ReviewBiological trace element research2026
Rethinking Zinc Requirements in Diabetes Mellitus: Comprehensive Review of Experimental and Clinical Studies Evidence.
Review in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Zinc deficiency in patients with type 2 diabetes increases risk of cardiovascular diseases: Tehran Lipid and Glucose Study.BMC cardiovascular disorders · 2026Article
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Authors and funding
1 author.
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Abstract
Dysregulated zinc homeostasis is a common feature of diabetes mellitus (DM), exacerbating β-cell dysfunction, impairing glycemic control, and promoting vascular, renal, neural, and cognitive complications. This review summarizes experimental and clinical evidence on hyperzincuria and impaired intestinal zinc absorption in type 1 (T1DM) and type 2 (T2DM) DM, focusing on their mechanisms and implications for revising dietary zinc recommendations. Experimental models showed tissue-specific zinc depletion, with pancreas, liver, and femur zinc levels reduced by 17-50%, while kidney, muscle, and intestine show variable changes depending on DM duration and dietary zinc. Radiolabeled zinc studies report a 53% reduction in intestinal uptake, while early-stage of DM may compensatory increase absorption up to ~ 70%. However, prolonged hyperglycemia and zinc transporter dysregulation (ZIP4/ZIP7/ZIP14 down, ZnT1/5/7 and metallothioneins up) cause persistent intracellular and systemic zinc depletion. Persistent urinary zinc (UZn) loss, a marker of disrupted zinc homeostasis in diabetes, increases 3- to 14-fold in T1DM models, 5- to 6-fold in db/db mice, and is 1.6- to 5-fold higher in humans with T1DM and 1.4- to 7-fold higher in T2DM. Hyperzincuria in DM is primarily driven by hyperglycemia-induced osmotic diuresis and glycosuria, exacerbated by diabetic nephropathy, proteinuria, and the use of certain antidiabetic and antihypertensive medications. Current zinc RDAs (8 mg/day for women, 11 mg/day for men) may be insufficient in diabetes, and a 30-50% higher intake could help restore zinc balance, improve glycemic control, and reduce the risk of complications. However, these estimates are based on experimental and observational data, and well-designed clinical studies are needed to confirm the optimal zinc intake in DM.
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