Early-phase insulin secretion is disturbed in obese subjects with glucose intolerance

Mizuno, Akira; Arai, Hidekazu; Fukaya, Makiko; Sato, Mitsuyo; Yamanaka-Okumura, Hisami; Takeda, Eiji; Doi, Toshio

doi:10.1016/j.metabol.2007.01.017

Cited by 11 publications

(14 citation statements)

References 35 publications

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“…The metabolic syndrome is characterized by hyperinsulinaemia [18]. The C‐peptide provides a better estimate of the synthesis of insulin than the concentration of insulin per se , as insulin but not the C‐peptide is rapidly metabolized in the liver [32]. Furthermore, studies on patients with coronary artery disease indicated that C‐peptide has a stronger correlation than insulin with high PAI‐1 [33].…”

Section: Discussionmentioning

confidence: 99%

Low PAI‐1 activity in relation to inflammatory parameters, insulin profile and body mass index

Ågren

Wiman

Schulman

2008

Journal of Internal Medicine

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Abstract. Å gren A, Wiman B, Schulman S (Karolinska Institute and Coagulation Unit and Karolinska University Hospital; Karolinska University Hospital, Stockholm, Sweden; and McMaster University, Hamilton, ON, Canada). Low PAI-1 activity in relation to inflammatory parameters, insulin profile and body mass index. J Intern Med 2008; 264: 586-592.Background and objective. High plasminogen activator inhibitor type 1 (PAI-1) activity is associated with inflammatory reactions and insulin resistance, but it is unclear what regulates PAI-1 activity at the low end. The purpose of this study was to investigate if patients with low PAI-1 activity have a lack of inflammatory response or a low insulin level.

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Section: Discussionmentioning

confidence: 99%

Low PAI‐1 activity in relation to inflammatory parameters, insulin profile and body mass index

Ågren

Wiman

Schulman

2008

Journal of Internal Medicine

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“…The top right panel shows the flow of FFA from adipose tissue to plasma, which has a similar form, but with k AA replacing k GL , see equation (4). The flux from liver TAG to plasma TAG is shown in the lower left panel.…”

Section: Graphs Of Fluxesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…The third of these causes is of most interest to us as this form of insulin resistance is common in some obese and all type 2 diabetic subjects, although early phase insulin secretion is inhibited in some type 2 diabetic subjects [3,4]. Both obese and diabetic subjects demonstrate a reduced rate of plasma glucose disposal and a higher than normal basal glucose level [3][4][5]. In the case of type 2 diabetes this can be partially explained by the fact that hepatic glucose uptake is impaired [4,6] and the suppression of hepatic glucose output by insulin is reduced [7]; also skeletal muscle glucose uptake is known to be impaired in type 2 diabetes [8].…”

Section: Introductionmentioning

confidence: 99%

“…Both obese and diabetic subjects demonstrate a reduced rate of plasma glucose disposal and a higher than normal basal glucose level [3][4][5]. In the case of type 2 diabetes this can be partially explained by the fact that hepatic glucose uptake is impaired [4,6] and the suppression of hepatic glucose output by insulin is reduced [7]; also skeletal muscle glucose uptake is known to be impaired in type 2 diabetes [8]. Similarly, with non-diabetic obese subjects there is reduced hepatic glucose output suppression from insulin [3,5] and reduced skeletal muscle glucose uptake [9].…”

Section: Introductionmentioning

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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The Effects of Insulin Resistance on Individual Tissues: An Application of a Mathematical Model of Metabolism in Humans

et al. 2016

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Whilst the human body expends energy constantly, the human diet consists of a mix of carbohydrates and fats delivered in a discontinuous manner. To deal with this sporadic supply of energy, there are transport, storage and utilisation mechanisms, for both carbohydrates and fats, around all tissues of the body. Insulin-resistant states such as type 2 diabetes and obesity are characterised by reduced efficiency of these mechanisms. Exactly how these insulin-resistant states develop, for example whether there is an order in which tissues become insulin resistant, is an active area of research with the hope of gaining a better overall understanding of insulin resistance. In this paper, we use a previously derived system of 12 first-order coupled differential equations that describe the transport between, and storage in, different tissues of the human body. We briefly revisit the derivation of the model before parametrising the model to account for insulin resistance. We then solve the model numerically, separately simulating each individual tissue as insulin resistant, and discuss and compare these results, drawing three main conclusions. The implications of these results are in accordance with biological intuition. First, insulin resistance in a tissue creates a knock-on effect on the other tissues in the body, whereby they attempt to compensate for the reduced efficiency of the insulin-resistant tissue. Second, insulin resistance causes a fatty liver, and the insulin resistance of tissues other than the liver can cause fat to accumulate in the liver. Finally, although insulin resistance in individual tissues can cause slightly reduced skeletal muscle metabolic flexibility, it is when the whole body is insulin resistant that the biggest effect on skeletal muscle flexibility is seen.

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Early-phase insulin secretion is disturbed in obese subjects with glucose intolerance

Cited by 11 publications

References 35 publications

Low PAI‐1 activity in relation to inflammatory parameters, insulin profile and body mass index

Low PAI‐1 activity in relation to inflammatory parameters, insulin profile and body mass index

A Mathematical Model of the Human Metabolic System and Metabolic Flexibility

The Effects of Insulin Resistance on Individual Tissues: An Application of a Mathematical Model of Metabolism in Humans

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