Evidence of mitochondrial dysfunction in obese adolescents
Article first published online: 15 DEC 2009
© 2009 The Author(s)/Journal Compilation © 2009 Foundation Acta Pædiatrica
Volume 99, Issue 6, pages 906–911, June 2010
How to Cite
Wilms, L., Larsen, J., Pedersen, P. and Kvetny, J. (2010), Evidence of mitochondrial dysfunction in obese adolescents. Acta Paediatrica, 99: 906–911. doi: 10.1111/j.1651-2227.2009.01635.x
- Issue published online: 4 MAY 2010
- Article first published online: 15 DEC 2009
- Received 28 May 2009; revised 27 October 2009; accepted 16 November 2009.
- Basal oxygen consumption;
- Mitochondrial dysfunction;
- Thyroid hormones
Aim: Although obesity and weight gain generally are anticipated to be caused by an imbalance between energy intake and energy expenditure, the significance of thyroid hormones (TH) remains unclear. Examination of mitochondrial function may reflect intracellular thyroid hormone effect and elucidate whether a lower metabolic rate is present.
Methods: In a group of 34 obese adolescents (age <16 years and body mass index above the age-related 95th percentile), and an age- and gender-matched group of 32 lean adolescent, thyroid stimulating hormone (TSH) and basal oxygen consumption were measured and mitochondrial function in peripheral blood monocytes was determined by flow cytometry.
Results: Significant increase in TSH (3.06 ± 1.56 mU/L vs. 2.33 ± 0.91 mU/L, p < 0.05) and a decrease in VO2 (129 ± 16 mL O2/m2*min vs. 146 ± 15 mL O2/m2*min, p < 0.05) were observed in obese adolescents compared with lean adolescents. Flow cytometry analysis demonstrated a lower mitochondrial mass (6385 ± 1962 a.u. vs. 7608 ± 2328 a.u., p < 0.05) and mitochondrial membrane potential (11426 ± 3861 a.u. vs. 14017 ± 5536 a.u., p < 0.05) in obese adolescents compared with lean adolescents. These results are even more pronounced in adolescents with obese mothers.
Conclusion: In obese adolescents, the increased TSH and lowered VO2 propose a lowered basal metabolic rate and the impaired mitochondrial function suggests a decreased thyroid hormone stimulation of mitochondrial energy production. The maternal in-heritage is suggestive of a basal metabolic defect or mitochondrial resistance for TH.