» Articles » PMID: 34882233

Alpha-to-beta Cell Trans-differentiation for Treatment of Diabetes

Overview
Specialty Biochemistry
Date 2021 Dec 9
PMID 34882233
Citations 7
Authors
Affiliations
Soon will be listed here.
Abstract

Diabetes mellitus is a significant cause of morbidity and mortality in the United States and worldwide. According to the CDC, in 2017, ∼34.2 million of the American population had diabetes. Also, in 2017, diabetes was the seventh leading cause of death and has become the number one biomedical financial burden in the United States. Insulin replacement therapy and medications that increase insulin secretion and improve insulin sensitivity are the main therapies used to treat diabetes. Unfortunately, there is currently no radical cure for the different types of diabetes. Loss of β cell mass is the end result that leads to both type 1 and type 2 diabetes. In the past decade, there has been an increased effort to develop therapeutic strategies to replace the lost β cell mass and restore insulin secretion. α cells have recently become an attractive target for replacing the lost β cell mass, which could eventually be a potential strategy to cure diabetes. This review highlights the advantages of using α cells as a source for generating new β cells, the various investigative approaches to convert α cells into insulin-producing cells, and the future prospects and problems of this promising diabetes therapeutic strategy.

Citing Articles

Decoding the Significance of Alpha Cell Function in the Pathophysiology of Type 1 Diabetes.

Carroll J, Chen J, Mittal R, Lemos J, Mittal M, Juneja S Cells. 2024; 13(22).

PMID: 39594662 PMC: 11593172. DOI: 10.3390/cells13221914.


Type 1 diabetes: immune pathology and novel therapeutic approaches.

Ling E, Lemos J, Hirani K, von Herrath M Diabetol Int. 2024; 15(4):761-776.

PMID: 39469552 PMC: 11512973. DOI: 10.1007/s13340-024-00748-z.


Hesperidin activates the GLP-1R/cAMP-CREB/IRS2/PDX1 pathway to promote transdifferentiation of islet α cells into β cells Across the spectrum.

Zhang W, Wu L, Qu R, Liu T, Wang J, Tong Y Heliyon. 2024; 10(16):e35424.

PMID: 39220963 PMC: 11365324. DOI: 10.1016/j.heliyon.2024.e35424.


Sex-based impact of pancreatic islet stressors in GluCreERT2/Rosa26-eYFP mice.

Tanday N, Coulter-Parkhill A, Moffett R, Suruli K, Dubey V, Flatt P J Endocrinol. 2023; 259(2).

PMID: 37650517 PMC: 10563506. DOI: 10.1530/JOE-23-0174.


EpiCRISPR targeted methylation of Arx gene initiates transient switch of mouse pancreatic alpha to insulin-producing cells.

dordevic M, Stepper P, Feuerstein-Akgoz C, Gerhauser C, Paunovic V, Tolic A Front Endocrinol (Lausanne). 2023; 14:1134478.

PMID: 37008919 PMC: 10063207. DOI: 10.3389/fendo.2023.1134478.


References
1.
Zhang Q, Ramracheya R, Lahmann C, Tarasov A, Bengtsson M, Braha O . Role of KATP channels in glucose-regulated glucagon secretion and impaired counterregulation in type 2 diabetes. Cell Metab. 2013; 18(6):871-82. PMC: 3851686. DOI: 10.1016/j.cmet.2013.10.014. View

2.
Ohlsson H, Karlsson K, Edlund T . IPF1, a homeodomain-containing transactivator of the insulin gene. EMBO J. 1993; 12(11):4251-9. PMC: 413720. DOI: 10.1002/j.1460-2075.1993.tb06109.x. View

3.
Hang Y, Stein R . MafA and MafB activity in pancreatic β cells. Trends Endocrinol Metab. 2011; 22(9):364-73. PMC: 3189696. DOI: 10.1016/j.tem.2011.05.003. View

4.
McKimpson W, Accili D . Reprogramming Cells to Make Insulin. J Endocr Soc. 2019; 3(6):1214-1226. PMC: 6546342. DOI: 10.1210/js.2019-00040. View

5.
Godinho R, Mega C, Teixeira-de-Lemos E, Carvalho E, Teixeira F, Fernandes R . The Place of Dipeptidyl Peptidase-4 Inhibitors in Type 2 Diabetes Therapeutics: A "Me Too" or "the Special One" Antidiabetic Class?. J Diabetes Res. 2015; 2015:806979. PMC: 4449938. DOI: 10.1155/2015/806979. View