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This Article Full Text Full Text (PDF) All Versions of this Article: 297/4/E856    most recent 91008.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Miller, R. Articles by Lowe, M. E. PubMed PubMed Citation Articles by Miller, R. Articles by Lowe, M. E.

Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice

¹Department of Pediatrics, Children's Hospital of Pittsburgh of The University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; ²Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri; and ³Department of Cell and Molecular Biology, Lund University Biomedical Center, Lund, Sweden

Submitted 17 December 2008 ; accepted in final form 20 July 2009

A pentapeptide released from procolipase, enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve and in the hypothalamus and amygdala, primarily in the central nucleus of the amygdala. To investigate the physiological role of endogenous enterostatin, we created an enterostatin-deficient, colipase-sufficient (Ent^–/–) mouse. Ent^–/– mice are viable, normally active, and fertile. They exhibit normal growth on low-fat and high-fat diets. Furthermore, Ent^–/– mice develop diet-induced obesity, as do Ent^+/+ mice, and have normal responses to a two-macronutrient choice diet and to a switch from a high-fat to a low-fat diet. Levels of total serum (P = 0.004) and non-HDL (P 0.001) cholesterol were higher and levels of HDL cholesterol (P = 0.01) were lower in Ent^–/– than in wild-type mice. To determine whether enterostatin contributed to the decreased survival or whether colipase deficiency was the sole contributor, we administered enterostatin to procolipase-deficient (Clps^–/–) mouse pups. Enterostatin significantly improved survival (P 0.001). Our results demonstrate that enterostatin is not critically required to regulate food intake or growth, suggesting that other pathways may compensate for the loss of enterostatin. Enterostatin has developmental effects on survival of newborns and alters cholesterol metabolism.

appetite regulation; fat intake; procolipase; satiety