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The effects of fat on gastric emptying (GE), gut hormones, and energy intake are dependent on digestion to free fatty acids (FFAs). In animals, small intestinal oleic acid inhibits energy intake more potently than the triacylglyceride (TG) triolein, but there is limited information about the comparative effects of FFA and TG in human beings. We compared the effects of FFA and TG on GE, gut hormone secretion, appetite, and energy intake in healthy males.Nine men (age, 23 +/- 2 y; body mass index, 22 +/- 1 kg/m(2)) were studied on 3 occasions to evaluate the effects of (1) 40 g oleic acid (FFA, 1830 kJ), (2) 40 g macadamia oil (TG, 1856 kJ; both 600-mL oil-in-water emulsions stabilized with 4% milk protein and labeled with 15 MBq (123)I), or (3) 600 mL 4% milk protein (control, 352 kJ), administered intragastrically, on GE, plasma cholecystokinin (CCK) and peptide-YY (PYY) levels, appetite perceptions, and subsequent energy intake.GE of FFA was much slower than that of TG (P.05), with greater retention of FFA, than TG, in the proximal stomach (P.001). Hunger was less (P.05), and fullness was greater (P.05), after FFA when compared with control and TG. Increases in plasma CCK and PYY levels were greater after FFA than TG or control (P.05). Energy intake tended to be less after FFA compared with TG (control, 4754 +/- 610 kJ; TG, 5463 +/- 662 kJ; FFA, 4199 +/- 410 kJ).FFAs empty from the stomach more slowly, but stimulate CCK and PYY and suppress appetite more potently than TG in healthy human beings.

Acute hyperglycaemia slows gastric emptying, reduces proximal gastric tone, inhibits antral motility, and stimulates pyloric contractions. The mechanisms mediating these effects are unknown, but nitric oxide (NO), a key inhibitory neurotransmitter in the gut, could potentially be involved. Aim: To determine whether the NO synthase inhibitor, L-NAME, reverses the effects of hyperglycaemia on gastric emptying and proximal and distal gastric motility. Methods: Seven healthy volunteers (4 male; age 30.3±3.8 yr; BMI 23.6±1.2 kg/m2) were studied in a 4-way randomised crossover design (hyperglycaemia vs. euglycaemia; L-NAME vs. placebo) after an overnight fast. After positioning a transnasal manometry catheter across the pylorus, the blood glucose was maintained at either 15 mmol/L or 5 mmol/L using a glucose/insulin clamp. Once the blood glucose was stabilised for 30 min, an intravenous infusion of L-NAME (180 mcg/kg/h) or placebo (0.9% saline) was commenced (t = 0) and continued for 150 min. At t = 30, subjects ingested a test drink containing 50g glucose made up to 300ml with water. Gastric emptying and intragastric distribution (proximal and distal stomach retention) were measured using 3-D ultrasound. Antropyloroduodenalmotility was recorded concurrently. Statistical analysis was performed using repeated measures ANOVA. Data presented as mean ± SEM. Results: Gastric half-emptying time (T50) was prolonged on the hyperglycaemia/placebo day compared to the remaining 3 study days, which were no different from each other (127±19min [hyperglycaemia/placebo] vs. 86±7min [hyperglycaemia/L-NAME] vs. 77±12min [euglycaemia/placebo] vs. 81±5min [euglycaemia/ L-NAME]; P = 0.01). The effect of hyperglycaemia on gastric emptying was completely abolished by L-NAME. The rate of total gastric emptying closely correlated to that of proximal (r = 0.970; P < 0.0001), but not distal (P = N.S.), gastric emptying. Fasting antral motility index was suppressed during hyperglycaemia (P < 0.05). Basal pyloric pressure was increased during hyperglycaemia (P < 0.001), and decreased with L-NAME (P < 0.001). Conclusions: Hyperglycaemia-induced delay in gastric emptying is associated with increased proximal retention and increased basal pyloric pressure; these effects are attenuated markedly by L-NAME.

BACKGROUND: There is evidence that the menstrual cycle affects appetite, such that energy intake is lower pre-ovulation than post-ovulation (Li et al, Appetite 1999; 33:109-118). Since changes in gastric emptying (GE) contribute to acute energy intake, an understanding of how the menstrual cycle affects GE is important. Furthermore, knowledge on day-to-day variations in energy intake, i.e. within the same phase of the menstrual cycle, is limited. AIMS: To assess the hypotheses that (i) GE is slower, and hunger and energy intake are less, pre-ovulation than post-ovulation, (ii) GE and energy intake are reproducible when assessed twice within a particular phase of the menstrual cycle (eg pre-ovulation) and (iii) the reduction in hunger and energy intake pre-ovulation will be related to slower GE. METHODS: 9 healthy, lean females (aged 32±1 years; BMI: 21.6±0.5 kg/m2) were studied on 3 separate occasions; twice pre-ovulation (between days 6-12; “Pre-V1” and “Pre-V2”), and once post-ovulation (between days 18-24; “Post”). Visits were randomized in singleblind fashion over consecutive menstrual cycles. Following consumption of a 300 ml glucose drink (815 kJ), GE (using 3D ultrasound) and hunger (using visual analogue scales) were measured for 90 min. Between 90-120 min, energy intake at a buffet meal was quantified. RESULTS: During pre-ovulation, GE was slower (P

Studies in animals indicate that endogenous nitric oxide (NO) is an important inhibitory neurotransmitter in the gastrointestinal tract and that it modulates food intake. We evaluate the role of NO mechanisms in mediating the effects of small intestinal nutrients on antropyloroduodenal motility and appetite in humans.On 2 separate days, 8 healthy adult men received intravenous L-NAME 180 microg/kg/h or 0.9% saline (0-150 min); between 30 min and 120 min, an intraduodenal lipid infusion (2 kcal/min) was administered, and at 120 min subjects were offered a buffet meal (120-150 min). Antropyloroduodenal pressures were measured with a sleeve/sidehole manometric assembly. During the infusions, perceptions of hunger and fullness were assessed with visual analog questionnaires and amount and macronutrient content of food consumed at the buffet meal were quantified. Blood pressure and heart rate were monitored at regular intervals.Intraduodenal lipid infusion was associated with increases in fullness (P0.05) and in frequency of isolated pyloric pressure waves (P0.05) and basal pyloric pressure (P0.05); and decreases in hunger (P0.05) and in frequency of antral (P0.05) and duodenal (P0.05) pressure waves. L-NAME increased diastolic blood pressure (P = 0.08) and decreased heart rate (P0.05), but had no effect on antropyloroduodenal pressures or food intake.Intravenous administration of the systemic NO synthase inhibitor, L-NAME, in a dose that affects cardiovascular function in healthy humans does not modify the antropyloroduodenal motor and appetite responses to intraduodenal lipid infusion.