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This Article Full Text Full Text (PDF) All Versions of this Article: 289/1/E40    most recent 00367.2004v1 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 Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Arsenijevic, D. Articles by Langhans, W. Search for Related Content PubMed PubMed Citation Articles by Arsenijevic, D. Articles by Langhans, W.

Enterostatin decreases postprandial pancreatic UCP2 mRNA levels and increases plasma insulin and amylin

¹Institute of Animal Sciences, Eidegnossische Technische Hochschule Zurich, Schwerzenbach; ²Institute of Veterinary Physiology, University of Zurich, Zurich, Switzerland; and ³Deptartment of Cell and Molecular Biology, Biomedical Center, Lund University, Lund, Sweden

Submitted 12 August 2004 ; accepted in final form 9 February 2005

This study investigated the chronic effect of enterostatin on body weight and some of the associated changes in postprandial metabolism. Rats were adapted to 6 h of food access/day and a choice of low-fat and high-fat (HF) food and then given enterostatin or vehicle by an intraperitoneally implanted minipump delivering 160 nmol enterostatin/h continuously over a 5-day infusion period. Enterostatin resulted in a slight but significant reduction of HF intake and body weight. After the last 6-h food access period, enterostatin-treated animals had lower plasma triglyceride and free fatty acid but higher plasma glucose and lactate levels than control animals. Enterostatin infusion resulted in increased uncoupling protein-2 (UCP2) expression in various tissues, including epididymal fat and liver. UCP2 was reduced in the pancreas of enterostatin-treated animals, and this was associated with increased plasma levels of insulin and amylin. Whether these two hormones are involved in the observed decreased food intake due to enterostatin remains to be determined. As lipid metabolism appeared to be altered by enterostatin, we measured peroxisome proliferator-activated receptor (PPAR) expression in tissues and observed that PPAR, -, -1, and -2 expression were modified by enterostatin in epididymal fat, pancreas, and liver. This further links altered lipid metabolism with body weight loss. Our data suggest that alterations in UCP2 and PPAR2 play a role in the control of insulin and amylin release from the pancreas. This implies that enterostatin changes lipid and carbohydrate metabolic pathways in addition to its effects on food intake and energy expenditure.

body weight; appetite; glutathione; peroxisome proliferator-activated receptors; uncoupling protein-2