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increased sucrose intake in mice lacking gut microbiota.pdf

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increased sucrose intake in mice lacking gut microbiota

Up-regulation of intestinal type 1 taste receptor 3 and sodium glucose luminal transporter-1 expression and increased sucrose intake in mice lacking gut microbiota T. D. Swartz1,2, F. A. Duca1,2, T. de Wouters1,2, Y. Sakar1 and M. Covasa1* 1INRA, Centre de Recherche de Jouy-en-Josas, UMR 1319, MICALIS, Neurobiology of Ingestive Behavior, Domaine de Vilvert, 78350 Jouy-en-Josas Cedex, France 2University Pierre and Marie Curie, Paris, France (Received 13 January 2011 – Revised 19 May 2011 – Accepted 20 May 2011 – First published online 25 July 2011) Abstract The chemosensory components shared by both lingual and intestinal epithelium play a critical role in food consumption and the regu- lation of intestinal functions. In addition to nutrient signals, other luminal contents, including micro-organisms, are important in signalling across the gastrointestinal mucosa and initiating changes in digestive functions. A potential role of gut microbiota in influencing food intake, energy homeostasis and weight gain has been suggested. However, whether gut microbiota modulates the expression of nutri- ent-responsive receptors and transporters, leading to altered food consumption, is unknown. Thus, we examined the preference for nutritive (sucrose) and non-nutritive (saccharin) sweet solutions in germ-free (GF, C57BL/6J) mice compared with conventional (CV, C57BL/6J) control mice using a two-bottle preference test. Then, we quantified mRNA and protein expression of the sweet signalling protein type 1 taste receptor 3 (T1R3) and a-gustducin and Na glucose luminal transporter-1 (SGLT-1) of the intestinal epithelium of both CV and GF mice. Additionally, we measured gene expression of T1R2, T1R3 and a-gustducin in the lingual epithelium. We found that, while the preference for sucrose was similar between the groups, GF mice consumed more of the high concentration (8 %) of sucrose solution than CV mice. There was no difference in either the intake of or the preference for saccharin. G