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New Drug Corrects Diet-Induced Obesity by Keeping Mitochondria from Fragmenting

Mitochondrial fragmentation is increased by a high-fat diet and excessive leptin, a signaling molecule released by adipose tissues that increases appetite. Scientists at University of California, Irvine, showed in mouse studies, oral administration of SH-BC-893, a small water-soluble, synthetic sphingolipid, inhibits endolysosomal trafficking of proteins required for mitochondrial fission, improving mitochondrial morphology and function in white adipose tissue and the brain, restoring normal leptin signaling, and reducing food intake to a level that maintains a negative energy balance resulting in weight loss.