by University of Texas Health Science Center at San Antonio
https://medicalxpress.com/news/2022-04- ... etite.html
Scientists from The University of Texas Health Science Center at San Antonio (UT Health San Antonio) today reported that inhibiting a liver enzyme in obese mice decreased the rodents' appetite, increased energy expenditure in adipose (fat) tissues and resulted in weight loss.
The finding, published in Cell Metabolism, provides a potentially desirable drug target to treat metabolic issues such as obesity and diabetes, the authors said.
"We first needed to discover this mechanism and, now that we have, we can develop drugs to improve metabolic syndrome," said senior author Masahiro Morita, Ph.D., assistant professor of molecular medicine in UT Health San Antonio's Sam and Ann Barshop Institute for Longevity and Aging Studies.
"We have an enzyme inhibitor that we want to make more specific to increase its effects," said first author Sakie Katsumura, DDS, Ph.D., postdoctoral fellow in the Morita laboratory.
The liver enzyme, called CNOT6L deadenylase, turns off messenger ribonucleic acids (mRNAs) that ordinarily carry genetic instructions from the nucleus to sites in the cell where two liver proteins are made.
One of the proteins, growth differentiation factor 15 (GDF15), sends signals to two regions of the hindbrain to control food intake. The other, fibroblast growth factor 21 (FGF21), sends signals to brown and white adipose tissues to increase energy expenditure. CNOT6L deadenylase impedes mRNA code-carrying for both GDF15 and FGF21, which reduces these benefits.