Helicobacter pylori infection can affect energy modulating hormones and body weight in germ free mice

Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess...

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Bibliographic Details
Main Authors: Loke, Mun Fai, Vadivelu, Jamuna, Tan, Tuan Lin, Wong, Whye Yen, Khosravi, Yalda, Seow, Shih Wee, Amoyo, Arlaine Anne, Chiow, Kher Hsin, Poh, Qian Hui, Sentosa, Ignatius Mario Doli, Bunte, Ralph M., Pettersson, Sven
Other Authors: Lee Kong Chian School of Medicine (LKCMedicine)
Format: Article
Language:English
Published: 2015
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Online Access:https://hdl.handle.net/10356/106989
http://hdl.handle.net/10220/25248
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Institution: Nanyang Technological University
Language: English
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Summary:Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.