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Related Concept Videos

Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Type II Diabetes II: Pathophysiology01:24

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PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
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Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...

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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
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Insulin resistance in nodular thyroid disease.

Hamiyet Yilmaz Yasar1, Ozden Ertuğrul, Bülent Ertuğrul

  • 1Department of Endocrinology, Aydın State Hospital, Aydın, Turkey. drhamiyetyilmaz@yahoo.com

Endocrine Research
|October 7, 2011
PubMed
Summary

Insulin resistance is linked to larger thyroid nodules and increased thyroid volume in patients with euthyroid nodular goiter. This suggests insulin resistance may be a risk factor for developing this condition.

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Area of Science:

  • Endocrinology
  • Thyroidology
  • Metabolic Syndrome

Background:

  • Insulin exhibits mitogenic effects on thyroid cells.
  • Euthyroid nodular goiter is a common thyroid condition.
  • The role of insulin resistance in goiter development requires further investigation.

Purpose of the Study:

  • To investigate the association between insulin resistance and euthyroid nodular goiter.
  • To compare insulin resistance markers in patients with nodular thyroid disease versus healthy controls.

Main Methods:

  • Study included 63 patients with nodular thyroid disease and 83 healthy controls.
  • All subjects were euthyroid, euglycemic, and normotensive, with no prior risk factors for insulin resistance.
  • Evaluations included serum insulin, biochemical parameters, thyroid ultrasound, and fine needle aspiration biopsy for nodules >1cm.

Main Results:

  • Patients with nodular goiter had significantly higher HOMA (Homeostatic Model Assessment) scores, indicating insulin resistance (p=0.007).
  • Thyroid volume was significantly greater in the patient group (p=0.03).
  • A significant correlation was observed between HOMA and nodule volume (p<0.001).

Conclusions:

  • Insulin resistance may contribute to thyroid cell proliferation, nodule formation, and increased thyroid volume.
  • Insulin resistance is proposed as a potential risk factor for euthyroid nodular goiter.