Myeloperoxidase and Protein-radicalization are Linked to Insulin Resistance in the Obese Adipose Tissue

Authors

SOLEDAD BARRERA¹ , CRITOFER LOPEZ¹ , FLORENCIA CLAVELES CASAS¹ , PAULA DISCIULLO¹ , DARIO RAMIREZ¹ , SANDRA GOMEZ MEJIBA¹

1. CONICET-SAN LUIS

Conference / event

27th annual conference SOCIETY FOR FREE RADICAL BIOLOGY AND MEDICINE, November 2020 (Virtual)

Poster summary

Our B6 mouse model of diet-induced obesity showed adipose tissue macrophages (ATM) forming typical crown-like structures in the adipose tissue (AT). These ATM from obese mice express 15-times more myeloperoxidase (MPO) mRNA than those from control mice. MPO protein, but not mRNA, was also found inside adipocytes in the obese AT. Treatment with the nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) improved insulin sensitivity in obese mice. DMPO-based immuno-spin trapping and MS-tandem showed the radicalization of specific components of the insulin-triggered signaling. These effects were prevented by resveratrol that scavenged intracellularly produced HOCl thus preventing loss of insulin sensitivity. DMPO also prevented HOCl-induced loss of insulin sensitivity in adipocytes by trapping radicalized protein. Scavenging HOCl produced inside adipocytes with resveratrol or preventing protein oxidation with spin traps can protect insulin signaling in adipocytes

Keywords

MYELOPEROXIDASE, ADIPOCYTE, PROTEIN FREE RADICAL, DMPO, OBESITY, INSULIN RESISTANCE

Research areas

Biochemistry, Molecular and Cellular Biosciences, Pharmacy and Pharmacology, Biological Sciences

References

No data provided

Funding

1. FONCYT (No. PICT-2021-I-A-0147)

Supplemental files

No data provided

Additional information

Competing interests

No competing interests were disclosed.

Data availability statement

Data sharing not applicable to this poster as no datasets were generated or analyzed during the current study.

Creative Commons license

Copyright © 2024 BARRERA et al. This is an open access work distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.