Mechanisms involved in malabsorption of dietary lipids

Vetten in de voeding zijn belangrijk voor het menselijk lichaam als bronnen van energie en als bouwstenen, vooral in periodes van groei en ontwikkeling. Gewoonlijk is het menselijk lichaam in staat om voedingsvetten zeer efficiënt op te nemen; meer dan 96% van de voedingsvetten wordt opgenomen in het lichaam. Er zijn echter verschillende aandoeningen waarbij de absorptie van voedingsvetten verstoord is. Voor een goede behandeling van patiënten met deze zogenaamde vetmalabsorptiesyndromen is inzicht in het vetabsorptieproces essentieel. Het proces dat verantwoordelijk is voor de opname van vetten uit de voeding speelt zich af in het maagdarmkanaal. Zie: Samenvatting

Detection of impaired intestinal absorption of long-chain fatty acids:validation studies of a novel test in a rat model of fat malabsorption

Background: Classic fat balance studies detect fat malabsorption but do not discriminate between the potential causes of malabsorption, such as impaired intestinal lipolysis or reduced uptake of fatty acids. Objective: We aimed to validate a novel test for the specific, sensitive detection of impaired intestinal uptake of long-chain unesterified fatty acids in an appropriate rat model of fat malabsorption. Design: The absorption and appearance in plasma of [C-13]palmitic acid were determined in control rats and in rats with fat malabsorption due either to chronic bile deficiency (permanent bile diversion) or to oral administration of the lipase inhibitor orlistat (200 mg/kg diet). [C-13]Palmitic acid results were compared with the percentage absorption of ingested dietary fat determined by fat balance. Results: Between 1 and 6 h after intraduodenal administration, plasma [C-13]palmitate concentrations in control rats were 4-10-fold higher than in bile-deficient rats (P <0.05) but were not significantly different between orlistat-supplemented rats and their controls. In control and bile-deficient rats, plasma [C-13]palmitate concentrations allowed complete discrimination between normal (>92%) and reduced ( Conclusions: The [C-13]palmitic acid absorption test detects impaired intestinal absorption of long-chain fatty acids selectively and sensitively in a rat model of fat malabsorption due to bile deficiency. Our data strongly support the use of the [C-13]palmitic acid absorption test for the diagnosis of clinical fat malabsorption syndromes

Fat malabsorption in cystic fibrosis patients receiving enzyme replacement therapy is due to impaired intestinal uptake of long-chain fatty acids

Background: Pancreatic enzyme replacement therapy frequently fails to correct intestinal fat malabsorption completely in cystic fibrosis (CF) patients. The reason for this failure is unknown. Objective: We investigated whether fat malabsorption in CF patients treated with pancreatic enzymes is caused by insufficient lipolysis of triacylglycerols or by defective intestinal uptake of long-chain fatty acids. Design: Lipolysis was determined on the basis of breath (CO2)-C-13 recovery in 10 CF patients receiving pancreatic enzyme replacement therapy after they ingested 1,3-distearoyl,2[1-C-13]octanoyl glycerol ([C-13]MTG). Intestinal uptake of long-chain fatty acids was determined by analyzing plasma [C-13]linoleic acid ([C-13]LA) concentrations after patients ingested [C-13]LA. For 3 d, dietary intakes were recorded and feces were collected. Results: Fecal fat excretion ranged from 5.1 to 27.8 g/d ((x) over bar +/- SD: 11.1 +/- 7.0 g/d) and fat absorption ranged from 79% to 93% (89 +/- 5%). There was no relation between breath (CO2)-C-13 recovery and dietary fat absorption (r = 0.04) after ingestion of [C-13]MTG. In contrast, there was a strong relation between 8-h plasma [C-13]LA concentrations and dietary fat absorption (r = 0.88, P <0.001). Conclusion: Our results suggest that continuing fat malabsorption in CF patients receiving enzyme replacement therapy is not likely due to insufficient lipolytic enzyme activity, but rather to incomplete intraluminal solubilization of long-chain fatty acids, reduced mucosal uptake of long-chain fatty acids, or both