"Omics" and "epi-omics" underlying the β-cell adaptation to insulin resistance
Background: Pancreatic β-cells adapt to high metabolic demand by expanding their β-cell mass and/or enhancing insulin secretion to maintain glucose homeostasis. Type 2 diabetes (T2D) is typically characterized by β-cell decompensation. Scope of the review: The current review focuses on summarizing t...
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| Main Authors: | , |
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| Format: | Book |
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Elsevier,
2019-09-01T00:00:00Z.
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| Summary: | Background: Pancreatic β-cells adapt to high metabolic demand by expanding their β-cell mass and/or enhancing insulin secretion to maintain glucose homeostasis. Type 2 diabetes (T2D) is typically characterized by β-cell decompensation. Scope of the review: The current review focuses on summarizing the "omics" and "epi-omics" approaches that particularly focus on addressing the β-cell adaptation to insulin resistance and T2D. Major conclusions: The molecular mechanisms underlying successful versus compromised β-cell adaptation to insulin resistance are not entirely understood. The last decade has seen an exponential increase in the use of "omics" and "epi-omics" approaches to dissect pathophysiology of metabolic diseases. One recent example is the emergence of m6A mRNA methylation as a new layer of regulation of gene expression with the potential to impact diverse physiological processes in metabolic cells. Keywords: β-cells, Insulin resistance, Genomics, Transcriptomics, Epigenomics, Epitranscriptomics |
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| Item Description: | 2212-8778 10.1016/j.molmet.2019.06.003 |