Carboxyl ester lipase from either mother's milk or the pancreas is required for efficient dietary triglyceride digestion in suckling mice.

Because dietary fats provide an important source of energy in the newborn, the efficient digestion of dietary fats is critical to their well-being. Despite the importance of dietary fat digestion, newborns have a deficiency of pancreatic triglyceride lipase, the predominant digestive lipase in adults. The efficient dietary fat digestion in newborns suggests that other lipases must compensate for the lack of pancreatic triglyceride lipase. In this study, we test the hypothesis that breast milk, pancreatic carboxyl ester lipase (CEL), or both contribute to dietary fat digestion in the newborn. To test this hypothesis, we determined the amount and composition of fecal fat in wild-type and CEL-deficient newborns nursed by either wild-type or CEL-deficient dams. We tested all genetic permutations of the nursing pairs. An interaction between the genotype of the dam and of the pup determined the amount of fecal fat (P < 0.001). Fecal fat was highest in CEL-deficient pups nursed by CEL-deficient dams. Furthermore, only the feces from the CEL-deficient pups nursed by CEL-deficient dams contained undigested lipids. Even with increased fecal fats, the CEL-deficient pups had normal weight gain. Our results demonstrate that CEL contributes significantly to dietary triglyceride digestion whether it originates from mother's milk or pancreatic secretions. However, only the absence of both mother's milk and pancreatic CEL produces fat maldigestion. The absence of a single CEL source makes no difference in the efficiency of dietary fat absorption.