucose tolerance. Therefore, the question is, why do we see this reversal in the CB1R SF1-RA mice?
In order to be able to measure the glucose content of the individual mice, we must use a method known as the Glucose Tolerance Test. In short, for a GTT you inject glucose and see how well the mice can clear the glucose bolus by measuring their blood glucose. This is dependent on insulin sensitivity and insulin secretion (i.e., how well is insulin causing glucose to be taken up by peripheral tissues), and glucagon response and secretion (i.e., is endogenous glucose production being shut down properly in response to the glucose bolus and responding insulin levels). The main aim of this research will be to determine if CB1R’s in the VMH are sufficient enough to regulate insulin sensitivity in mice.
Biochemistry & Molecular Biology
When & Where
Gallahue Hall 105