Scholarlink

<p>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 <i>db/db</i> 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&#xa0;mg/day for women, 11&#xa0;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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Rethinking Zinc Requirements in Diabetes Mellitus: Comprehensive Review of Experimental and Clinical Studies Evidence

  • 期刊论文

  • 发表日期：

    2026年1月9日

查看全文
  • Zahra Bahadoran

摘要

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.