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Zinc and Adipose Organ Dysfunction: Molecular Insights into Obesity and Metabolic Disorders
Zahra Bahadoran1,2, Fateme Ghafouri-Taleghani3, Marijana Todorčević4
1Micronutrient Research Center, Research Institute for Endocrine Disorders, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. zahrabahadorabn@yahoo.com.
Purpose Of Review:
This review explores the emerging role of zinc (Zn) as a critical regulator of adipose organ structure and function, highlighting how Zn-related molecular networks contribute to the pathogenesis of obesity and associated metabolic disorders.
Recent Findings:
Experimental Zn-deficient models, and genetically-modified Zn-associated proteins, including Zn transporters [i.e., ZnTs (SLC30 family) and Zips (SLC39 family)], zinc-α2-glycoprotein (ZAG), metallothioneins (MTs), and zinc finger proteins (ZFPs), demonstrate that Zn is indispensable for maintaining adipose organ integrity. Loss of these proteins disrupts adipogenesis, promotes adipocyte hypertrophy, induces macrophage infiltration and M1 polarization, and drives pathological visceral fat expansion, resulting in systemic metabolic dysregulation. Zn plays a pivotal role in preserving adipose organ health and systemic metabolic balance. Further investigation is needed to elucidate depot-specific effects of Zn and the coordinated roles of Zn-handling proteins in adipose tissue, which may open new avenues for therapeutic strategies against obesity and metabolic diseases.
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