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Originally published In Press as doi:10.1074/jbc.M203912200 on July 11, 2002

J. Biol. Chem., Vol. 277, Issue 37, 34117-34124, September 13, 2002
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Leptin Promotes Biliary Cholesterol Elimination during Weight Loss in ob/ob Mice by Regulating the Enterohepatic Circulation of Bile Salts*

Hideyuki HyogoDagger §, Suheeta RoyDagger , Beverly Paigen, and David E. CohenDagger ||**

From the Departments of Dagger  Medicine and || Biochemistry, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461 and  The Jackson Laboratory, Bar Harbor, Maine 04609

Leptin administration to obese C57BL/6J (ob/ob) mice results in weight loss by reducing body fat. Because adipose tissue is an important storage depot for cholesterol, we explored evidence that leptin-induced weight loss in ob/ob mice was accompanied by transport of cholesterol to the liver and its elimination via bile. Consistent with mobilization of stored cholesterol, cholesterol concentrations in adipose tissue remained unchanged during weight loss. Plasma cholesterol levels fell sharply, and microscopic analyses of gallbladder bile revealed cholesterol crystals as well as cholesterol gallstones. Surprisingly, leptin reduced biliary cholesterol secretion rates without affecting secretion rates of bile salts or phospholipids. Instead, cholesterol supersaturation of gallbladder bile was due to marked decreases in bile salt hydrophobicity and not to hypersecretion of biliary cholesterol per se, such as occurs in humans during weight loss. In addition to regulating bile salt composition, leptin treatment decreased bile salt pool size. The smaller, more hydrophilic bile salt pool was associated with substantial decreases in intestinal cholesterol absorption. Within the liver, leptin treatment reduced the activity of 3-hydroxy-3-methylglutaryl-CoA reductase, but it did not change activities of cholesterol 7alpha -hydroxylase or acyl-CoA:cholesterol acyltransferase. These data suggest that leptin regulates biliary lipid metabolism to promote efficient elimination of excess cholesterol stored in adipose tissue. Cholesterol gallstone formation during weight loss in ob/ob mice appears to represent a pathologic consequence of an adaptive response that prevents absorption of biliary and dietary cholesterol.

* This work was supported by National Institutes of Health Grants DK48873 (to D. E. C.) and DK51568 (to B. P.) and Grant DK 20514 from the Albert Einstein College of Medicine Diabetes Research & Training Center.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Recipient of a grant from the Japan-North America Medical Exchange Foundation and a Dr. Charles Trey Memorial American Liver Foundation Postdoctoral Fellowship.

** To whom correspondence should be addressed: Liver Research Center, Ullmann 625, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461. Tel.: 718-430-2098; Fax: 718-430-8975; E-mail: dcohen@aecom.yu.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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Copyright © 2002 by the American Society for Biochemistry and Molecular Biology.