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dc.contributor.authorPuntip Toghawen_US
dc.contributor.authorAlice Matoneen_US
dc.contributor.authorYongwimon Lenburyen_US
dc.contributor.authorAndrea De Gaetanoen_US
dc.contributor.otherKasetsart Universityen_US
dc.contributor.otherConsiglio Nazionale delle Ricercheen_US
dc.contributor.otherSouth Carolina Commission on Higher Educationen_US
dc.contributor.otherMahidol Universityen_US
dc.date.accessioned2018-06-11T04:57:43Z-
dc.date.available2018-06-11T04:57:43Z-
dc.date.issued2012-05-16en_US
dc.identifier.citationTheoretical Biology and Medical Modelling. Vol.9, No.1 (2012)en_US
dc.identifier.issn17424682en_US
dc.identifier.other2-s2.0-84860910951en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84860910951&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/14399-
dc.description.abstractBackground: Consensus exists that several bariatric surgery procedures produce a rapid improvement of glucose homeostasis in obese diabetic patients, improvement apparently uncorrelated with the degree of eventual weight loss after surgery. Several hypotheses have been suggested to account for these results: among these, the antiincretin, the ghrelin and the lower-intestinal dumping hypotheses have been discussed in the literature. Since no clear-cut experimental results are so far available to confirm or disprove any of these hypotheses, in the present work a mathematical model of the glucose-insulin- incretin system has been built, capable of expressing these three postulated mechanisms. The model has been populated with critically evaluated parameter values from the literature, and simulations under the three scenarios have been compared. Results: The modeling results seem to indicate that the suppression of ghrelin release is unlikely to determine major changes in short-term glucose control. The possible existence of an anti-incretin hormone would be supported if an experimental increase of GIP concentrations were evident post-surgery. Given that, on the contrary, collected evidence suggests that GIP concentrations decrease post-surgery, the lower-intestinal dumping hypothesis would seem to describe the mechanism most likely to produce the observed normalization of Type 2 Diabetes Mellitus (T2DM) after bariatric surgery. Conclusions: The proposed model can help discriminate among competing hypotheses in a context where definitive data are not available and mechanisms are still not clear. © 2012 Toghaw et al.; licensee BioMed Central Ltd.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84860910951&origin=inwarden_US
dc.subjectMathematicsen_US
dc.subjectMedicineen_US
dc.titleBariatric surgery and T2DM improvement mechanisms: A mathematical modelen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1186/1742-4682-9-16en_US
Appears in Collections:Scopus 2011-2015

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