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This Article Full Text (Publish Ahead of Print[PDF]) All Versions of this Article: 90/3/756S    most recent ajcn.2009.27462Lv1 Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bachmanov, A. A Articles by Beauchamp, G. K Search for Related Content PubMed PubMed Citation Articles by Bachmanov, A. A Articles by Beauchamp, G. K Agricola Articles by Bachmanov, A. A Articles by Beauchamp, G. K

Glutamate taste and appetite in laboratory mice: physiologic and genetic analyses^1,2,3,4

¹ From the Monell Chemical Senses Center, Philadelphia, PA (AAB, MI, HJ, MGT, and GKB); the Laboratory of Cellular Neurobiology, Department of Life Science, Tokyo University of Pharmacy and Life Science, Hachioji, Tokyo, Japan (MI); and the National Research Institute of Fisheries Science, Yokohama, Japan (YM).

² Presented at the "100th Anniversary Symposium of Umami Discovery: The Roles of Glutamate in Taste, Gastrointestinal Function, Metabolism, and Physiology," held in Tokyo, Japan, September 10–13, 2008.

³ Supported by R01DC00882 from the National Institutes of Health (to AAB), and the Ajinomoto Amino Acid Research Program (Ajinomoto is a manufacturer of food and amino acids including glutamate).

⁴ Address correspondence to AA Bachmanov, Monell Chemical Senses Center, 3500 Market Street, Philadelphia, PA 19104. E-mail: bachmanov{at}monell.org.

ABSTRACT

This article provides an overview of our studies of variation in voluntary glutamate consumption in mice. In 2-bottle preference tests, mice from the C57BL/6ByJ (B6) strain consume more monosodium L-glutamate (MSG) than do mice from the 129P3/J (129) strain. We used these mice to study physiologic and genetic mechanisms that underlie the strain differences in glutamate intake. Our genetic analyses showed that differences between B6 mice and 129 mice in MSG consumption are unrelated to strain variation in consumption of sodium or sweeteners and therefore are attributed to mechanisms specific for glutamate. These strain differences could be due to variation in responses to either taste or postingestive effects of glutamate. To examine the role of taste responsiveness, we measured MSG-evoked activity in gustatory nerves and showed that it is similar in B6 and 129 mice. On the other hand, strain-specific postingestive effects of glutamate were evident from our finding that exposure to MSG increases its consumption in B6 mice and decreases its consumption in 129 mice. We therefore examined whether B6 mice and 129 mice differ in postingestive metabolism of glutamate. We showed that, after intragastric administration of MSG, the MSG is preferentially metabolized through gluconeogenesis in B6 mice, whereas thermogenesis is the predominant process for 129 mice. We hypothesize that a process related to gluconeogenesis of the ingested glutamate generates the rewarding stimulus, which probably occurs in the liver before glucose enters the general circulation, and that the glutamate-induced postingestive thermogenesis generates an aversive stimulus. Our animal model studies raise the question of whether humans also vary in glutamate metabolism in a manner that influences their glutamate preference, consumption, and postingestive processing.

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