Event Title
The Potential Mechanism of Leptin on Lipolysis in Brown Adipose Tissue
Start Date
15-4-2021 9:30 AM
End Date
15-4-2021 10:30 AM
Student's Major
Biological Sciences
Student's College
Science, Engineering and Technology
Mentor's Name
Charles Krois
Mentor's Department
Chemistry and Geology, Biological Sciences
Mentor's College
Science, Engineering and Technology
Description
Using mainly fatty acids for energy, brown fat produces heat in order to maintain body temperature through thermogenesis. Lipolysis, the release of fatty acids from stored triglyceride, is mediated (in part) by the protein hormone sensitive lipase (HSL). Activation of HSL occurs when it is phosphorylated by protein kinase A (PKA), which is itself activated due to signaling via a G protein-coupled receptor (GPCR). Leptin, a hormone, signals to cells by activating a cascade called the JAK-STAT pathway. In short, activation of Janus kinases (JAK) leads to phosphorylation and activation of STAT (signal transducers and activators of transcription) to alter the expression of specific target genes (1,5). In addition, leptin can also exhibit crosstalk affecting the GPCR pathway. Zhang and colleagues identified an example where leptin signaling inhibited PKA in endothelial cells (5,6). However, whether this crosstalk occurs in brown fat is unclear.
The Potential Mechanism of Leptin on Lipolysis in Brown Adipose Tissue
Using mainly fatty acids for energy, brown fat produces heat in order to maintain body temperature through thermogenesis. Lipolysis, the release of fatty acids from stored triglyceride, is mediated (in part) by the protein hormone sensitive lipase (HSL). Activation of HSL occurs when it is phosphorylated by protein kinase A (PKA), which is itself activated due to signaling via a G protein-coupled receptor (GPCR). Leptin, a hormone, signals to cells by activating a cascade called the JAK-STAT pathway. In short, activation of Janus kinases (JAK) leads to phosphorylation and activation of STAT (signal transducers and activators of transcription) to alter the expression of specific target genes (1,5). In addition, leptin can also exhibit crosstalk affecting the GPCR pathway. Zhang and colleagues identified an example where leptin signaling inhibited PKA in endothelial cells (5,6). However, whether this crosstalk occurs in brown fat is unclear.
