Volume 25, Issue 3 (7-2025)                   ijdld 2025, 25(3): 171-182 | Back to browse issues page


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Nezhadali M. Associations of Adipocytokines with Insulin Resistance and Type 2 Diabetes: A Review Study. ijdld 2025; 25 (3) :171-182
URL: http://ijdld.tums.ac.ir/article-1-6390-en.html
Department of Biology, IsI.C., Islamic Azad University, Islamshahr, Iran , ma-nejadali@yahoo.com
Abstract:   (2169 Views)
Background: Type 2 Diabetes Mellitus (T2DM) is a chronic metabolic disease characterized by insulin resistance and inadequate insulin secretion by pancreatic beta cells. Insulin resistance is the most important characteristic of T2DM, in which the peripheral tissues, including the liver, skeletal muscles, and adipose tissue, shows a lower response to the presence of insulin and insulin function is impaired. Adipose tissue, in addition to storing fat, synthesizes and secretes several bioactive peptides called adipokine and cytokine, which play an important role in regulating metabolism, inflammation, obesity and diabetes.
Methods: In the present study, searches were conducted in the Persian and Latin databases PubMed, Science Direct, Google Scholar, SID, and Magiran using keywords such as Diabetes, Insulin Resistance, Adipokine, Adiponectin, Leptin, Resistin, TNF-α, IL-6, RBP-4, Chemerin, Vaspin, Visfatin, Omentin, and Aplin to retrieve articles published from 2011 to 2024.
Results: The results indicated that adiponectin levels are reduced in patients with T2DM and insulin resistance. Elevated levels of leptin and retinol-binding protein-4 play a crucial role in the development of insulin resistance and T2DM. According to the evidence, adiponectin, resistin, TNF-α, interleukin-6, vaspin, and visfatin are associated with insulin resistance and T2DM. Contradictory results were found regarding the associations of omentin, apelin, and chemerin with insulin resistance and T2DM.
Conclusion: Adipocytokines may serve as biomarkers for predicting and early diagnosis of insulin resistance and T2DM. 
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Type of Study: Review | Subject: Special

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