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Type II Diabetes and Obesity: A Control Theoretic Model

机译:II型糖尿病和肥胖症:一种控制理论模型

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Diabetes mellitus can be further classified as Type I diabetes (TID) or Type II diabetes (TIID). TID is recognized as a complete failure in the pancreas β-cell islet. TIID is a failure in the body's ability to regulate glucose plasma concentration within the blood. Two aspects of TIID are well recognized: impaired insulin secretion and insulin resistance. Insulin resistance inhibits the organs' to glucose uptake and the response to insulin secretion. Insulin resistance can be linked to increased levels of Free Fatty Acid (FFA) concentration within exhibited in obese individuals and di-abetes patients' offspring. Offspring of diabetes patients exhibit an extreme reduction in mitochondrial function; whereas obese individuals demonstrate high FFA concentration due to an excess of adipose tissue. FFA is linked to insulin resistance with TIID patients. Simulating glucose regulation in the body is considered to be an interesting control theory problem with significant impact. The suggested model in the paper is an attempt to address glucose regulation from a control theoretic viewpoint using the pharmacokinetic approach. The model identifies the contribution of glucose, insulin, incretins, glucagon, and FFA on glucose regulation within the body. The model con-sists of sub-models addressing the factors production rate (source) and clearance rate (sinks) based upon physiological responses. The model emphasizes the effect of FFA on glucose regulation, therefore creating a base for a mathematical model to simulate the behavior of early TIID diabetes glucose regulation under the effect of insulin resistance with a decreased rate in insulin secretion. The model would remain unable to simulate other behaviors of insulin impairment response exhibited within the TIID. Finally; the model creates a better understanding of TIID, further insight into prevention meth-ods, new disease managements options in the form of diet, a better understanding of the impact of obesity on diabetes, and it can be used to investigate a possible link to cardiovascular diseases.
机译:糖尿病可以进一步分类为I型糖尿病(TID)或II型糖尿病(TIID)。 TID被认为是胰腺β-细胞胰岛的完全失败。 TIID是体内调节血液内葡萄糖血浆浓度的能力的失败。 TIID的两个方面得到了很好的认可:胰岛素分泌受损和胰岛素抵抗力。胰岛素抗性抑制葡萄糖摄取的器官和对胰岛素分泌的反应。胰岛素抵抗可以与肥胖个体和Di-Pearbes患者后代的展示中的游离脂肪酸(FFA)浓度的水平增加。糖尿病患者的后代表现出对线粒体功能的极度减少;而肥胖个体由于过量的脂肪组织而表现出高FFA浓度。 FFA与TIID患者有关的胰岛素抵抗。模拟体内的葡萄糖调节被认为是一个有趣的控制理论问题,具有显着影响。本文的建议模型是尝试使用药代动力学方法来解决来自控制理论观点的葡萄糖调节。该模型识别葡萄糖,胰岛素,Incretins,胰高血糖素和FFA对体内葡萄糖调节的贡献。基于生理反应的子模型的模型与子模型的模型共同分子解决了因素生产率(源)和清除率(下沉)。该模型强调FFA对葡萄糖调节的影响,因此为数学模型产生了基础,以模拟胰岛素抗性在胰岛素分泌率降低的胰岛素抵抗力下的早期TIID糖尿病葡萄糖调节的行为。该模型将仍然无法模拟在TIID内展示的胰岛素损伤反应的其他行为。最后;该模型创造了更好地理解TIID,进一步了解预防臭氧,新的疾病管理选择以饮食的形式,更好地了解肥胖对糖尿病的影响,可用于研究可心血管的可能链接疾病。

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