Infection with Giardia lamblia often causes only minor mucosal changes to the small intestine yet frank fat malabsorption may still occur. Some evidence suggests abtext-abstract pancreatic exocrine function in subjects with giardiasis although the mechanism and significance of this is unclear. Studies were conducted in vitro to determine the effect of G. lamblia trophozoites or culture filtrates from the organism on lipolysis of triglyceride by porcine pancreatic lipase. Live trophozoites significantly inhibited lipolysis. The degree of inhibition increased with longer duration of lipase exposure to trophozoites. Total amounts of enzyme inhibited were proportional to enzyme concentration, while the percentage inhibition was greatest at lowest concentration. At a lipase concentration of 1·7 i.u./ml, enzyme activity was reduced by 89·7% compared to controls after incubation for 4 h with trophozoites. The effect was abolished using killed, intact trophozoites. Culture filtrates of G. lamblia did not inhibit lipolysis. Specificity of the effect was suggested by the failure of another flagellate protozoan, Trichomonas vaginalis, to inhibit lipase. In this assay system the inhibition of lipolysis was not dependent on the bile salt concentration present. The impact of this effect in vivo remains to be determined but it may contribute to fat malabsorption in giardiasis.

The lipase inhibitor, orlistat, is used in the treatment of obesity and reduces fat absorption by about 30%. However, the mean weight loss induced by orlistat is less than expected for the degree of fat malabsorption. It was hypothesised that lipase inhibition with orlistat attenuates the suppressive effects of oral fat on subsequent energy intake in normal-weight subjects. Fourteen healthy, lean subjects (nine males, five females; aged 25±1·3 years) were studied twice, in a double-blind fashion. The subjects received a high-fat yoghurt ‘preload’ (males 400g (2562kJ); females 300g (1923kJ)), containing orlistat (120mg) on one study day (and no orlistat on the other ‘control’ day), 30min before ad libitum access to food and drinks; energy intake was assessed during the following 8h. Blood samples were taken at regular intervals for the measurement of plasma cholecystokinin (CCK). Each subject performed a 3d faecal fat collection following each study. Energy intake during the day was greater following orlistat (10220 (sem 928) kJ) v. control (9405 (sem 824) kJ) (P=0·02). On both days plasma CCK increased (P<0·05) after the preload. Plasma CCK 20min following ingestion of the preload was less after orlistat (4·1 (sem 0·9) pmol/l) v. control (5·3) (sem 0·9) pmol/l (P=0·028); however there was no difference in the area under the curve 0–510min between the two study days. Fat excretion was greater following orlistat (1017 (sem 168) kJ) v. control (484 (sem 90) kJ) (P=0·004). In conclusion, in healthy, lean subjects the acute inhibitory effect of fat on subsequent energy intake is attenuated by orlistat and the increase in energy intake approximates the energy lost due to fat malabsorption.