Redox implications in adipose tissue (dys)function—A new look at old acquaintances

• Adipose tissue (AT) buffers nutrient excess determining overall metabolic health.
• Redox insight in lipid storage and adipogenesis of AT is reviewed.
• Redox modulation of AT as therapeutic target in obesity/syndrome X is considered.

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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