Development of a computational model of glucose toxicity in the progression of diabetes mellitus

  • Received: 01 October 2015 Accepted: 29 June 2018 Published: 01 July 2016
  • MSC : Primary: 92B05; Secondary: 92C50.

  • Diabetes mellitus is a disease characterized by a range of metabolic complications involving an individual's blood glucose levels, and its main regulator, insulin. These complications can vary largely from person to person depending on their current biophysical state. Biomedical research day-by-day makes strides to impact the lives of patients of a variety of diseases, including diabetes. One large stride that is being made is the generation of techniques to assist physicians to ``personalize medicine''.From available physiological data, biological understanding of the system, and dimensional analysis, a differential equation-based mathematical model was built in a sequential matter, to be able to elucidate clearly how each parameter correlates to the patient's current physiological state. We developed a simple mathematical model that accurately simulates the dynamics between glucose, insulin, and pancreatic $\beta$-cells throughout disease progression with constraints to maintain biological relevance. The current framework is clearly capable of tracking the patient's current progress through the disease, dependent on factors such as latent insulin resistance or an attrite $\beta$-cell population. Further interests would be to develop tools that allow the direct and feasible testing of how effective a given plan of treatment would be at returning the patient to a desirable biophysical state.

    Citation: Danilo T. Pérez-Rivera, Verónica L. Torres-Torres, Abraham E. Torres-Colón, Mayteé Cruz-Aponte. Development of a computational model of glucose toxicity in the progression of diabetes mellitus[J]. Mathematical Biosciences and Engineering, 2016, 13(5): 1043-1058. doi: 10.3934/mbe.2016029

    Related Papers:

  • Diabetes mellitus is a disease characterized by a range of metabolic complications involving an individual's blood glucose levels, and its main regulator, insulin. These complications can vary largely from person to person depending on their current biophysical state. Biomedical research day-by-day makes strides to impact the lives of patients of a variety of diseases, including diabetes. One large stride that is being made is the generation of techniques to assist physicians to ``personalize medicine''.From available physiological data, biological understanding of the system, and dimensional analysis, a differential equation-based mathematical model was built in a sequential matter, to be able to elucidate clearly how each parameter correlates to the patient's current physiological state. We developed a simple mathematical model that accurately simulates the dynamics between glucose, insulin, and pancreatic $\beta$-cells throughout disease progression with constraints to maintain biological relevance. The current framework is clearly capable of tracking the patient's current progress through the disease, dependent on factors such as latent insulin resistance or an attrite $\beta$-cell population. Further interests would be to develop tools that allow the direct and feasible testing of how effective a given plan of treatment would be at returning the patient to a desirable biophysical state.


    加载中
    [1] Accessed: 2014-04-03.
    [2] Metabolism, 61 (2012), 221-228.
    [3] 5th edition, 2002.
    [4] in Biochemistry, 5th edition, Section 21.5, W H Freeman, New York, 2002.
    [5] Journal of Clinical Investigation, 68 (1981), 1456-1467.
    [6] Journal of Clinical Investigation, 108 (2001), 655-659.
    [7] Biochem. J, 15 (1998), 19-31.
    [8] Physiological reviews, 85 (2005), 1255-1270.
    [9] Diabetes, 52 (2003), 102-110.
    [10] http://www.mayoclinic.org/diseases-conditions/type-2-diabetes/expert-answers/hyperinsulinemia/faq-20058488, Accessed: 2014-04-03.
    [11] American Journal of Physiology-Renal Physiology, 296 (2009), F298-F305.
    [12] Endocrinology, 133 (1993), 208-214.
    [13] Journal of Clinical Investigation, 50 (1971), 1702-1711.
    [14] Endocrine reviews, 19 (1998), 491-503.
    [15] Journal of Biological Chemistry, 272 (1997), 30261-30269.
    [16] Pediatric Clinics of North America, 52 (2005), 1553-1578.
    [17] Journal of Clinical Investigation, 81 (1988), 872-878.
    [18] Diabetes & metabolism, 34 (2008), S56-S64.
    [19] Applied numerical mathematics, 56 (2006), 559-573.
    [20] Diabetes, 48 (1999), 524-530.
    [21] Diabetes care, 28 (2005), S37.
    [22] http://www.healthline.com/health/diabetes/insulin-and-glucagon#Overview1, Accessed: 2014-04-03.
    [23] McGraw Hill Professional, 2012.
    [24] The American Journal of Medicine, 79 (1985), 1-7.
    [25] Diabetologia, 38 (1995), 1295-1299.
    [26] The American journal of medicine, 119 (2006), S10-S16.
    [27] Endocrinology, 143 (2002), 339-342.
    [28] Journal of Clinical Investigation, 81 (1988), 435-441.
    [29] Role of Insulin Resistance in Human Disease, 1 (1992), 91-97.
    [30] Pearson Higher Education AU, 2011.
    [31] Diabetes, 52 (2003), 581-587.
    [32] Diabetes, 53 (2004), S119-S124.
    [33] Diabetes, 43 (1994), 1085-1089.
    [34] http://healthyeating.sfgate.com/expected-blood-glucose-after-highcarb-meal-3529.html, Accessed: 2014-04-03.
    [35] http://www.phlaunt.com/diabetes/14046621.php, Accessed: 2014-04-03.
    [36] Endocrinology, 127 (1990), 1580-1589.
    [37] http://www.diabetesselfmanagement.com/managing-diabetes/blood-glucose-management/strike-the-spike-ii/, Accessed: 2014-04-03.
    [38] Molecular Systems Biology, 4 (2008), p214.
    [39] http://www.medicinenet.com/hyperglycemia/article.htm, Accessed: 2014-04-03.
    [40] Diabetes care, 23 (2000), 295-301.
    [41] Journal of the Intensive Care Society, 10 (2009), 216-217.
    [42] Journal of Theoretical Biology, 206 (2000), 605-619.
    [43] Mathematical biosciences, 235 (2012), 8-18.
    [44] Diabetes, 53 (2004), S16-S21.
    [45] Journal of Biological Chemistry, 279 (2004), 12126-12134.
    [46] Journal of Clinical Investigation, 93 (1994), 870-876.
  • Reader Comments
  • © 2016 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
通讯作者: 陈斌, bchen63@163.com
  • 1. 

    沈阳化工大学材料科学与工程学院 沈阳 110142

  1. 本站搜索
  2. 百度学术搜索
  3. 万方数据库搜索
  4. CNKI搜索

Metrics

Article views(3133) PDF downloads(732) Cited by(0)

Article outline

/

DownLoad:  Full-Size Img  PowerPoint
Return
Return

Catalog