Abstract
BackgroundThe aim of a recent research project was the investigation of the mechanisms involved in the onset of type 2 diabetes in the absence of familiarity. This has led to the development of a computational model that recapitulates the aetiology of the disease and simulates the immunological and metabolic alterations linked to type-2 diabetes subjected to clinical, physiological, and behavioural features of prototypical human individuals.ResultsWe analysed the time course of 46,170 virtual subjects, experiencing different lifestyle conditions. We then set up a statistical model able to recapitulate the simulated outcomes.ConclusionsThe resulting machine learning model adequately predicts the synthetic dataset and can, therefore, be used as a computationally-cheaper version of the detailed mathematical model, ready to be implemented on mobile devices to allow self-assessment by informed and aware individuals. The computational model used to generate the dataset of this work is available as a web-service at the following address: http://kraken.iac.rm.cnr.it/T2DM.
Highlights
The aim of a recent research project was the investigation of the mechanisms involved in the onset of type 2 diabetes in the absence of familiarity
Insulin resistance or insulin-deficient states leads to a reduced response of tissues, such as the skeletal muscle, liver, and adipose tissue, to insulin, M-Type 2 diabetes (T2D) implements the effects of insulin resistance on the glucose uptake by peripheral organs [45]
In general we indicate the vector corresponding to the initial condition as follows: x = [S, A, W, H, (NPA, Duration of physical activity sessions in minutes (DPA), Intensity of physical activity sessions (IPA)), (CME, Mean protein intake per day (PME), Mean fat intake per day (FME))]
Summary
The aim of a recent research project was the investigation of the mechanisms involved in the onset of type 2 diabetes in the absence of familiarity. The term metaflammation well describes this kind of inflammation caused by a high caloric and sugar-rich diet which mainly originates in the visceral adipose tissue [4]. This inflammatory-eliciting insult triggers a cellular response consisting of the release of several intracellular signals and a low levels of cytokines such as Tumour Necrosis Factor-α (TNF-α), and Interleukin-6 (IL-6) [5]. Summarising, the prolonged condition of a pro-inflammatory response alters the metabolic functions of the adipocytes [7] and, in the long term, causes hyperglycemia and eventually full-blown type 2 diabetes [8]
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