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Peer-reviewedCC BY-NC-ND 4.0npj Metabolic Health and Disease

Multifaceted role of genetic and epigenetic architecture of glucose homeostasis and diabetes

  • Manoj Khokhar1,2
  1. 1Department of Biochemistry, All India Institute of Medical Sciences Rewari, Rewari, 123102 Haryana India
  2. 2Department of Biochemistry, All India Institute of Medical Sciences Jodhpur, Jodhpur, 342005 Rajasthan India
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Abstract

Glucose homeostasis depends on coordinated genetic and epigenetic regulation of pancreatic beta-cells, insulin-sensitive tissues, and neuroendocrine circuits. This review synthesises evidence from over 600 GWAS loci and the primary literature published between 2008 and 2026, and emerging single-cell functional genomics, CRISPR-based perturbation screens, deep-learning variant-effect predictors (DeepSEA, Enformer, AlphaGenome), and polygenic risk frameworks to explain insulin secretion, insulin signalling, and diabetes susceptibility, converting GWAS associations into mechanistic insight and genotype-guided precision therapies.

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Cite

BibTeXRIS
BibTeX
@article{khokhar2026multifaceted,
  title = {{Multifaceted role of genetic and epigenetic architecture of glucose homeostasis and diabetes}},
  author = {Manoj Khokhar},
  journal = {npj Metabolic Health and Disease},
  year = {2026},
  month = oct,
  doi = {10.1038/s44324-026-00135-z},
  url = {https://doi.org/10.1038/s44324-026-00135-z},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Multifaceted role of genetic and epigenetic architecture of glucose homeostasis and diabetes
AU  - Manoj Khokhar
PY  - 2026
DA  - 2026/10/26
JO  - npj Metabolic Health and Disease
DO  - 10.1038/s44324-026-00135-z
UR  - https://doi.org/10.1038/s44324-026-00135-z
AB  - Glucose homeostasis depends on coordinated genetic and epigenetic regulation of pancreatic beta-cells, insulin-sensitive tissues, and neuroendocrine circuits. This review synthesises evidence from over 600 GWAS loci and the primary literature published between 2008 and 2026, and emerging single-cell functional genomics, CRISPR-based perturbation screens, deep-learning variant-effect predictors (DeepSEA, Enformer, AlphaGenome), and polygenic risk frameworks to explain insulin secretion, insulin signalling, and diabetes susceptibility, converting GWAS associations into mechanistic insight and genotype-guided precision therapies.
SN  - 2948-2828
ER  -