Abstract
Small bowel contractility may be more prominent in obese subjects, such that there is enhanced nutrient absorption and hunger stimulation. However, there is little evidence to support this. This study examined in vitro small bowel contractility in obese patients versus non-obese patients.Samples of histologically normal small bowel were obtained at laparoscopic Roux-en-Y gastric bypass from obese patients. Control specimens were taken from non-obese patients undergoing small bowel resection for benign disease or formation of an ileal pouch-anal anastamosis. Samples were transported in a pre-oxygenated Krebs solution. Microdissected circular smooth muscle strips were suspended under 1 g of tension in organ baths containing Krebs solution oxygenated with 95% O2/5% CO2 at 37°C. Contractile activity was recorded using isometric transducers at baseline and in response to receptor-mediated contractility using prostaglandin F2a, a nitric oxide donor and substance P under both equivocal and non-adreneregic, non-cholinergic conditions (guanethidine and atropine).Following equilibration, the initial response to the cholinergic agonist carbachol (0.1 mmol/L) was significantly increased in the obese group (n = 63) versus the lean group (n = 61) with a mean maximum response: weight ratio of 4.58 ± 0.89 vs 3.53 ± 0.74; (p = 0.032). Following washout and re-calibration, cumulative application of substance P and prostaglandin F2a produced concentration-dependent contractions of human small bowel smooth muscle strips. Contractile responses of obese small bowel under equivocal conditions were significantly increased compared with non-obese small bowel (p < 0.05 for all agonists). However, no significant differences were shown between the groups when the experiments were performed under NANC conditions. There were no significant differences found between the groups when challenged with nitric oxide, under either equivocal or NANC conditions.Stimulated human small bowel contractility is increased in obese patients suggesting faster enteric emptying and more rapid intestinal transit. This may translate into enhanced appetite and reduced satiety.
Highlights
The development of obesity results from a person's inadequate energy expenditure and/or excessive caloric intake
In relation to caloric intake, the gastrointestinal (GI) system plays a vital role in the controlling nutrient ingestion, digestion, and absorption
These functions depend on an intact, coordinated GI motility, which regulates the rates at which nutrients are processed and participates in the control of appetite and satiety
Summary
The development of obesity results from a person's inadequate energy expenditure and/or excessive caloric intake. In relation to caloric intake, the gastrointestinal (GI) system plays a vital role in the controlling nutrient ingestion, digestion, and absorption. These functions depend on an intact, coordinated GI motility, which regulates the rates at which nutrients are processed and participates in the control of appetite and satiety. Intestinal transit plays a crucial role in the absorption of nutrients. Variations in intestinal motility control the transit and absorption of the ingested nutrients through negative feedback [3,4] and hormonal methods [5], affecting satiety. If obese patients demonstrate increased intestinal motility and transit, does this indicate that they have enhanced absorptive capacity? If obese patients demonstrate increased intestinal motility and transit, does this indicate that they have enhanced absorptive capacity? if they have a decreased transit time, what factor is present that blocks the negative feedback on satiety in these patients? It has been speculated that the intestinal absorption is more rapid and efficient in obesity, irrespective of the intestinal transit rate, but the supporting evidence is very limited
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