Mild subclinical hypothyroidism (mSCH) in obese boys has drawn increasing attention due to its potential impact on growth and metabolism. Recent studies suggest a complex interplay between insulin – like growth factor (IGF – 1), metabolic parameters, and mSCH in this population.
IGF – 1: A Key Link in Growth – Metabolism Crosstalk
IGF – 1, primarily regulated by growth hormone, plays a central role in linear growth and metabolic homeostasis. In obese boys with mSCH (defined by elevated TSH with normal free T4), IGF – 1 levels often show a paradoxical decrease despite increased body mass. This reduction may stem from thyroid hormone – mediated suppression of hepatic IGF – 1 synthesis, as thyroid hormones enhance growth hormone receptor expression. Clinically, lower IGF – 1 correlates with impaired growth velocity and altered body composition, such as increased visceral fat.
Metabolic Parameters: Insulin Resistance and Lipid Dysregulation
Obesity – associated insulin resistance is a hallmark in this group. Studies show that mSCH exacerbates insulin resistance, as thyroid hormones directly influence glucose uptake and glycogen synthesis. Fasting insulin and HOMA – IR (homeostatic model assessment of insulin resistance) often correlate with TSH levels in obese boys with mSCH. Additionally, lipid profiles exhibit dysregulation: elevated total cholesterol, LDL – C, and triglycerides, alongside reduced HDL – C, which may be further worsened by thyroid hormone deficiency.
Mechanistic Insights: Inflammation and Adipokine Imbalance
Adipose tissue in obesity secretes proinflammatory cytokines (e.g., TNF – α, IL – 6), which interfere with thyroid hormone conversion (T4 to T3) and disrupt hypothalamic – pituitary – thyroid axis feedback. This inflammation may also suppress IGF – 1 signaling. Adipokines like leptin, elevated in obesity, can cross – regulate thyroid function by affecting TSH pulsatility, while adiponectin (reduced in obesity) may modulate IGF – 1 sensitivity.
Clinical Implications
The interplay between mSCH, IGF – 1, and metabolic parameters highlights the need for integrated monitoring in obese boys. While the threshold for thyroid hormone replacement in mSCH remains controversial, evidence suggests that treating boys with low IGF – 1 and severe insulin resistance may improve metabolic markers. Longitudinal studies are needed to clarify whether correcting mSCH can restore IGF – 1 – mediated growth and mitigate long – term metabolic risks.
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