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Thyroid function in obese children with non-alcoholic fatty liver disease

To investigate the relationships between thyroid function and metabolic risk factors in obese adolescents with non-alcoholic fatty liver disease (NAFLD). One hundred sixty obese adolescents and 40 control subjects were enrolled in the study. The obese subjects were divided into two groups based on p...

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Bibliographic Details
Published in:Journal of clinical research in pediatric endocrinology 2014-09, Vol.6 (3), p.152-157
Main Authors: Bilgin, Hüseyin, Pirgon, Özgür
Format: Article
Language:English
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Summary:To investigate the relationships between thyroid function and metabolic risk factors in obese adolescents with non-alcoholic fatty liver disease (NAFLD). One hundred sixty obese adolescents and 40 control subjects were enrolled in the study. The obese subjects were divided into two groups based on presence or absence of liver steatosis (NAFLD group and non-NAFLD group). Serum samples were assayed for glucose, insulin, cholesterol, alanine aminotransferase, aspartate aminotransferase, free thyroxine (fT4), free triiodothyronine (fT3) and thyroid-stimulating hormone (TSH). The ratio of fT3 to fT4 was evaluated as an indirect index of deiodinase activity. Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR) from fasting samples. NAFLD and non-NAFLD groups had slightly higher fasting blood glucose values than the control group. Fasting insulin levels in the NAFLD group were significantly higher than those in the non-NAFLD and control groups. The NAFLD group had significantly greater HOMA-IR values compared with the non-NAFLD group and also with the control group. The NAFLD group had significantly higher fT3/fT4 ratio values compared to both non-NAFLD and control groups. fT3/fT4 was positively correlated with serum insulin levels in the NAFLD group. This study showed that obese adolescents with hepatosteatosis had elevated values for fT3/fT4 ratio. This finding suggested a high conversion of T4 to T3 due to increased deiodinase activity as a compensatory mechanism for fat accumulation.
ISSN:1308-5727
1308-5735
DOI:10.4274/jcrpe.1488