Key result
Redox imbalance in fat tissue acts as a potential instigator of adipocyte dysfunction in obesity, leading to failure in safe storage of metabolic substrates and subsequent glucose and lipid overflow.
Highlights the role of redox imbalance in adipose tissue dysfunction and the metabolic complications of obesity.
May support redox modulation as a therapeutic target in obesity; hypothesis-generating and requires prospective validation.
Obesity is an energy balance disorder associated with dyslipidemia, insulin resistance and diabetes type 2, also summarized with the term metabolic syndrome or syndrome X. Increasing evidence points to "adipocyte dysfunction", rather than fat mass accretion per se, as the key pathophysiological factor for metabolic complications in obesity. The dysfunctional fat tissue in obesity characterizes a failure to safely store metabolic substrates into existing hypertrophied adipocytes and/or into new preadipocytes recruited for differentiation. In this review we briefly summarize the potential of redox imbalance in fat tissue as an instigator of adipocyte dysfunction in obesity. We reveal the challenge of the adipose redox changes, insights in the regulation of healthy expansion of adipose tissue and its reduction, leading to glucose and lipids overflow.
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Janković et al. (2015) conducted a review in Obesity and metabolic syndrome. Redox imbalance was evaluated. Redox imbalance in fat tissue acts as a potential instigator of adipocyte dysfunction in obesity, leading to failure in safe storage of metabolic substrates and subsequent glucose and lipid overflow.
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