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    • Although the serum levels of some inflammatory cytokines suc

    2018-11-14

    Although the serum levels of some inflammatory cytokines such as TNF-α were not elevated in H. pylori-infected HFD mice, the increased abundance of Desulfovibrionaceae which can produce endotoxins and the compromised intestinal barrier s ibuprofen some doubt on the role of inflammation. In addition to inflammation hypothesis, increasing evidence indicates that H. pylori infection can influence the production of metabolic hormones involved in energy homeostasis both in human and animal studies, which is another potential mechanism for H. pylori-associated insulin resistance (Boltin and Niv, 2012; Khosravi et al., 2015; Roper et al., 2008). In our study, we also found remarkable changes of metabolic hormones after H. pylori infection given HFD. Both GIP and resistin which have been reported to play a cardinal role in IR and associated metabolic disturbances were observed to increase significantly in H. pylori-infected mice with HFD at the early stage (Gault et al., 2005; Muse et al., 2004). Moreover, the HFD itself induced dramatic elevation of circulating resistin after long-term treatment, and thus no statistical difference was observed between H. pylori-infected and non-infected groups. The changes of resistin are consistent with the alteration in body IR, which indicates the role of metabolic hormones in H. pylori-associated IR. Both H. pylori strains used in this study are observed to promote HFD-induced metabolic disorders, although the degree of their pathogenicity is not identical. The discrepancies in the association of H. pylori and IR in epidemiological studies are likely due to the infection of different strains as well as diet consumption. Further experiments using germ-free animals are highly warranted to elucidate the causal relationship between gut microbiota and H. pylori-associated IR in the presence of HFD. In conclusion, we found that H. pylori infection promoted HFD-induced central obesity and IR at the early stage, the extent of which is close to the effect of long-term HFD. Meanwhile, we observed a dynamic alteration in the gut microbiota that is consistent with the changes of metabolic phenotype (Supplement Fig. 4). Thus, there may be an interaction among H. pylori, diet and gut microbiota, which dysregulates host metabolic homeostasis and the treatment of H. pylori may be beneficial to the patients with impaired glucose tolerance in addition to diet control. The following are the supplementary data related to this article.
    Funding Sources This work was supported in part by grants from the National Natural Science Foundation of China (81470832) and the Graduate Innovation Fund of Jiangxi Province (YC2014-B021).
    Conflicts of Interest
    Author Contributions
    Acknowledgments We thank Prof. JZ Zhang at the National Institute for Communicable Diseases and Prevention of Chinese Center for Disease Control and Prevention for providing the H. pylori type strains SS1 and NCTC11637.
    Introduction Transplantation has been considered one of the medical miracles which can cure incurable diseases (Dalal, 2015). On the other hand, transplantation has been associated with the donor shortage which leads to organ trafficking s ibuprofen and organ tourism (Dalal, 2015). The Istanbul declaration, supported by World Health Organization, has emphasized the importance of changing this situation (Dalal, 2015). One of the ultimate solutions for this situation is xenotransplantation. Among the xenotransplantation options, islet xenotransplantation using porcine islets has been considered to be the closest to the clinical reality (Groth et al., 1994). In fact, the initial islet xenotransplantation was conducted in 90s (Groth et al., 1994). Since then several clinical trials of islet xenotransplantation were conducted; however, clear clinical benefits were rarely shown (Matsumoto et al., 2014; Valdes-Gonzalez et al., 2005; Valdes-Gonzalez et al., 2010). The standard therapy for the type 1 diabetes is intensive insulin therapy which can reduce HbA1c. However the drawback is increasing hypoglycemic episodes (The Diabetes Control and Complications Trial Research Group, 1997). Beta-cell replacement therapy including pancreas and islet transplantation can normalize HbA1c without increasing hypoglycemic episodes; however, the donor shortage and the necessity of immunosuppressant are major issues to apply the treatments widely (Matsumoto, 2010). To alleviate the donor shortage, islet transplantation using non-heart beating human donor was conducted (Matsumoto et al., 2006), and a living donor (Matsumoto et al., 2005), but these approaches can never solve this issue generally. Islet xenotransplantation may be one of the ultimate solutions to solve the shortage of donated organs.