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In this study, we investigated the analogies between the physiological effects of simmondsin, a satiety-inducing glycoside extracted from jojoba seeds, and the gastro-intestinal satiation peptide, cholecystokinin. The effects of intraperitoneal injection of the biological active CCK-octapeptide on the pancreas, interscapular brown adipose tissue, growth performance and energy metabolism in normal-fed, severely food intake-restricted (50 % of normal food intake) or moderately food intake-restricted (65 % of normal food intake) growing rats were compared to the effects of 0.25 % simmondsin mixed in the food, inducing moderate food intake reduction (65 % of normal) in rats. Cholecystokinin induced pancreatic hypertrophy. In normal fed rats, cholecystokinin had no effect on brown adipose tissue or growth, while, in severely food intake-restricted rats, it caused brown adipose tissue hypertrophy and reduced growth. In moderately food intake-restricted rats, both cholecystokinin and simmondsin induced pancreatic hypertrophy, increased brown adipose weight and metabolism and caused a slight decrease in growth. We conclude that cholecystokinin may decrease growth performance in fast growing severely food intake-restricted rats by stimulating brown adipose tissue metabolism, probably because of protein shortage induced by pancreatic hyperstimulation. Simmondsin has similar effects. These results support the hypothesis that endogenous cholecystokinin is involved in the effects of simmondsin in rats.

Adult rats received simmondsin by intragastric intubation (ig) or intraperitoneal injection (ip) or mixed in with food (MF). Food intake inhibition was noted after administration by any of these routes, starting within minutes after ig or MF administration and continuing for ±2 h in the former case and for 20 h in the latter. Following ip administration, food intake inhibition started after approximately 0.5 h and continued for about 2 h and was followed by a hyperphagic period. Simmondsin was measurable in the blood, but the concentration did not correlate with the anorexic effect. Only a fraction of the ingested or ip-administered simmondsin was excreted unmodified in the urine or feces. Ip administered simmondsin was detectable in the feces, indicating passage from the blood into the gut. The presence of simmondsin in the proximal gut seems to be necessary for the induction of anorexia. Keywords: Simmondsin; jojoba; absorption; excretion; rats