Thyroid hormones are considered to be the major regulator of genomic and non-genomic pathways of mitochonddal biogenesis and consequently of mitochondrial bioactivity and oxygen uptake.Mitochondrial membrane potentials (MMP) have recently been demonstrated to be stimulated by thyroid hormones, and thus reflect the functional status of mitochondria.In obese adolescents a number of observations have suggested an impaired mitochondrial function and also evidence of impaired peripheral thyroid hormone effect (increased TSH and lowered VO2) Besides depressed MMP, depressed mitochondrial related gene expression (PGC1b and NRF2) have been demonstrated in obese adolescents compared to lean and evidence of impaired mitochondrial function in the lean mothers with obese offspring suggests on a genetic component.Furthermore, there exists a correlation between T3 and PBC1 b expression.The observation of a pre diabetic state (increased insulin resistance (HOMA2-IR)) and signs of the metabolic syndrome in obese adolescents are linked to mitochondrial function, as gene expression of PGC1 b are correlated to HOMA2-IR.These observations suggest that an important determinate in obesity in children may be an impaired T3-PGC-1β axis leading to mitochondrial dysfunction.