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.

中文翻译：

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β细胞对胰岛素抵抗的适应性的“组学”和“表观组学”。

背景技术胰腺β细胞通过扩大其β细胞质量和/或增强胰岛素分泌以维持葡萄糖稳态来适应高代谢需求。2型糖尿病（T2D）通常以β细胞代偿失调为特征。综述的范围当前的综述着重于总结“组学”和“表观组学”方法，这些方法特别着重于解决β细胞对胰岛素抵抗和T2D的适应性问题。主要结论尚不完全了解成功的和受损的β细胞适应胰岛素抵抗的分子机制。在过去的十年中，使用“组学”和“表组学”方法剖析代谢性疾病的病理生理学已呈指数级增长。