Hormonal
Chronic elevation of reactive oxygen species (ROS) in adipose tissue causes insulin resistance and metabolic dysfunction by impairing insulin signaling and reducing adiponectin secretion.
In obesity, fat cells produce too much oxidative stress (ROS) over time, which blocks insulin from working properly. This isn't about 'bad' stress in small amounts, but chronic overload. Managing weight and reducing fat mass is the primary way to reduce this specific source of oxidative stress and restore insulin sensitivity.
Whereas transient ROS produced by physiological stimuli such as insulin may be beneficial, sustained ROS generation impairs insulin response and might therefore initiate WAT dysfunction... chronic elevation of intracellular ROS levels in adipocytes subsequent to mitochondrial dysfunction results in insulin resistance through attenuation of insulin signaling [64].
Why this rating
The paper cites multiple in vivo rodent models and human clinical correlations, though it is a review article summarizing these findings.
Source
Oxidative Stress and Metabolic Pathologies: From an Adipocentric Point of View
Soazig Le Lay et al. · Oxidative Medicine and Cellular Longevity · 2014
DOI 10.1155/2014/908539
More from this paper
- Hypertrophied (enlarged) adipocytes are a significant source of ROS production, primarily via NADPH oxidase (Nox4) and mitochondrial dysfunction, driving local inflammation and metabolic dysfunction.Good
- Physiological levels of ROS act as beneficial second messengers that promote insulin sensitivity and adipogenesis, whereas chronic elevation leads to insulin resistance.Good
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