Effects of small-intestinal fat and carbohydrate infusions on appetite and food intake in obese and nonobese men

Abstract

To determine whether the satiating effects of nutrients in the small intestine are lower in obese than in nonobese people, 9 healthy, obese men [age: 18-33 y; body mass index (BMI; in kg/m2) 30.4-40.8] and 11 healthy, nonobese men (age: 18-33 y; BMI: 19.1-26.4) received an intraduodenal infusion of saline (control), lipid ( 11.97 kJ/min, or 2.86 kcal/min), or glucose (11.97 kJ/min) for 120 min on separate days. Fullness, hunger, and nausea were assessed by visual analogue scales. After the infusions, a meal was offered and food intake was quantified. There was no difference in appetite ratings between the obese and nonobese subjects during the infusions, in the amount or macronutrient composition of food eaten after the infusions, or in the time taken to eat the meals. Both the lipid and glucose infusions were associated with greater fullness than the control infusion. The energy content of the food eaten was less after the lipid infusion than after either the control or glucose infusion (P < 0.01): lipid infusion suppressed energy intake by 22% compared with the control infusion and by 15% compared with the glucose infusion. Suppression of energy intake after intraduodenal nutrient infusions was due to slower eating (P < 0.01). Intraduodenal infusions of fat suppressed appetite and food intake more than did equienergetic infusions of carbohydrate in both obese and nonobese young men, and the responses to intraduodenal fat and glucose were not affected by obesity. The latter observation suggests that established obesity is not associated with reduced small-intestinal responses to dietary fat or carbohydrate.

Dose-related effects of lauric acid on antropyloroduodenal motility, gastrointestinal hormone release, appetite, and energy intake in healthy men

“…Thirteen healthy males were included in the study; the number of subjects was based on power calculations derived from a previous study (6). We calculated that with 13 subjects we would observe a 10% decrease in energy intake at ␣ ϭ 0.05, with a power of 80%.…”

Jejunal Infusion of Glucose Decreases Energy Intake to a Greater Extent than Fructose in Adult Male Rats

“…Intraduodenal fructose, but not glucose, infusions in humans resulted in decreases in energy intake compared with saline infusions (10,11). Intraileal glucose infusions have been found to suppress energy intake to a greater extent than intraduodenal infusions in rats (12).…”

“…The rats were then divided into 3 groups to ensure an equal average body weight and SEM per group (GLU = 384 6 11.7 g, FRU = 394 6 12.9 g, and SAL = 392 6 9.8 g). Each group received either an equal kilocalorie load of GLU or FRU (11.4 kcal; Sigma-Aldrich), or SAL at a rate of 0.2 mL/h for 7 h at the beginning of the daily dark period for 5 d. An isotonic saline solution has been used previously as a control solution in human (10,11) and nonhuman animal (12,13) intestinal infusion studies. The parameters were chosen on the basis of previous research that showed a reduction in energy intake over a multiday infusion of an equal caloric load and duration of infusion of glucose and other nutrients, which we have used previously (8) and that have been used by others (13).…”

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.…”

“…A large body of literature suggests that some of these meal-related signals originate in the gastrointestinal tract and serve to terminate ingestion (5,11). Previously, studies have shown that intraintestinal infusions of long-chain fatty acids significantly reduced voluntary food intake (4,16): the mechanisms that control this response are complex, but likely involve gut-initiated satiety signals (9). Numerous gastrointestinal peptide hormones are released during and immediately after food intake, including cholecystokinin, peptide YY, glucagon-like peptide 1, and oxyntomodulin, which act either distally, signaling satiety and suppressing food intake via receptors located in the central nervous system, or proximally, by slowing gastric emptying (22,27).…”