Notebooks, datasets and additional files for D-Xylose mechanistic modeling from Minipigs Datasets

<p>PrmEstLOG.ipynb and PrmEst_LOG2_models.ipynb must be run with Julia 1.8.2 or 1.9.3 kernel. </p><p>Both extracting inputs from Inputs_PrmEst.ipynb <i>and</i> InputsPrmEst<i>_</i>2models.ipynb, respectively.</p><p>displayResults.ipynb displays the results to make it as readable as possible, stored in new_figs/</p&gt

Modeling Intestinal Glucose Absorption from D-xylose Data

International audienceType 2 Diabetes (T2D) is one of the main epidemics of this century. One of the hypothesis of medical research is that an important cause of T2D may be the abnormal regulation of intestinal glucose absorption (IGA). Early detection of IGA disorders, and, more generally, precision medicine, may help to prevent the risk of T2D. This could be achieved by predictive models of glucose dynamics in blood following an oral ingestion. Even though many such models have been proposed, they either do not cope with IGA at all, or their calibration requires the use of complex and invasive tracer protocols that make them clinically unusable on a daily basis. To overcome this issue, D-xylose may be used as an IGA marker. Indeed, it is a glucose analogue with similar intestinal absorption mechanisms but, contrary to glucose, its dynamics in blood only results from gastric emptying, intestinal absorption and elimination by the kidney. In this paper, we investigate, for the first time, a model-based assessment of IGA based on D-xylose dynamics in blood after oral absorption. We show that a multi-compartment model of instestinal absorption can fit very well D-xylose data obtained from different experimental conditions and be a good qualitative estimate of IGA. And addition, because gastric emptying is a possible confounding factor with intestinal absorption, we explore the relative contribution of both mechanisms to the rate of D-xylose (and thus glucose) appearance in blood

Limits of a Glucose-Insulin Model to Investigate Intestinal Absorption in Type 2 Diabetes

International audienceAbnormal regulation of glucose absorption in the small intestine is an important cause of Type 2 Diabetes (T2D). Even if this hypothesis is clinically well-known, it has not been fundamentally validated yet, mainly due to a lack of reliable metabolic knowledge on the glucose regulation. The main objective of this paper is to test this hypothesis on a highly referenced model composed of ordinary differential equations. This model is tested on an original dataset featuring the observations of obese diabetic patients. It shows its limits to predict our post-prandial glycemia and insulinemia time series especially with regard to the crucial complexity of gastro-intestinal regulation

Limits of a Glucose-Insulin Model to Investigate Intestinal Absorption in Type 2 Diabetes

International audienceAbnormal regulation of glucose absorption in the small intestine is an important cause of Type 2 Diabetes (T2D). Even if this hypothesis is clinically well-known, it has not been fundamentally validated yet, mainly due to a lack of reliable metabolic knowledge on the glucose regulation. The main objective of this paper is to test this hypothesis on a highly referenced model composed of ordinary differential equations. This model is tested on an original dataset featuring the observations of obese diabetic patients. It shows its limits to predict our post-prandial glycemia and insulinemia time series especially with regard to the crucial complexity of gastro-intestinal regulation