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Sips2015 - Glucose and non-esterified fatty acids (NEFA) metabolism

ABSTRACT: This a model from the article: Model-Based Quantification of the Systemic Interplay between Glucose and Fatty Acids in the Postprandial State. Fianne L. P. Sips, Elin Nyman, Martin Adiels, Peter A. J. Hilbers, Peter Strålfors, Natal A. W. van Riel, Gunnar Cedersund.PLoS ONE 10(9): e0135665. link,

SUBMITTER: Fianne Sips

PROVIDER: MODEL1806080001 | BioModels | 2019-01-17

REPOSITORIES: BioModels

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Model-Based Quantification of the Systemic Interplay between Glucose and Fatty Acids in the Postprandial State.

Sips Fianne L P FL Nyman Elin E Adiels Martin M Hilbers Peter A J PA Strålfors Peter P van Riel Natal A W NA Cedersund Gunnar G

PloS one 20150910 9

In metabolic diseases such as Type 2 Diabetes and Non-Alcoholic Fatty Liver Disease, the systemic regulation of postprandial metabolite concentrations is disturbed. To understand this dysregulation, a quantitative and temporal understanding of systemic postprandial metabolite handling is needed. Of particular interest is the intertwined regulation of glucose and non-esterified fatty acids (NEFA), due to the association between disturbed NEFA metabolism and insulin resistance. However, postprandi ...[more]

PMID: 26356502

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Project description:The number of circulating endothelial progenitor cells (EPCs) predicts future development of atherosclerotic cardiovascular disease (ASCVD) and is reduced in patients with type 2 diabetes (T2DM) or impaired glucose tolerance (IGT). Recent studies revealed the contribution of tight control of glycolysis and mitochondrial oxidative phosphorylation (OXPHOS), as well as fatty acid oxidation in the regulation of stem cell behavior. In this study, we show that how dysregulated glucose and triglyceride metabolism in T2DM/IGT affects the homeostasis of EPCs, i.e. bone marrow stem/progenitor cells (BMSCs). In our clinical study, consistent with previous reports, the patients with IGT or T2DM showed reduced level of circulating EPCs, as compared normal glucose tolerance. On the other hand, fasting or postprandial hypertriglyceridemia (hTG) itself did not affect the level of circulating EPCs. However, further analysis using single and multiple regression analyses strongly suggested that, in the presence of postprandial hTG, postprandial hyperglycemia exerts devastating effect on EPC homeostasis. We therefore carried out the proof of concept study in mice. Our experimental study revealed that repetitive glucose+lipid (G+L) spikes, but not repetitive glucose (G) spikes or lipid (L) spikes, rapidly upregulated p53 in BMSCs and induced premature aging phenotype of bone marrow cells, i.e. the impairment of BMSC quiescence and function, and myeloid-biased differentiation. Subsequent analysis implicated that p53-mediated augmentation of mitochondrial OXPHOS plays pivotal role for the impairment of BMSC quiescence and function. On the other hand, it is still not clear how repetitive G+L injection induced myeloid-biased differentiation. Because cell-fate decisions are executed by transcription factors in response to extracellular signals, and the best-known function of p53 is as a transcription factor, we asked to what extent repetitive glucose spikes and repetitive glucose+TG spikes affect transcriptional regulation in LSK cells.

Dataset Information

Sips2015 - Glucose and non-esterified fatty acids (NEFA) metabolism

Publications

Model-Based Quantification of the Systemic Interplay between Glucose and Fatty Acids in the Postprandial State.

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