Suppression of food intake, body weight, and body fat by jejunal fatty acid infusions

Abstract

Three experiments investigated effects of jejunal lipid infusions given on 4 or 21 consecutive days in adult, male Sprague-Dawley rats. In experiment 1, 7-h infusions of linoleic or oleic acid (0.2 ml/h for 7 h; total load = 11.5 kcal) on 4 consecutive days reduced total intake (ad libitum consumption of the liquid diet Boost, Mead Johnson, plus load) by approximately 15% and decreased weight gain compared with 4-day tests with saline administration. In experiment 2, linoleic acid at 0.1 ml/h for 7 h (5.7 kcal) was ineffective, whereas the same load delivered in 3.5 h produced effects similar in magnitude to those in the first experiment. In experiment 3, jejunal infusions of linoleic acid (0.2 ml/h for 7 h) on 21 consecutive days reduced mean total intake by 16%, body weight by 10%, and carcass fat by 48% compared with controls receiving saline. The net decrease in caloric intake may reflect the combined activation of pre- and postabsorptive mechanisms, and it suggests a possible treatment for obesity.

Food intake is inhibited by oral oleoylethanolamide

“…However, we also tested the effect of oral ethanolamine (1.88 mg/kg ϭ 30.72 mol/kg) and oleate (8.68 mg/kg ϭ 30.72 mol/ kg) separately and found no effect on food intake, with 131.6 Ϯ 26.8% (mean Ϯ SEM, n ϭ 4, P ϭ 0.30) and 94.7 Ϯ 9.2% (mean Ϯ SEM, n ϭ 12, P ϭ 0.62), respectively, of the amount measured in control rats (n ϭ 4, n ϭ 12). Also, rat and human studies investigating the appetite-regulating effect of oleate suggest that the dose of oleate needed to elicit a hypophagic effect may be several times higher than the dose we used (16,17).…”

Structure–effect relation of C18 long-chain fatty acids in the reduction of body weight in rats

“…Together, these data suggest that the adipose tissue-plasma leptinhypothalamus axis was functioning properly in oleic acidand 2-OHOA-treated rats and that the reduction of food intake must be provoked by another mechanism, which was able to compensate the increase of hypothalamic NPY. In this context, Cox et al 16 have shown that jejunal infusion of oleic acid is able to reduce food intake, most probably by celiac vagal afferent stimulation through cholecystokinin. 17 Nonetheless, intestinal infusions of oleic acid can be problematic, because this fatty acid can affect mucosal cells, leading to transient intestinal damage and decrease of food intake when administered as sodium oleate, 18 whereas others have also criticized that intestinal infusion of lipids may create false results when flux rates are exceeding physiological values of gastric emptying.…”

Voluntary consumption of ethyl oleate reduces food intake and body weight in rats

“…Intragastric and intraintestinal infusions of either linoleic or oleic acid have been demonstrated to reduce food intake and body weight in humans, rats and other animal models (4,6,7,8). Numerous studies have indicated a role for CCK, signaling via vagal afferent neurons in the gut and setting in motion a robust gut-satiety cascade.…”

“…Numerous studies have described a reduction in food intake following infusion of fatty acids directly into the small intestine: French et al demonstrated that upper intestinal infusions of 20% oil emulsions enriched with either stearic, oleic, or linoleic acid significantly reduced food intake compared controls infused with saline, and that this reduction in food intake was accompanied with increased plasma CCK concentrations (9); Meyer et al described reductions in food intake following intraintestinal infusions of either fatty or amino acids (16); Cox et al have reported that jejunal infusions of linoleic or oleic acid elicit increased satiety, decreased food intake and decreased body weight in rats (6). Matzinger et al demonstrated that this effect is mediated by cholecystokinin, abolishing the effects of intraduodenal fat infusions on food intake with a specific CCK-A receptor antagonist (15).…”