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Pathophysiology of Diabetes01:20

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Related Experiment Video

Updated: Jun 15, 2025

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Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes.

Tomohiro Nishino1,2, Sanjeev S Ranade1,2, Angelo Pelonero1,2

  • 1Gladstone Institutes; San Francisco, CA, USA.

Nature Cardiovascular Research
|August 26, 2024
PubMed
Summary

Maternal diabetes mellitus impacts specific embryonic cell populations, altering their epigenomic landscape and leading to birth defects. This study identifies key cellular mechanisms behind these developmental abnormalities.

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Area of Science:

  • Developmental biology
  • Epigenetics
  • Genomics

Background:

  • Maternal diabetes mellitus is a significant risk factor for congenital birth defects, including heart and craniofacial anomalies.
  • The specific cell types and underlying mechanisms affected by maternal diabetes during embryogenesis remain largely unknown.

Purpose of the Study:

  • To investigate the impact of maternal diabetes on the epigenomic landscape of embryonic progenitor cells.
  • To identify specific cell subpopulations and molecular mechanisms involved in diabetes-induced developmental defects.

Main Methods:

  • Utilized multi-modal single-cell analyses to examine epigenomic changes in cardiac and craniofacial progenitors.
  • Analyzed chromatin accessibility and gene expression patterns in response to maternal diabetes exposure.

Main Results:

  • Maternal diabetes selectively altered the epigenomic landscape of specific cardiac and craniofacial progenitor subpopulations.
  • A novel cardiac progenitor subset expressing ALX3 exhibited chromatin changes and adopted a posterior identity.
  • Neural crest-derived cells in the second pharyngeal arch showed epigenetic abnormalities and axial patterning defects.
  • Observed increases in retinoic acid signaling correlated with chromatin accessibility changes in affected progenitor cells.

Conclusions:

  • Maternal diabetes causes highly selective epigenomic consequences on distinct cell types during development.
  • These epigenomic alterations disrupt normal developmental patterning, contributing to congenital anomalies.
  • Understanding these specific cellular and molecular effects provides insights into preventing diabetes-associated birth defects.