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"Omics" and "epi-omics" underlying the β-cell adaptation to insulin resistance.

Abstract：

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.

journal_name

Mol Metab

journal_title

Molecular metabolism

authors

De Jesus DF,Kulkarni RN

doi

10.1016/j.molmet.2019.06.003

subject

Has Abstract

pub_date

2019-09-01 00:00:00

pages

S42-S48

issn

2212-8778

pii

S2212-8778(19)30563-0

journal_volume

27S

pub_type

杂志文章,评审

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