Obesity—A Disease With Many Aetiologies Disguised in the Same Oversized Phenotype

Has the Overeating Theory Failed?

Peter Stenvinkel

Disclosures

Nephrol Dial Transplant. 2015;30(10):1656-1664. 

In This Article

Healthy Mitochondria—The Key for a Lean Phenotype

Complicated interactions exist between the redox state and adipose tissue biology. Insulin resistance is associated with a metabolic inflexibility, i.e. a low capacity to adapt fuel oxidation to the availability of fuel. Thus, it may be possible to counteract obesity and its associated metabolic disorders by inducing thermogenesis via mitochondrial uncoupling proteins. As changes in whole-body energy homeostasis have effects on fat mass accumulation, studies linking defective mitochondrial biogenesis to obesity and impaired cell metabolism are of interest.[52] Indeed, the complex phenotype of the lean, but insulin resistant and metabolically morbid, caveolin-1 null mice is caused by altered mitochondrial function.[25] Fleischman et al.[53] demonstrated that normal mitochondrial function is associated with a healthier metabolic phenotype in children with overweight. Moreover, offsprings of patients with type 2 diabetes exhibit impaired mitochondrial function.[54] As dietary antioxidant and anti-inflammatory bioactive compounds increase thermogenesis and energy expenditure,[55] stimulation of mitochondrial oxidative capacity may be key for a lean phenotype.

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