During digestion, macronutrients are sensed within the small intestine. This sensory process is dependent upon the action of gut mediators, such as cholecystokinin (CCK) or serotonin (5-HT), on vagal afferents that, in turn, convey peripheral information to the brain to influence the control of food intake. Recent studies have suggested that dietary conditions alter vagal sensitivity to CCK and 5-HT. This phenomenon may be of importance to the onset of eating disorders. The aim of the present study was thus to investigate the effects of subjecting mice to 15 days of either an HF diet (30% fat, 54% carbohydrate) or an NF diet (10% fat, 74% carbohydrate) on 1) daily and short-term food intake, 2) vagal sensitivity to peripheral anorectic factors and macronutrient loads, and 3) vagal afferent neuron receptor expression. The results indicated that compared with an NF diet, and while increasing food intake and body weight gain, an HF diet altered the short-term response to CCK-8 and intragastric macronutrient loads, while decreasing vagal activation by CCK-8 and modifying the receptor expression of vagal neurons. These findings, therefore, suggest that dietary intervention effect on food intake could be linked to changes in vagal afferent receptor profiles.

Long term exposure to high fat (HF), high protein (HP) or high carbohydrates (HC) diets may lead to alterations of short term control of food intake, especially through their effects on peripheral sensitivity to gut hormones such as cholecystokinin and macronutrients. METHODS: Mice were submitted to either HF, HP or HC diet for 2 weeks. Neuronal activation was measured within the first central relay of vagal ascending fibers, the Nucleus of the Tractus Solitarius (NTS) in response to either intragastric gavage of calibrated diet load or peripheral injections of increasing doses of CCK. NTS activation was measured using immunohistochemical quantification of c‐fos expression performed on brainstem slices. RESULTS: We observed that HP‐induced NTS activation of HP adapted animals was greater than HF‐induced NTS activation of HF adapted animals. This result was consistent with a marked decrease in CCK sensitivity in HF adapted mice when compared to HP adapted mice. CONCLUSIONS: This study suggests that adaptation to HP diet increases sensitivity to gut anorectic signals whereas HF diet supresses this effect.

No abstract

No abstract