As it turns out, forskolin exerts its thermogenic and lipolytic actions via cAMP activation in adipocytes. It does this completely independently of epinephrine and stimulants. By activating cAMP in adipocytes, forkolin activates an enzyme, hormone-sensitive lipase (HSL), that modulates the liberation of fatty acids from adipocytes to be metabolized for energy. This induces significant lipolytic action.
Furthermore, forskolin stimulates thyroid function, not only by enhancing the production of the thyroid hormones, T4 and T3, but also by promoting the conversion of T4 to the more bioactive T3. Forskolin does this via modulation of the action of the enzyme type II deiodinase. This enhanced thyroid activity ultimately leads to enhanced thermogenic action.
Relatedly, forskolin also exerts cAMP-dependent anti-catabolic action. In particular, muscle-tissue breakdown is modulated by calpains. These are calcium-dependent enzymes that are themselves inhibited by agents known as calpastatins. Now, calpastatin activation is cAMP-dependent. Consequently, by activating cAMP, forskolin triggers calpain inhibition via calpastatin recruitment. This calpain inhibition ultimately leads to lean-tissue preservation, and an enhancement of the lean mass:fat mass ratio.
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