UC researchers may have identified molecular method of reducing obesity
University of Cincinnati (UC) pathologists have identified a new molecular target that may eventually help scientists develop drugs to reduce fat transport to adipocytes (fat cells) in the body and prevent obesity and related disorders, like diabetes, according to the finding in the Oct. 18 online edition of the Journal of Clinical Investigation.
The researchers found that a specific cell receptor, known as the adipocyte LDL receptor-related protein 1 (LRP1), provides clues about the underlying biological mechanisms that control fat transport in the body.
Using genetically altered mice, David Hui, PhD, author and professor of pathology and laboratory medicine at UC, and colleagues demonstrated how “knocking out” LRP1 in fat cells has a direct impact on how many lipids are transferred and deposited to different tissues. Hui said the experimental mice gained less weight, stored less fat, tolerated glucose better and expended more energy as compared with a control group.
“This receptor is expressed in numerous tissues throughout the body—including the heart, muscles, liver and vascular wall—but its specific functions in the different tissues are still relatively unknown,” Hui said. “Our study has shown this molecule directly impacts the rate of fat transport in the body, so with further study it could be a new target for drugs aimed at controlling obesity.”
For the study, two independent groups of LPR1-knockout mice were developed: one studied by Hui and his team at UC; the second monitored by co-author Joachim Herz, PhD, at the University of Texas Southwestern Medical Center.
The researchers discovered that when the LRP1 receptor was active, adipocytes absorbed more fat, triggering a series of cell-signaling activities, that caused the body to increase overall fat storage. Although both groups of mice were fed the same low-fat diet, the LRP1 knockout mice stored less fat and experienced no significant weight gain.
The researchers found that a specific cell receptor, known as the adipocyte LDL receptor-related protein 1 (LRP1), provides clues about the underlying biological mechanisms that control fat transport in the body.
Using genetically altered mice, David Hui, PhD, author and professor of pathology and laboratory medicine at UC, and colleagues demonstrated how “knocking out” LRP1 in fat cells has a direct impact on how many lipids are transferred and deposited to different tissues. Hui said the experimental mice gained less weight, stored less fat, tolerated glucose better and expended more energy as compared with a control group.
“This receptor is expressed in numerous tissues throughout the body—including the heart, muscles, liver and vascular wall—but its specific functions in the different tissues are still relatively unknown,” Hui said. “Our study has shown this molecule directly impacts the rate of fat transport in the body, so with further study it could be a new target for drugs aimed at controlling obesity.”
For the study, two independent groups of LPR1-knockout mice were developed: one studied by Hui and his team at UC; the second monitored by co-author Joachim Herz, PhD, at the University of Texas Southwestern Medical Center.
The researchers discovered that when the LRP1 receptor was active, adipocytes absorbed more fat, triggering a series of cell-signaling activities, that caused the body to increase overall fat storage. Although both groups of mice were fed the same low-fat diet, the LRP1 knockout mice stored less fat and experienced no significant weight gain.