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J. Biol. Chem., Vol. 278, Issue 44, 42899-42905, October 31, 2003

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Pancreatic Triglyceride Lipase Deficiency Minimally Affects Dietary Fat Absorption but Dramatically Decreases Dietary Cholesterol Absorption in Mice^*

Kevin W. Huggins, Lisa M. Camarota, Philip N. Howles, and David Y. Hui

From the Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267

This study generated pancreatic triglyceride lipase (PTL)-null mice to test the hypothesis that PTL-mediated hydrolysis of dietary triglyceride is necessary for efficient dietary cholesterol absorption. The PTL^–/– mice grew normally and displayed similar body weight as their PTL^+/+ littermates. Plasma lipid levels between animals of various PTL genotypes were similar when they were maintained on either a basal low fat diet or a western-type high fat/high cholesterol diet. Although the lack of a functional PTL delayed fat absorption during the initial hour of feeding a bolus load of olive oil containing [³H]triolein and [¹⁴C]cholesterol, the rate of [³H]triolein absorption was similar between PTL^+/+ and PTL^–/– mice after the initial 1-h period. Importantly, comparison of fecal fat content revealed similar overall fat absorption efficiency between PTL^+/+ and PTL^–/– mice. In contrast, the PTL^–/– mice displayed significant decrease in both the rate and the amount of cholesterol absorbed after a single meal. The plasma appearance of [¹⁴C]cholesterol was found to be 75% lower (p < 0.0005) in PTL^–/– mice compared with PTL^+/+ mice after 4 h. The total amount of [¹⁴C]cholesterol excreted in the feces was 45% higher (p < 0.0004) in PTL^–/– mice compared with PTL^+/+ mice over a 24-h period. These results indicate that the delayed fat digestion due to PTL deficiency results in a significant reduction in cholesterol absorption, although other enzymes in the digestive tract may compensate for the lack of PTL in PTL^–/– mice in fat digestion and absorption.

Received for publication, April 2, 2003 , and in revised form, July 30, 2003.

^* This work was supported by National Institutes of Health Program Project Grant DK54504 (to D. Y. H.) and National Research Service Award DK10065 (to K. W. H.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Present address: Dept. of Nutrition and Food Science, 328 Spidle Hall, Auburn University, Auburn, AL 36849.

To whom correspondence should be addressed: Dept. of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0529. Tel.: 513-558-9152; Fax: 513-558-2141; E-mail: huidy{at}email.uc.edu.

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