By inhibiting autoreceptors on presynaptic noradrenergic neurons, Yohimbine may increase norepinephrine release as the negative feedback inhibition cycle is interrupted.
Yohimbine acts on the adrenergic receptor system of fat cells, which regulates thermogenesis.
The beta subunits of adrenergic receptors (targets of ephedrine) can be considered stimulants for fat loss, since they increase the activity of the enzyme adenyl cyclase and subsequently the levels of cAMP.
Alpha subunits are more suppressive of fat metabolism, in which their activation reduces adenyl cyclase activity and lowers cAMP (specifically alpha-2) levels.
Yohimbine is a selective alpha-2 adrenergic receptor antagonist (inactivator), which inhibits the activation of the suppressor set of receptors and preserves the activity of adenyl cyclase and the effects mediated through beta receptors, also yohimbine can induce the fat loss indirectly through the release of adrenaline; adrenaline itself is an activator of beta-adrenergic receptors, however this increase in adrenaline may disappear over time reaching negligible levels 2 weeks after daily intake,
Increases in plasma free fatty acids and alpha2-adrenergic receptor density remain similar at both time points, suggesting that yohimbine selectively misses the spike in epinephrine but not the direct fat-burning effects of the receptor.
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