Effect of Adrenergic Signaling On All-Trans-Retinoic Acid Synthesis In Brown Adipose Tissue
Start Date
15-4-2021 9:30 AM
End Date
15-4-2021 10:30 AM
Student's College
Science, Engineering and Technology
Mentor's Name
Charles Krois
Mentor's Department
Chemistry and Geology
Mentor's College
Science, Engineering and Technology
Description
Thermogenesis is a process where our body maintains its temperature by producing heat. Nerves release norepinephrine to signal a thermogenic response in brown adipose tissue (BAT), which uses the activity of uncoupling proteins 1 (UCP1) to make heat. All-trans-retinoic acid (atRA), synthesized from dietary vitamin A, also affects an animal’s ability to carry out thermogenesis. Both atRA and norepinephrine independently increase the amount of UCP1, however, their interrelationship is not well understood. This experiment is focused on how norepinephrine effects atRA production in BAT, by examining norepinephrine’s effect on the mRNA levels of atRA synthesizing proteins. First, we determined the optimal dose of isoproterenol, a norepinephrine mimic, to elicit changes in UCP1 mRNA in cultured BAT tissue cells. Presently, we are determining whether treatment with a PKA inhibitor affects isoproterenol’s effect the mRNAs of atRA synthesis enzymes.
Effect of Adrenergic Signaling On All-Trans-Retinoic Acid Synthesis In Brown Adipose Tissue
Thermogenesis is a process where our body maintains its temperature by producing heat. Nerves release norepinephrine to signal a thermogenic response in brown adipose tissue (BAT), which uses the activity of uncoupling proteins 1 (UCP1) to make heat. All-trans-retinoic acid (atRA), synthesized from dietary vitamin A, also affects an animal’s ability to carry out thermogenesis. Both atRA and norepinephrine independently increase the amount of UCP1, however, their interrelationship is not well understood. This experiment is focused on how norepinephrine effects atRA production in BAT, by examining norepinephrine’s effect on the mRNA levels of atRA synthesizing proteins. First, we determined the optimal dose of isoproterenol, a norepinephrine mimic, to elicit changes in UCP1 mRNA in cultured BAT tissue cells. Presently, we are determining whether treatment with a PKA inhibitor affects isoproterenol’s effect the mRNAs of atRA synthesis enzymes.
