Direct assessment of liver glycogen storage by 13C nuclear magnetic resonance spectroscopy and regulation of glucose homeostasis after a mixed meal in normal subjects.

Taylor, Roy; Magnusson, Inger; Rothman, Douglas L.; Cline, Gary W.; Caumo, Andrea; Cobelli, Claudio; Shulman, Gerald I.

doi:10.1172/jci118379

Cited by 234 publications

(230 citation statements)

References 45 publications

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“…In Appendix C, we plot more complex combinations of concentrations which describe the other fluxes in the system. The quantitative agreement with experimental data for these results is fairly good, as can be seen by comparing Figure 5 with the experimental data of Taylor et al [12] plotted in Figure 6. Comparing the two meals we see that plasma insulin and glucose concentrations do not reach as high in the high fat meal as in the balanced meal, due to less glucose entering the system which also directly affects the rate of insulin secretion.…”

Section: Numerical Resultssupporting

confidence: 80%

“…Hepatic glycogen shows good qualitative and quantitative agreement with experimental data [12]. Following ingestion of the meal glucose is taken up from the plasma to be stored in the liver and within a few hours the liver is almost full to its maximum.…”

Section: Numerical Resultssupporting

confidence: 67%

“…We can however take some data from our simulations to get an idea of the effect of the different meals on adipose tissue by looking specifically at adipose tissue TAG uptake. We will produce the results for adipose tissue TAG uptake in dimensional form by plotting the following expression , assessed by the percentage of total oxidation due to glucose oxidation, and experimental data on respiratory quotient, taken from Taylor et al [12]. In all panels, time is in hours.…”

Section: Numerical Resultsmentioning

confidence: 99%

“…β G , k L -Taylor et al [12] carried out a study into hepatic glycogen storage in healthy subjects. Three different studies where done order to measure different rates and concentrations.…”

Section: Parameter Assessmentmentioning

confidence: 99%

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A Mathematical Model of the Human Metabolic System and Metabolic Flexibility

et al. 2014

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A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription. Abstract In healthy subjects some tissues in the human body display metabolic flexibility, by this we mean the ability for the tissue to switch its fuel source between predominantly carbohydrates in the post prandial state and predominantly fats in the fasted state. Many of the pathways involved with human metabolism are controlled by insulin, and insulin-resistant states such as obesity and type-2 diabetes are characterised by a loss or impairment of metabolic flexibility.In this paper we derive a system of 12 first-order coupled differential equations that describe the transport between and storage in different tissues of the human body. We find steady state solutions to these equations and use these results to nondimensionalise the model. We then solve the model numerically to simulate a healthy balanced meal and a high fat meal and we discuss and compare these results. Our numerical results show good agreement with experimental data where we have data available to us and the results show behaviour that agrees with intuition where we currently have no data with which to compare.

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Section: Numerical Resultssupporting

confidence: 80%

Section: Numerical Resultssupporting

confidence: 67%

Section: Numerical Resultsmentioning

confidence: 99%

Section: Parameter Assessmentmentioning

confidence: 99%

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A Mathematical Model of the Human Metabolic System and Metabolic Flexibility

et al. 2014

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“…This alteration was mainly due to altered suppression of EGP. Furthermore, after the ingestion of a mixed meal, plasma insulin concentration increases rapidly with a 30-min peak [16]. The quick rise in plasma insulin concentration is associated with a marked decrease in the glucagon to insulin ratio and concomitant suppression of EGP and glycogen accretion in the liver.…”

Section: Early-phase Insulin Secretion and Glucose Homeostasismentioning

confidence: 99%

Loss of early insulin secretion leads to postprandial hyperglycaemia

2003

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Aims/Hypothesis. A loss of early-phase insulin response is common in Type 2 diabetic patients and in people with impaired glucose metabolism. It is hypothesized that this alteration is not simply a marker for the risk of developing diabetes, rather it is a an important pathogenetic mechanism causing excessive postprandial hyperglycaemia. Methods. Relevant literature on the epidemiology, physiopathology, and therapeutic intervention related to loss of early insulin secretion and postprandial hyperglycaemia has been analysed. Results. In response to intravenous glucose, insulin secretion is biphasic. This behaviour translates as a rapid release of insulin into the blood stream in response to the ingestion of carbohydrates or a mixed meal. The rapid increase in portal insulin concentration and the avid binding of the hormone to its receptor on liver cell membranes, account for a prompt suppression of endogenous glucose production and reduction of the rate of increase in plasma glucose concentrations. This has been supported by experimental studies carried out in both animals and humans: the selective abolition of early insulin secretion in healthy subjects results in impaired glucose tolerance, excessive glucose excursions, and possible hampering of the thermic effects of ingested carbohydrates. In nondiabetic subjects, the loss of early insulin secretion is a determinant for developing diabetes. The critical role of the early-phase insulin response in determining postprandial hyperglycaemia, is supported by an amelioration of glucose tolerance by restoring the acute rise in plasma insulin concentrations after the ingestion of both glucose and a mixed meal. This amelioration in plasma glucose profile can prevent late hyperglycaemia and hyperinsulinaemia. Conclusion/interpretation. Therapeutic approaches aimed at restoring a physiological pattern of insulin secretion could prove effective in reducing postprandial glucose excursions particularly in the early stage of Type 2 diabetes. [Diabetologia (2003)

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Normal Insulin Secretion in Humans

Utzschneider

Porte

2003

International Textbook of Diabetes Mellitus

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Normal insulin secretion in humans is mainly regulated by glucose, but additional factors including other nutrients, hormones, and neural input play an important role. In the basal state, insulin is released in a rapid pulsatile manner, with pulses occurring every 6–10 min. These pulses are superimposed on an oscillatory pattern of 11–15 oscillations per 24 h. Dynamic insulin release also occurs in response to stimuli. The insulin response to intravenous glucose has been shown to have two distinct phases: an early first phase response lasting for 10 min, and a slower longer second phase response lasting as long as the glucose level is elevated. Preexistent elevations in the plasma glucose level are able to increase the insulin response to a subsequent glucose stimulus, an effect called priming. Glucose is also capable of potentiating the insulin response to non‐glucose secretagogues such as amino acids, peptides, and sulfonylureas. Non‐glucose factors that affect insulin secretion include amino acids, free fatty acids, medications, and the response to stress. Neural inputs regulate islet secretory function through both the sympathetic and parasympathetic nervous systems. The gastrointestinal peptides glucagon‐like peptide 1 (GLP‐1) and glucose‐dependent insulinotropic polypeptide (GIP), released from the intestine during oral intake, have been found to play a significant role in augmenting insulin release, an effect known as the incretin effect. When assessing the effect of all these different secretagogues on β‐cell function, it is important to take into account the prevailing insulin sensitivity, as variations in insulin sensitivity lead to compensatory changes in insulin release. Understanding the dynamics and complex regulation of normal insulin secretion in humans provides the basis for understanding the consequences of β‐cell dysfunction observed in diabetes.

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Direct assessment of liver glycogen storage by 13C nuclear magnetic resonance spectroscopy and regulation of glucose homeostasis after a mixed meal in normal subjects.

Cited by 234 publications

References 45 publications

A Mathematical Model of the Human Metabolic System and Metabolic Flexibility

A Mathematical Model of the Human Metabolic System and Metabolic Flexibility

Loss of early insulin secretion leads to postprandial hyperglycaemia

Normal Insulin Secretion in Humans

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