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Introduction
There is a concurrent increase in the incidence of thyroid carcinoma and obesity. Insulin resistance, adipokines, increased aromatase activity, inflammation, immunological response alterations, and oxidative stress have all been proposed as mechanisms for this association [1].
Metabolic syndrome (Mets) denotes problems constellation, including raised triglycerides, hypertension (HTN), low HDL cholesterol, insulin resistance, poor glucose tolerance, and abdominal obesity.
Incidence is rising in tandem with people number who are overweight or obese, with 25 percent of the Western population are expected to suffer from this condition [2].
Nodularity of thyroid tissue is extremely common, more than one-half of everyone living will acquire a thyroid nodule at some point in their life, and nodules appear to grow with age, because older persons have more nodules than younger ones [3].
Thyroid nodules (TNs) prevalence escalates with age, increasing from 2% and 2.7% in men and women aged 26 to 30, to 6.7% and 8.7% in those aged 36 to 40, 12.4% and 14.1% in individuals aged 45 to 50, and 14.5% and 18% in men and women over 55 years [4]. Another study reported that approximately 50% of individuals aged 65 years have thyroid nodules detected by ultrasonography [5]. And a cross-sectional survey of asymptomatic adults in Germany using ultrasonography to detect thyroid nodules demonstrated an even higher prevalence of 80% in women and 74% in men over 60 years old [6].
Concerning insulin resistance: the augmentation of cellular proliferation has been elucidated through various mechanisms; the initial phase involves mitogen-activated protein kinase (MAPK) pathway activation, and to counteract the inhibition and reinstate the phosphatidylinositide 3-kinase (PI3K) pathway, which is integral to insulin-mediated glucose regulation and is often blocked in insulin resistance. Second, through modifying the insulin like growth factor (IGF) system, insulin can have an indirect effect on carcinogenesis [7].
An increase in insulin levels causes insulin to attach to IGF-binding proteins, resulting in displacement and elevated free IGF1levels. Additionally, Insulin resistance is linked to increased IGF1 synthesis and decreased IGFBP synthesis in liver, resulting in higher amounts of bioactive IGF1. Additionally, it has recently been reported that insulin resistance and nodular thyroid disease are positively correlated [8].
Considering Mets prevalence in the elderly, which is associated with both type 2 diabetes mellitus(DM) and insulin resistance,...