Food intake is controlled by complex physiological systems that are not yet fully understood. Neurotransmitters and hormones certainly play a key role. For instance, cholecystokinin (CCK), produced by endocrine cells in the duodenal mucoase, is known to induce satiety ans is a very potent food intake depressor.
Food intake depression also occurs after consuming seeds of the jojoba plant (Simmondsia chinensis), a desert shrub native to the Sonoran desert from the Southern States of the USA. A series of related glycosides have been extracted from the deoiled jojoba meal. The principal molecule is simmondsin [2-(cyanomethylene)-3-hydroxy-4,5-dmethoxycyclohexyl beta-D glucoside] (up to 7 % by weight of defatted jojoba meal). As simmondsin induces food intake depression and emaciation, it was thought to be toxic. However, actual toxicity had never been unambiguously demonstrated and no pair-feeding studies had been performed to discriminate between te effects of food intake reduction and possible toxic effects. In actual fact, the acute toxicity of simmondsin si very low and no pathological changes could be attributed to simmondsin. It therefore remained to prove that simmondsin reduces food intake by its toxicity.
The aim of our research on simmondsin and defatted jojoba meal was to unravel the mechanism of action of simmondsin, to study possible toxic influences and to investigate its potential as a food intake depressant.