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Review
. 2023 Sep 7;24(18):13782.
doi: 10.3390/ijms241813782.

Mitochondrial Dynamics and Insulin Secretion

Affiliations
Review

Mitochondrial Dynamics and Insulin Secretion

Uma D Kabra et al. Int J Mol Sci. .

Abstract

Mitochondria are involved in the regulation of cellular energy metabolism, calcium homeostasis, and apoptosis. For mitochondrial quality control, dynamic processes, such as mitochondrial fission and fusion, are necessary to maintain shape and function. Disturbances of mitochondrial dynamics lead to dysfunctional mitochondria, which contribute to the development and progression of numerous diseases, including Type 2 Diabetes (T2D). Compelling evidence has been put forward that mitochondrial dynamics play a significant role in the metabolism-secretion coupling of pancreatic β cells. The disruption of mitochondrial dynamics is linked to defects in energy production and increased apoptosis, ultimately impairing insulin secretion and β cell death. This review provides an overview of molecular mechanisms controlling mitochondrial dynamics, their dysfunction in pancreatic β cells, and pharmaceutical agents targeting mitochondrial dynamic proteins, such as mitochondrial division inhibitor-1 (mdivi-1), dynasore, P110, and 15-oxospiramilactone (S3).

Keywords: diabetes; fission; fusion; glucose-stimulated insulin secretion; mitochondrial dynamics; pancreatic beta cell.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
A schematic model showing the steps involved in glucose-stimulated insulin secretion by the pancreatic β cell.
Figure 2
Figure 2
Regulation of mitochondrial dynamics by fission, fusion, and mitophagy.
Figure 3
Figure 3
Domain structure and posttranslational modification of Drp1 at different amino acid residues, along with commonly used dominant-negative mutant (K38A).
Figure 4
Figure 4
Effect of manipulation of mitochondrial dynamic regulating players on insulin secretion. (A) Mitofusins (Mfn1/2), (B) Optic Atrophy 1 (Opa1), (C) Mitochondrial Fission 1 Protein (Fis1), and (D) Dynamin Related Protein 1 (Drp1).

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References

    1. Debono M., Cachia E. The impact of diabetes on psychological well being and quality of life. The role of patient education. Psychol. Health Med. 2007;12:545–555. doi: 10.1080/13548500701235740. - DOI - PubMed
    1. Chou C.Y., Hsu D.Y., Chou C.H. Predicting the Onset of Diabetes with Machine Learning Methods. J. Pers. Med. 2023;13:406. doi: 10.3390/jpm13030406. - DOI - PMC - PubMed
    1. Baynes H.W. Classification, pathophysiology, diagnosis and management of diabetes mellitus. J. Diabetes Metab. 2015;6:1–9. doi: 10.4172/2155-6156.1000541. - DOI
    1. DeFronzo R.A. Pathogenesis of type 2 diabetes mellitus. Med. Clin. 2004;88:787–835. doi: 10.1016/j.mcna.2004.04.013. - DOI - PubMed
    1. Weyer C., Tataranni P.A., Bogardus C., Pratley R.E. Insulin resistance and insulin secretory dysfunction are independent predictors of worsening of glucose tolerance during each stage of type 2 diabetes development. Clin. Diabetol. 2001;2:167–172. doi: 10.2337/diacare.24.1.89. - DOI - PubMed

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