What is it about?

Objectives: The mechanisms of obesity-associated thyroid dysfunction in children are incompletely deciphered. We aimed to evaluate whether visceral adipose tissue (VAT), insulin resistance (IR), inflammation, oxidative stress (OS) are involved in thyroid morpho-functional changes in pubertal obese children. Methods: We recruited 43 obese pubertal children without history of thyroid pathology. Metabolic and thyroid parameters (visceral fat thickness [VFT], waist/hip ratio [WHR], waist/ height ratio [WHtR], insulin, glucose, liver parameters, thyroid stimulation hormone [TSH], free thyroxine [FT4], free triiodothyronine [FT3], thyroid and abdominal ultrasonography) were evaluated. Serum monocyte chemoattractant protein-1 (MCP-1) and malondialdehyde (MDA) levels were quantified as markers of inflammation and OS. Results: VFT correlated positively both with WHR (p= 0.034) and the presence of thyroid nodules (p= 0.036). WHR associated with TSH (p= 0.005), FT3/FT4 (p= 0.033) and was independently associated with FT3/FT4 increase (p< 0.001). HOMA-IR increased with visceral obesity (waist circumference, p= 0.001; WHR, p= 0.018; WHtR: p< 0.001), hepatic impairment (alanine aminotransferase, p= 0.019) and hepatic steatosis (HS; p= 0.013) and correlated positively with FT3/FT4 (p= 0.036). TSH was significantly higher in subjects with HS versus those without HS (p= 0.007) and logistic regression analysis identified TSH as a risk factor for HS (p= 0.014). MDA correlated positively with MCP-1 (p= 0.021). Conclusion: VAT and IR may be responsible for changes in thyroid parameters associated with obesity: elevated TSH, FT3/FT4 levels and increased prevalence of thyroid nodules. WHR was predictive of increased FT3/FT4. In obese children, there is an interdependent relationship between HS and thyroid function.

Featured Image

Why is it important?

Increased visceral adiposity may be responsible for changes in thyroid parameters associated with obesity: increased levels of TSH, FT3/FT4, FT3, and frequency of thyroid nodules.WHR is a simple VAT measurement and a predictive factor for FT3/FT4 elevation. At the same time, ultrasound VFT measurement is a good indicator of the prevalence of thyroid nodules. FT3 and FT3/FT4 increase can be considered a reliable marker for the severity of metabolic damage represented by IR. The presence of HS was higher in IR patients and associated with increased TSH. Moreover, TSH was an independent factor associated with HS, supporting a bidirectional relationship between hepatic impairment and TSH elevation. Obese children had a lower prevalence of MS and IR than obese adults. Inflammation and OS were not involved in thyroid changes in obese children.

Perspectives

An exponential increase in childhood obesity at progressively younger ages is observed, leading to early metabolic comorbidities and severely impaired life quality in adulthood. Along with genetic predisposition, current determinants of obesity in children include an unbalanced and hypercaloric diet and a reduced physical activity . Excessive visceral adipose tissue (VAT) and/or insulin resistance (IR) associated with obesity interfere with thyroid function and morphology through mechanisms not yet completely understood. Although the impact of thyroid dysfunction on glucose, proteins, lipids, and basal metabolism is well established , the effect of obesity and IR on the hypothalamic-pituitary-thyroid (HPT) axis is still unclear. Obese children may present elevation in thyroid stimulating hormone (TSH) level with or without substantial oscillations in thyroid hormones (TH), and the normalization of these parameters after weight loss supports the hypothesis that changes in the HPT axis represent an effect rather than a cause of obesity

PhD, MD racataianu nicoleta
UMF Iuliu Hatieganu Cluj-Napoca Romania

Read the Original

This page is a summary of: Interplay between metabolic and thyroid parameters in obese pubertal children. Does visceral adipose tissue make the first move?, Acta Clinica Belgica, August 2019, Taylor & Francis,
DOI: 10.1080/17843286.2019.1660021.
You can read the full text:

Read

Contributors

The following have contributed to this page