osteum and maltodextrin

To determine whether damage to the intestinal mucosa by oleic acid causes the suppression of food intake observed in response to intraintestinal infusion of the fatty acid, we measured lactate dehydrogenase (LDH) activity, a marker for cell damage, in the intestinal lumen after intestinal infusion of fatty acid under conditions similar to those employed in studies of eating behavior. Infusions of 25 or 51 mM sodium oleate (neutralized oleic acid) markedly and rapidly increased LDH activity, whereas infusions of saline had little or no effect. Infusion of octanoate, which has been reported to be ineffective in reducing eating behavior, did not increase intestinal LDH activity relative to saline infusion. Similarly, infusion of ethyl oleate or free (nonneutralized) oleic acid neither increased luminal LDH activity nor suppressed food intake. Infusion of sodium oleate also produced a strong conditioned aversion to sucrose. The results strongly suggest that the suppression of food intake induced by intraintestinal infusion of sodium oleate is due to the injurious effects of this unphysiological form of the fatty acid.

Topics: Animals; Duodenum; Enteral Nutrition; Fat Emulsions, Intravenous; Feeding Behavior; Food Deprivation; Gastrointestinal Contents; L-Lactate Dehydrogenase; Learning; Male; Oleic Acid; Polysaccharides; Rats; Rats, Inbred Strains; Satiety Response; Taste