ABSTRACT
Studies in the early 1970s showed that (–)-HCA inhibits citrate cleavage enzyme and fatty acid synthesis in vivo in the rat liver.5 Further work revealed that (–)-HCA decreased the rate of lipogenesis (when administered intravenously or interperitonally), and oral administration reduced fatty acid and cholesterol synthesis only when given before feeding. This lead to the supposition that if (– )-HCA could inhibit lipogenesis, but not affect normal energy production by cell mitochondria in humans, it could be of value in treating certain lipid disorders and obesity.6
