The progression of secondary diabetes: A review of modeling studies

被引:2
|
作者
Yang, Boya [1 ]
Li, Jiaxu [2 ]
Haller, Michael J. J. [3 ]
Schatz, Desmond A. A. [3 ]
Rong, Libin [1 ]
机构
[1] Univ Florida, Dept Math, Gainesville, FL 32611 USA
[2] Univ Louisville, Dept Math, Louisville, KY USA
[3] Univ Florida, Dept Pediat, Gainesville, FL USA
来源
关键词
mathematical model; secondary diabetes; hyperthyroidism; glucocorticoids; epinephrine; growth hormone; INSULIN REGULATORY SYSTEM; GROWTH-HORMONE; GLUCOSE-HOMEOSTASIS; MATHEMATICAL-MODEL; EPINEPHRINE; RESISTANCE; OSCILLATIONS; SENSITIVITY; METABOLISM; MECHANISMS;
D O I
10.3389/fendo.2022.1070979
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Mathematical modeling has provided quantitative information consistent with experimental data, greatly improving our understanding of the progression of type 1 and type 2 diabetes. However, diabetes is a complex metabolic disease and has been found to be involved in crosstalk interactions with diverse endocrine diseases. Mathematical models have also been developed to investigate the quantitative impact of various hormonal disorders on glucose imbalance, advancing the precision treatment for secondary diabetes. Here we review the models established for the study of dysglycemia induced by hormonal disorders, such as excessive glucocorticoids, epinephrine, and growth hormone. To investigate the influence of hyperthyroidism on the glucose regulatory system, we also propose a hyperthyroid-diabetes progression model. Model simulations indicate that timely thyroid treatment can halt the progression of hyperglycemia and prevent beta-cell failure. This highlights the diagnosis of hormonal disorders, together withblood sugar tests, as significant measures for the early diagnosis and treatment of diabetes. The work recapitulates updated biological research on the interactions between the glucose regulatory system and other endocrine axes. Further mathematical modeling of secondary diabetes is desired to promote the quantitative study of the disease and the development of individualized diabetic therapies.
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收藏
页数:16
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