SH-BC-893 could be a promising therapy for managing diet-induced obesity
A team of scientists at University of California, US has discovered a novel pharmacological approach to attenuate the mitochondrial dysfunction that drives diet-induced obesity.
Consuming a high-fat diet can lead to obesity and metabolic disorders such as diabetes and fatty liver. Palmitate, a fat abundant in a Western diet, triggers metabolic dysfunction by causing excessive mitochondrial fission within cells.
Mitochondria play a crucial role in a cell’s energy production, but also coordinate cell stress responses. Too much mitochondrial fission impairs their function, undermining metabolism and increasing toxic by-products associated with insulin resistance in some tissue types.
“Elegant genetic studies in mice show that maintaining mitochondrial networks in a fused state can overcome high fat diet-induced obesity. Our study uses a small molecule to re-shape mitochondria in multiple tissues simultaneously, reversing obesity and correcting metabolic disease even though mice continue to consume the unhealthy diet,” said senior author Aimee Edinger, UCI Chancellor’s Fellow and professor of developmental & cell biology.
The study’s findings suggest that SH-BC-893 could be a promising therapy for managing diet-induced obesity. The authors found the drug to be safe and effective in the mouse model and plan on further investigating the compound for possible use in human patients.