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A delay differential equation model for metabolic feedback among glucose, insulin and glucagon, and some thoughts on dual pump artificial pancreas

时间:2024-06-26 来源: 作者: 摄影: 编辑:张恩斯 上传:

报告人:李嘉旭教授

报告人单位:美国路易维尔大学

报告时间:2024年6月27日(星期四)9:00

报告地点:笃行楼316-1

举办单位:数理科学学院

报告人简介

李嘉旭,博士,美国路易维尔大学教授。1996年获美国亚利桑那州立大学计算机科学硕士学位,2004年获美国亚利桑那州立大学数学博士学位。自2007年8月起在美国路易维尔大学数学系任助理教授,副教授,教授。主要从事于动力系统,泛函微分方程,数学生物学的研究,特别集中于基因转化,代谢系统及糖尿病的研究,任Frontier Systems Biology和Mathematical Bioscience and Engineering等杂志编委。在主要专业杂志如SIAM Journal on Applied Mathematics、Journal of Theoretical Biology、Journal of Mathematical Biology等发表多篇有影响力的论文,主持和参与多个美国卫生研究院、能源部项目以及子项目。他的研究成果大多处于国际领先水平,被多个生物学家、控制专家所应用。此外,在2007年回归学术界之前,李教授曾在美国高科技工业领域工作十余年,历任程序员、工程师、高级工程师、资深高级工程师等,主要从事数据库,控制软件的研发工作。

报告摘要

Glucose, insulin, and glucagon together form a complete endocrine metabolic feedbackloop. Most existing modeling work pertaining to this loop focuses mainly on the regulationsbetween glucose and insulin. The role of glucagon in these works is summarized by hepaticglucose production (HGP) dependent solely on insulin levels. In this talk, we carefully analyzethe secretion of glucagon, its role in HGP, and its interactions with insulin, and then formulatea dynamical system model to further analyze its effects in balancing blood sugar levels. Thepresence of glucagon allows us to examinethe impacts of HGP governed by insulin andglucagon separately. This reveals insight about how a very recent concept, glucagon resistance,can affect blood glucose levels and lead to rampant glucagon production and consequentlyblood sugar levels. We also show that a form of insulin resistance in hepatic cells can leadto excess insulin secretion, a characteristic of type 2 diabetes mellitus. We also present somethoughts on modeling the feedback loop in a dual pump artificial pancreas.

审核人:蔡亚峰

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