Effect of triglyceride structure on fecal excretion of 13C-labeled triglycerides.

OBJECTIVE

The aim of this work was to determine the effects of specific changes in the structure of (13)C-labeled triglyceride (TG*) on its fecal excretion relative to total stool fat excretion determined simultaneously in patients with reduced exocrine pancreatic function.

METHODS

A series of 47 studies were conducted in 26 young cystic fibrosis (CF) patients and 11 adult patients with chronic pancreatitis over a five year period. Each test consisted of ingesting a single high fat test meal containing both (13)C-labeled triglyceride (TG*) and dysprosium chloride (DyCl(3)) a nonabsorbable marker of intestinal transit; in most studies the food colorant brilliant blue (FD&C blue #1) was administered along with the DyCl(3). The TGs tested were: PPP = TRIPALMITIN-1,1,1-(13)C(3); SOS = 2-OCTANOYL-1,3-DISTEARIN-2-octanoyl-1,2-(13)C(2); and PLP* = 2-LAURYL-1,3-DIPALMITIN-dipalmitoyl-1,1,2,2-(13)C(4). Ingestion of the test meal was followed by collection of individual stools for at least 72 hours. Stools were analyzed for (13)C-Excess ((13)C*), total fat, and Dy.

RESULTS

Excretion of PLP showed a high degree of linear correlation with stool fat (r(2) = 0.924) over a wide-range of fecal fat values. Excretion of SOS was also significantly correlated with stool fat, but its excretion was less than 10% at all levels of steatorrhea and the slope of the regression line relating TG excretion to stool fat was some four to five times smaller than observed for PLP. Fecal excretion of PPP* was highly correlated with stool fat (r(2) = 0.941) in patients with moderate steatorrhea (<25 g fat/24 hours) and the slope of the regression line (3.20) was considerably greater than for P*LP*. Only results from those studies in which stool collections were complete (Dy excretion >90%) were utilized in the statistical comparisons (36 of 47 studies).

CONCLUSIONS

The observed highly significant linear correlation between PLP and stool fat over the entire range of steatorrhea suggests that PLP excretion may be a suitable surrogate for fecal fat in patients with reduced exocrine pancreatic function. Because fecal excretion of TG* administered as described can be accurately determined by sampling only two visually marked stools, development of a noninvasive test to replace the current 72-hour stool fat test using this approach is possible. Use of other engineered TG*s and/or labeled fatty acids, may provide a method for non-invasive in vivo assessment of the specific defect(s) leading to steatorrhea in other patient groups.