Editorial, Endocrinol Diabetes Res Vol: 11 Issue: 6

Thyroid Dysfunction and Insulin Resistance: Interactions Between Thyroid Hormones and Glucose Metabolism in Metabolic Health

Dr. Mohamed El-Sayed^*

Dept. of Internal Medicine, Cairo Biomedical University, Egypt

*Corresponding Author:

Dr. Mohamed El-Sayed
Dept. of Internal Medicine, Cairo Biomedical University, Egypt
E-mail: mohamed.elsayed@cbu.eg

Received: 01-Dec-2025, Manuscript No. ecdr-26-183235; Editor assigned: 4-Dec-2025, Pre-QC No. ecdr-26-183235 (PQ); Reviewed: 19-Dec-2025, ecdr-26-183235; Revised: 25-Dec-2025, Manuscript No. ecdr-26-183235 (R); Published: 31-Dec-2025, DOI: 10.4172/2324-8777.1000453

Citation: Mohamed E (2025) Thyroid Dysfunction and Insulin Resistance: Interactions Between Thyroid Hormones and Glucose Metabolism in Metabolic Health. Endocrinol Diabetes Res 11:453

Introduction

Thyroid hormones play a vital role in regulating energy balance, basal metabolic rate, and glucose and lipid metabolism. Disorders of thyroid function, including hypothyroidism and hyperthyroidism, are common endocrine conditions that can significantly influence metabolic health. Insulin resistance, a key pathophysiological feature of type 2 diabetes mellitus and metabolic syndrome, has been increasingly linked to abnormalities in thyroid hormone action. Understanding the relationship between thyroid dysfunction and insulin resistance is essential for early diagnosis and effective management of metabolic disorders [1,2].

Discussion

Thyroid hormones, primarily triiodothyronine (T3) and thyroxine (T4), influence glucose homeostasis through their effects on hepatic glucose production, insulin secretion, and peripheral glucose uptake. In hypothyroidism, reduced thyroid hormone levels are associated with decreased glucose utilization in skeletal muscle and adipose tissue, leading to impaired insulin-mediated glucose disposal. Additionally, hypothyroidism is often accompanied by weight gain, dyslipidemia, and increased visceral adiposity, all of which contribute to insulin resistance.

Hyperthyroidism also affects insulin sensitivity, though through different mechanisms. Excess thyroid hormones increase hepatic gluconeogenesis and intestinal glucose absorption, resulting in elevated blood glucose levels. Enhanced lipolysis and increased free fatty acid concentrations further impair insulin signaling in peripheral tissues. Although insulin secretion may initially increase to compensate, chronic hyperthyroidism can lead to β-cell stress and worsening glycemic control [3,4].

Subclinical thyroid dysfunction, characterized by abnormal thyroid-stimulating hormone (TSH) levels with normal circulating T3 and T4, has also been associated with insulin resistance. Elevated TSH may directly influence adipocyte function, inflammation, and insulin signaling pathways. Emerging evidence suggests that even mild thyroid hormone imbalances can have meaningful metabolic consequences [5].

Inflammation, oxidative stress, and altered adipokine secretion represent shared mechanisms linking thyroid dysfunction and insulin resistance. Leptin, adiponectin, and resistin levels are influenced by thyroid status and play important roles in modulating insulin sensitivity. Importantly, treatment of thyroid disorders has been shown to improve insulin sensitivity and glycemic parameters in many patients, underscoring the clinical relevance of this interaction.

However, the relationship between thyroid function and insulin resistance is complex and bidirectional. Insulin resistance itself may alter thyroid hormone metabolism and TSH regulation, creating a metabolic feedback loop that exacerbates disease progression.

Conclusion

Thyroid dysfunction and insulin resistance are closely interconnected through multiple hormonal and metabolic pathways. Both overt and subclinical thyroid disorders can impair insulin sensitivity and contribute to metabolic dysregulation. Recognizing and addressing thyroid abnormalities in individuals at risk of insulin resistance may improve metabolic outcomes and support integrated endocrine care.

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