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Sustained O-GlcNAcylation reprograms mitochondrial function to regulate energy metabolism.

Ee Phie Tan1, Steven R McGreal2, Stefan Graw3

  • 1From the Departments of Biochemistry and Molecular Biology.

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Altering O-GlcNAcylation, a protein modification, impacts cellular energy metabolism and mitochondrial function. Sustained increases in O-GlcNAcylation reprogram energy pathways, affecting chronic disease development.

Keywords:
O-GlcNAcaseO-GlcNAcylationOGTbioenergeticsmitochondrianuclear factor 2 (erythroid-derived 2-like factor) (NFE2L2) (Nrf2)reactive oxygen species (ROS)

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Area of Science:

  • Biochemistry
  • Cellular Metabolism
  • Mitochondrial Biology

Background:

  • Mitochondrial dysfunction and reactive oxygen species (ROS) are implicated in chronic diseases.
  • Post-translational modification of proteins with O-linked N-acetylglucosamine (O-GlcNAcylation) is crucial for cellular regulation.
  • Previous work showed O-GlcNAcylation disruption impairs mitochondrial function.

Purpose of the Study:

  • To investigate the effects of sustained alterations in O-GlcNAcylation on cellular and organismal metabolic function.
  • To elucidate the molecular mechanisms linking O-GlcNAcylation to metabolic reprogramming.
  • To explore the implications for metabolic diseases.

Main Methods:

  • Pharmacological and genetic manipulation of O-GlcNAcylation in SH-SY5Y neuroblastoma cells.
  • Assessment of cellular respiration, ROS generation, mitochondrial morphology, and membrane potential.
  • RNA-sequencing for transcriptome analysis, including NRF2 pathway evaluation.
  • In vivo studies in mouse brain and liver, including OGT knockdown and indirect calorimetry.

Main Results:

  • Sustained O-GlcNAc elevation reduced cellular respiration and ROS generation, elongated mitochondria, and increased mitochondrial membrane potential.
  • Transcriptome analysis revealed reprogramming and down-regulation of the NRF2-mediated antioxidant response.
  • In vivo, elevated O-GlcNAc levels promoted weight loss, lowered respiration, and shifted metabolism towards carbohydrate dependence.
  • OGT knockdown in the liver increased ROS, impaired respiration, and enhanced the NRF2 antioxidant response.

Conclusions:

  • Sustained elevation of O-GlcNAcylation, alongside increased OGA expression, reprograms cellular energy metabolism.
  • These metabolic changes have significant implications for the etiology, development, and management of metabolic diseases.
  • O-GlcNAcylation is a key regulator of metabolic homeostasis and a potential therapeutic target.