1. ^*These authors contributed equally to this work
2. ^†German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany
3. ^‡Obesity Research Center, Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio
4. ^§Department of Pathology, Otto-von-Guericke-University, Magdeburg, Germany
5. ^¶Department of Gastroenterology, Innenstadt University Hospital, Munich, Germany
6. ^**Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York
7. ^††Charité University Medicine, Berlin, Germany
8. ^‡‡Department of Nutrition, University of California, Davis, California

Correspondence: Hella S. Jürgens, Department of Pharmacology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Arthur-Scheunert-Allee 114–116, 14558 Nuthetal, Germany. E-mail: juergens@mail.dife.de

^**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. 1734 solely to indicate this fact.

Received 13 September 2004; Accepted 14 April 2005.

Abstract

Objective: The marked increase in the prevalence of obesity in the United States has recently been attributed to the increased fructose consumption. To determine if and how fructose might promote obesity in an animal model, we measured body composition, energy intake, energy expenditure, substrate oxidation, and several endocrine parameters related to energy homeostasis in mice consuming fructose.

Research Methods and Procedures: We compared the effects of ad libitum access to fructose (15% solution in water), sucrose (10%, popular soft drink), and artificial sweetener (0% calories, popular diet soft drink) on adipogenesis and energy metabolism in mice.

Results: Exposure to fructose water increased adiposity, whereas increased fat mass after consumption of soft drinks or diet soft drinks did not reach statistical significance (n = 9 each group). Total intake of energy was unaltered, because mice proportionally reduced their caloric intake from chow. There was a trend toward reduced energy expenditure and increased respiratory quotient, albeit not significant, in the fructose group. Furthermore, fructose produced a hepatic lipid accumulation with a characteristic pericentral pattern.

Discussion: These data are compatible with the conclusion that a high intake of fructose selectively enhances adipogenesis, possibly through a shift of substrate use to lipogenesis.