Effect of triglycerides with different fatty acid chain length on superior mesenteric artery blood flow.

Fat stimulates superior mesenteric artery (SMA) blood flow. Little is known, however, about the influence of fatty acid chain length on SMA flow. The present study was performed to compare the effect of long chain triglycerides (LCT, corn oil), very long chain triglycerides (VLCT, fish oil) and medium chain triglycerides (MCT) on SMA flow. A total of seven healthy volunteers (four men, three women; aged 26 +/- 4 years) participated in three experiments, performed in random order during 60 min continuous intra-duodenal infusion of either LCT (30 mL h(-1); 240 kcal h-1), equicaloric VLCT (30 mL h(-1); 240 kcal h(-1)) or MCT in equimolar (15 mL h(-1); 113 kcal h(-1)) and equicaloric amount (30 mL h(-1); 225 kcal h(-1)). Basal and stimulated SMA blood flow were measured by Doppler ultrasonography. At regular intervals blood samples were taken for measurement of plasma cholecystokinin (CCK) and plasma peptide YY (PYY). Basal SMA blood flow volumes were not significantly different among the LCT, VLCT and MCT experiments (426 +/- 135, 460 +/- 114 and 503 +/- 177 mL min(-1), respectively). The SMA flow increased significantly (P < 0.05) during fat infusion but was significantly higher during LCT (1460 +/- 692 mL min-1) compared with VLCT (1061 +/- 384 mL min-1), MCT 15 mL h(-1) (870 +/- 286 mL min(-1)) and MCT 30 mL h-1 (904 +/- 223 mL min(-1)). Plasma CCK levels increased significantly (P < 0.05) during LCT and VLCT but not during MCT infusion. No correlation was found between SMA flow and plasma CCK levels (r = 0.27; P = 0.2) The SMA blood flow in response to triglycerides is dependent on fatty acid chain length. This chain length-dependent blood flow response is, however, not linear and is not related to plasma CCK levels.

Antroduodenal motility in chronic pancreatitis: are abnormalities related to exocrine insufficiency?

In patients with chronic pancreatitis (CP) the relation among exocrine pancreatic secretion, gastrointestinal hormone release, and motility is disturbed. We studied digestive and interdigestive antroduodenal motility and postprandial gut hormone release in 26 patients with CP. Fifteen of these patients had pancreatic insufficiency (PI) established by urinary para-aminobenzoic acid test and fecal fat excretion. Antroduodenal motility was recorded after ingestion of a mixed liquid meal. The effect of pancreatic enzyme supplementation was studied in 8 of the 15 CP patients with PI. The duration of the postprandial antroduodenal motor pattern was significantly (P < 0.01) prolonged in CP patients (324 +/- 20 min) compared with controls (215 +/- 19 min). Antral motility indexes in the first hour after meal ingestion were significantly reduced in CP patients. The interdigestive migrating motor complex cycle length was significantly (P < 0.01) shorter in CP patients (90 +/- 8 min) compared with controls (129 +/- 8 min). These abnormalities were more pronounced in CP patients with exocrine PI. After supplementation of pancreatic enzymes, these alterations in motility reverted toward normal. Digestive and interdigestive antroduodenal motility are abnormal in patients with CP but significantly different from controls only in those with exocrine PI. These abnormalities in antroduodenal motility in CP are related to maldigestion.

Medium chain triglycerides activate distal but not proximal gut hormones.

BACKGROUND AND AIMS: Compared to long chain triglycerides (LCT), medium chain triglycerides (MCT) are considered an attractive caloric source in malabsorptive diseases because of their favorable physico-chemical characteristics. The use of MCTis, however, limited by the occurrence of gastrointestinal symptoms such as diarrhoea. We have, therefore, investigated the effects of MCT and LCT on proximal (cholecystokinin; CCK) and distal (peptide YY; PYY) gut hormone secretion. METHODS: Eight healthy volunteers participated in four experiments performed in random order during continuous intraduodenal administration for 360 min of a) saline (control); b) LCT15 mmol/h; c) MCT15mmol/h (equimolar); d) MCT 30 mmol/h (equicaloric). Plasma CCK and PYY were determined at regular intervals (radioimmunoassay). Duodenocecal transit (DCTT) was measured by lactulose H(2)breath test. RESULTS: DCTT during LCT (105 +/- 11 min) was not significantly different from saline (111 +/- 10 min). Both low dose MCT (54 +/- 5 min) and high dose MCT (61 +/- 6 min) significantly accelerated DCTT (P< 0.05). Plasma CCK increased significantly (P< 0.05) during LCT but not during MCT or saline. PYY increased significantly (P< 0.05) not only during LCT, but also during low and high dose MCT but not during saline. CONCLUSIONS: Intraduodenal MCTs a) accelerate intestinal transit; b) do not stimulate CCK release; c) but stimulate release of the distal gut hormone PYY. These results suggest that MCTs are not rapidly absorbed in the proximal gut but probably reach the ileocolonic region and stimulate PYY release.