Abstract
BACKGROUND
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 anti-incretin, 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.
Links
Authors
Toghaw P, Matone A, Lenbury Y, De Gaetano A
Institution
Department of Mathematics, Faculty of Science, Kasetsart University, Bangkok, Thailand.
Source
Theoretical biology & medical modelling 9: 2012 pg 16MeSH
Bariatric SurgeryDiabetes Mellitus, Type 2
Dipeptidyl Peptidase 4
Gastric Inhibitory Polypeptide
Ghrelin
Glucagon-Like Peptide 1
Glucose
Humans
Incretins
Insulin
Intestines
Mathematical Concepts
Models, Biological
Obesity
Treatment Outcome
Pub Type(s)
Journal ArticleResearch Support, Non-U.S. Gov't
Language
eng
PubMed ID
22587410
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