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Model-Based Quantif...
Model-Based Quantification of the Systemic Interplay between Glucose and Fatty Acids in the Postprandial State
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- Sips, F. L. P. (författare)
- Eindhoven University of Technology, Netherlands
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- Nyman, Elin (författare)
- Linköpings universitet,Institutionen för medicinsk teknik,Tekniska fakulteten,CVMD iMED DMPK AstraZeneca RandD, Sweden
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- Adiels, Martin, 1976 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine,University of Gothenburg,University of Gothenburg, Sweden
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- Hilbers, P. A. J. (författare)
- Eindhoven University of Technology, Netherlands
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- Strålfors, Peter (författare)
- Linköpings universitet,Avdelningen för cellbiologi,Medicinska fakulteten
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- van Riel, N. A. W. (författare)
- Eindhoven University of Technology, Netherlands
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- Cedersund, Gunnar, 1978 (författare)
- Linköpings universitet,Institutionen för medicinsk teknik,Tekniska fakulteten,Avdelningen för cellbiologi,Medicinska fakulteten
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(creator_code:org_t)
- 2015-09-10
- 2015
- Engelska.
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Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 10:9
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Abstract
Ämnesord
Stäng
- 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, postprandial glucose metabolism is characterized by a dynamic interplay of simultaneously responding regulatory mechanisms, which have proven difficult to measure directly. Therefore, we propose a mathematical modelling approach to untangle the systemic interplay between glucose and NEFA in the postprandial period. The developed model integrates data of both the perturbation of glucose metabolism by NEFA as measured under clamp conditions, and postprandial time-series of glucose, insulin, and NEFA. The model can describe independent data not used for fitting, and perturbations of NEFA metabolism result in an increased insulin, but not glucose, response, demonstrating that glucose homeostasis is maintained. Finally, the model is used to show that NEFA may mediate up to 30-45% of the postprandial increase in insulin-dependent glucose uptake at two hours after a glucose meal. In conclusion, the presented model can quantify the systemic interactions of glucose and NEFA in the postprandial state, and may therefore provide a new method to evaluate the disturbance of this interplay in metabolic disease.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine (hsv//eng)
Nyckelord
- HEPATIC INSULIN-RESISTANCE
- NUCLEAR-MAGNETIC-RESONANCE
- DIACYLGLYCEROL
- ACTIVATION
- CARDIOVASCULAR-DISEASE
- LIPOPROTEIN METABOLISM
- DIABETES-MELLITUS
- OBESE-PATIENTS
- MINIMAL MODEL
- HUMANS
- LIVER
- Multidisciplinary Sciences
- HUMANS
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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