Delay in ATP-dependent calcium inflow may affect insulin secretion from pancreatic beta-cell

被引:8
作者
Das, Phonindra Nath [1 ]
Halder, Suvankar [2 ]
Bairagi, Nandadulal [3 ]
Chatterjee, Samrat [2 ]
机构
[1] Memari Coll, Dept Math, Purba Bardhaman 713146, W Bengal, India
[2] Translat Hlth Sci & Technol Inst, NCR Biotech Sci Cluster, Complex Anal Grp, Faridabad 121001, India
[3] Jadavpur Univ, Ctr Math Biol & Ecol, Dept Math, Kolkata 700032, India
关键词
Type; 2; diabetes; Beta cell; Mathematical model; Delay differential equation; Oscillations; Glucose-calcium relation; GLUCOSE RESPONSE CURVE; TYPE-2 DIABETES RISK; ULTRADIAN OSCILLATIONS; REGULATORY SYSTEM; MODEL; MECHANISMS; METABOLISM; TOLERANCE; TIME; HOMEOSTASIS;
D O I
10.1016/j.apm.2020.03.030
中图分类号
T [工业技术];
学科分类号
08 ;
摘要
Any dysfunction in the secretion of insulin and/or in its use is critical in the development of type 2 diabetes. Calcium plays a very important role in the insulin secretion mechanism from beta-cell. In this paper, we studied the dynamic interaction of glucose-induced insulin secretion mechanism through glucose metabolism and ATP-dependent calcium influx. We proposed and analyzed a four dimensional system of nonlinear delay differential equations to give insights into different possible mechanisms for maintaining plasma glucose homeostasis through calcium-induced insulin secretion. The time duration between ATP formation and subsequent calcium influx through cell membrane has been found to be critical in maintaining insulin homeostasis. How variational effects of system parameters lead to various glycemic states are demonstrated. Possibility of new potential drug therapies is also discussed through parameter recalibration. (C) 2020 Elsevier Inc. All rights reserved.
引用
收藏
页码:202 / 221
页数:20
相关论文
共 101 条
[1]   HYPERCOMPLEX MODELS OF INSULIN AND GLUCOSE DYNAMICS - DO THEY PREDICT EXPERIMENTAL RESULTS [J].
ALBISSER, AM ;
YAMASAKI, Y ;
BROEKHUYSE, H ;
TIRAN, J .
ANNALS OF BIOMEDICAL ENGINEERING, 1980, 8 (4-6) :539-557
[2]  
American Diabetes Association, 2000, CLIN DIABETES, V18
[3]  
[Anonymous], 2016, World Health Organization - Global Report on Diabetes
[4]   GLUCOSE INDUCES CLOSURE OF SINGLE POTASSIUM CHANNELS IN ISOLATED RAT PANCREATIC BETA-CELLS [J].
ASHCROFT, FM ;
HARRISON, DE ;
ASHCROFT, SJH .
NATURE, 1984, 312 (5993) :446-448
[5]   ELECTROPHYSIOLOGY OF THE PANCREATIC BETA-CELL [J].
ASHCROFT, FM ;
RORSMAN, P .
PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY, 1989, 54 (02) :87-143
[6]   Diabetes Mellitus and the β Cell: The Last Ten Years [J].
Ashcroft, Frances M. ;
Rorsman, Patrik .
CELL, 2012, 148 (06) :1160-1171
[7]   Glucose metabolism in vivo in four commonly used inbred mouse strains [J].
Berglund, Eric D. ;
Li, Candice Y. ;
Poffenberger, Greg ;
Ayala, Julio E. ;
Fueger, Patrick T. ;
Willis, Shannon E. ;
Jewell, Marybeth M. ;
Powers, Alvin C. ;
Wasserman, David H. .
DIABETES, 2008, 57 (07) :1790-1799
[8]   Metabolic and electrical oscillations: partners in controlling pulsatile insulin secretion [J].
Bertram, Richard ;
Sherman, Arthur ;
Satin, Leslie S. .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2007, 293 (04) :E890-E900
[9]  
Birkhoff Garrett, 1978, ORDINARY DIFFERENTIA, V4
[10]   SENSITIVITY AND UNCERTAINTY ANALYSIS OF COMPLEX-MODELS OF DISEASE TRANSMISSION - AN HIV MODEL, AS AN EXAMPLE [J].
BLOWER, SM ;
DOWLATABADI, H .
INTERNATIONAL STATISTICAL REVIEW, 1994, 62 (02) :229-243