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. 2013 Mar 27:4:37.
doi: 10.3389/fendo.2013.00037. eCollection 2013.

Beta cell dysfunction and insulin resistance

Marlon E Cerf  1
Affiliations

Beta cell dysfunction and insulin resistance

Marlon E Cerf. Front Endocrinol (Lausanne). .

Abstract

Beta cell dysfunction and insulin resistance are inherently complex with their interrelation for triggering the pathogenesis of diabetes also somewhat undefined. Both pathogenic states induce hyperglycemia and therefore increase insulin demand. Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion therefore elevated glucose concentrations prevail. Persistently elevated glucose concentrations above the physiological range result in the manifestation of hyperglycemia. With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres. Beta cell dysfunction supersedes insulin resistance in inducing diabetes. Both pathological states influence each other and presumably synergistically exacerbate diabetes. Preserving beta cell function and insulin signaling in beta cells and insulin signaling in the glucose recipient tissues will maintain glucose homeostasis.

Keywords: beta cell compensation; diabetes; obesity; oxidative stress; proliferation.

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Figures

Figure 1
Figure 1
Hyperglycemia-induced beta cell dysfunction, insulin resistance, and type 2 diabetes.
Figure 2
Figure 2
Beta cell proliferation and compensation counters beta cell demise and dysfunction but promotes beta cell survival. Factors are encircled; proliferating factors are in bold.
Figure 3
Figure 3
Beta cell dysfunction and insulin resistance dynamics.
See this image and copyright information in PMC

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References

    1. Alonso L. C., Yokoe T., Zhang P., Scott D. K., Kim S. K., O’Donnell C. P., et al. (2007). Glucose infusion in mice: a new model to induce beta-cell replication. Diabetes 56, 1792–180110.2337/db06-1513 - DOI - PMC - PubMed
    1. Ashcroft F. M., Rorsman P. (2012). Diabetes mellitus and the beta cell: the last ten years. Cell 148, 1160–117110.1016/j.cell.2012.02.010 - DOI - PMC - PubMed
    1. Bergman R. N. (2005). Minimal model: perspective from 2005. Horm. Res. 64(Suppl. 3), 8–1510.1159/000089312 - DOI - PubMed
    1. Blandino-Rosano M., Alejandro E. U., Sathyamurthy A., Scheys J. O., Gregg B., Chen A. Y., et al. (2012). Enhanced beta cell proliferation in mice overexpressing a constitutively active form of Akt and one allele of p21 (Cip). Diabetologia 55, 1380–138910.1007/s00125-012-2465-9 - DOI - PMC - PubMed
    1. Boj S. F., Petrov D., Ferrer J. (2010). Epistasis of transcriptomes reveals synergism between transcriptional activators Hnf1alpha and Hnf4alpha. PLoS Genet. 6:e1000970.10.1371/journal.pgen.1000970 - DOI - PMC - PubMed