Study zeros in on mitochondrial dysfunction to treat obesity

According to new research in the journal EMBO Molecular Medicine, researchers at the University of California unveiled how centering on mitochondria may aid in treating obesity.

“Here, we reveal that these compounds are either unable to block ceramide-induced mitochondrial fission or require extended incubation periods to be effective,” the authors wrote in their findings.

“In contrast, targeting endolysosomal trafficking events important for mitochondrial fission rapidly and robustly prevented ceramide-induced disruptions in mitochondrial form and function.”

In the study, researchers used a synthetic sphingolipid known as SH-BC-893 and found it inhibited mitochondrial dysfunction in the liver, brain, and white adipose tissue of rodents who had consumed a Western diet. The subsequent end result was a normalization of leptin and adiponectin, resulting in weight loss, improvement of fatty liver disease, and enhanced glucose handling, even in spite of continued consumption of a high-fat diet.

“As an interventional agent, SH-BC-893 restored normal body weight, glucose disposal, and hepatic lipid levels in mice consuming a HFD,” the study concluded.

“In sum, the sphingolipid analog SH-BC-893 robustly and acutely blocks ceramide-induced mitochondrial dysfunction, correcting diet-induced obesity and its metabolic sequelae.”

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