Safety Issues

The p-agonist clenbuterol was the subject of considerable negative publicity in the early 1990s when its illegal use was linked to cases of acute food poisoning in Europe.[11] Clenbuterol was initially designed with a long half-life as a pharmaceutical medicine used in treatment of respiratory and other diseases, and the desired properties of such medicines are totally opposite to what is required for a feed ingredient. Later generation p-agonists were developed with structural differences that resulted in shorter

ß-Adrenergic Agonist

ß-Adrenergic Agonist

Fig. 3 Mechanism of signal transduction from p adrenergic receptors (pAR). The p adrenergic receptor is activated by an agonist and interacts with Gs proteins. The Gs proteins stimulate adenylyl cyclase (AC) to convert adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), which acts as an intracellular signaling molecule. Increased levels of cAMP activate protein kinase A (PKA) to phosphorylate many enzymes and regulatory factors important in metabolic regulation. (From Ref. [7].)

Phosphorylation

Fig. 3 Mechanism of signal transduction from p adrenergic receptors (pAR). The p adrenergic receptor is activated by an agonist and interacts with Gs proteins. The Gs proteins stimulate adenylyl cyclase (AC) to convert adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), which acts as an intracellular signaling molecule. Increased levels of cAMP activate protein kinase A (PKA) to phosphorylate many enzymes and regulatory factors important in metabolic regulation. (From Ref. [7].)

half-lives and lower oral potencies allowing safe development for use in livestock.[12] Therefore, the problems that arose from the illegal treatment of animals with clenbuterol are no longer problems with current p-agonists. Any approved p-agonists' lean efficiency enhancer must meet or exceed stringent human food safety standards.

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