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NADPH Oxidases Connecting Fatty Liver Disease, Insulin Resistance and Type 2 Diabetes: Current Knowledge and Therapeutic Outlook

Published in

Antioxidants, vol. 11, no. 6, 1131

Publication date

2022-06-09

First online date

2022-06-09

Abstract

Nonalcoholic fatty liver disease (NAFLD), characterized by ectopic fat accumulation in hepatocytes, is closely linked to insulin resistance and is the most frequent complication of type 2 diabetes mellitus (T2DM). One of the features connecting NAFLD, insulin resistance and T2DM is cellular oxidative stress. Oxidative stress refers to a redox imbalance due to an inequity between the capacity of production and the elimination of reactive oxygen species (ROS). One of the major cellular ROS sources is NADPH oxidase enzymes (NOX-es). In physiological conditions, NOX-es produce ROS purposefully in a timely and spatially regulated manner and are crucial regulators of various cellular events linked to metabolism, receptor signal transmission, proliferation and apoptosis. In contrast, dysregulated NOX-derived ROS production is related to the onset of diverse pathologies. This review provides a synopsis of current knowledge concerning NOX enzymes as connective elements between NAFLD, insulin resistance and T2DM and weighs their potential relevance as pharmacological targets to alleviate fatty liver disease.

Keywords

  • Hepatosteatosis
  • Nonalcoholic fatty liver disease
  • NAFLD
  • Reactive oxygen species
  • ROS
  • NADPH oxidase
  • NOX
  • Insulin resistance
  • Diabetes
  • Oxidative stress

Citation (ISO format)

NASCÈ, Alberto et al. NADPH Oxidases Connecting Fatty Liver Disease, Insulin Resistance and Type 2 Diabetes: Current Knowledge and Therapeutic Outlook. In: Antioxidants, 2022, vol. 11, n° 6, p. 1131. doi: 10.3390/antiox11061131

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Article (Published version)

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Additional URL for this publication

https://www.mdpi.com/2076-3921/11/6/1131

Journal ISSN

2076-3921
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Technical informations

Creation

24/06/2022 07:54:00

First validation

24/06/2022 07:54:00

Update

06/01/2025 08:24:10

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06/01/2025 08:24:10

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