Multiscale Modeling of Insulin Secretion
(2011) In IEEE Transactions on Biomedical Engineering 58(10). p.3020-3023- Abstract
- Insulin secretion from pancreatic beta cells is a fundamental physiological process, and its impairment plays a pivotal role in the development of diabetes. Mathematical modeling of insulin secretion has a long history, both on the level of the entire body and on the cellular and subcellular scale. However, little direct communication between these disparate scales has been included in mathematical models so far. Recently, we have proposed a minimal model for the incretin effect by which the gut hormone glucagon-like peptide 1 (GLP-1) enhances insulin secretion. To understand how this model couples to cellular events, we use a previously published mechanistic model of insulin secretion, and show mathematically that induction of glucose... (More)
- Insulin secretion from pancreatic beta cells is a fundamental physiological process, and its impairment plays a pivotal role in the development of diabetes. Mathematical modeling of insulin secretion has a long history, both on the level of the entire body and on the cellular and subcellular scale. However, little direct communication between these disparate scales has been included in mathematical models so far. Recently, we have proposed a minimal model for the incretin effect by which the gut hormone glucagon-like peptide 1 (GLP-1) enhances insulin secretion. To understand how this model couples to cellular events, we use a previously published mechanistic model of insulin secretion, and show mathematically that induction of glucose competence in beta cells by GLP-1 can underlie derivative control by GLP-1. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2179901
- author
- Pedersen, Morten Gram LU ; Dalla Man, Chiara and Cobelli, Claudio
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Derivative control, glucagon-like peptide 1 (GLP-1), incretins, insulin, granules, threshold distribution
- in
- IEEE Transactions on Biomedical Engineering
- volume
- 58
- issue
- 10
- pages
- 3020 - 3023
- publisher
- IEEE - Institute of Electrical and Electronics Engineers Inc.
- external identifiers
-
- wos:000295102600021
- scopus:80053156336
- pmid:21846600
- ISSN
- 1558-2531
- DOI
- 10.1109/TBME.2011.2164918
- language
- English
- LU publication?
- yes
- id
- a52e9ef2-b895-4394-99bf-e308709354f7 (old id 2179901)
- date added to LUP
- 2016-04-01 14:49:07
- date last changed
- 2022-03-22 02:02:50
@article{a52e9ef2-b895-4394-99bf-e308709354f7,
abstract = {{Insulin secretion from pancreatic beta cells is a fundamental physiological process, and its impairment plays a pivotal role in the development of diabetes. Mathematical modeling of insulin secretion has a long history, both on the level of the entire body and on the cellular and subcellular scale. However, little direct communication between these disparate scales has been included in mathematical models so far. Recently, we have proposed a minimal model for the incretin effect by which the gut hormone glucagon-like peptide 1 (GLP-1) enhances insulin secretion. To understand how this model couples to cellular events, we use a previously published mechanistic model of insulin secretion, and show mathematically that induction of glucose competence in beta cells by GLP-1 can underlie derivative control by GLP-1.}},
author = {{Pedersen, Morten Gram and Dalla Man, Chiara and Cobelli, Claudio}},
issn = {{1558-2531}},
keywords = {{Derivative control; glucagon-like peptide 1 (GLP-1); incretins; insulin; granules; threshold distribution}},
language = {{eng}},
number = {{10}},
pages = {{3020--3023}},
publisher = {{IEEE - Institute of Electrical and Electronics Engineers Inc.}},
series = {{IEEE Transactions on Biomedical Engineering}},
title = {{Multiscale Modeling of Insulin Secretion}},
url = {{http://dx.doi.org/10.1109/TBME.2011.2164918}},
doi = {{10.1109/TBME.2011.2164918}},
volume = {{58}},
year = {{2011}},
}