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Purpose of Review <p>This narrative review aims to synthesize evidence regarding plasma taurine concentrations in individuals with type 2 diabetes mellitus (T2DM), explore the underlying mechanisms involved and evaluate the therapeutic potential of taurine as an adjuvant treatment. Finally, it highlights key knowledge gaps and perspectives for future clinical research. Taurine, a sulfur-containing amino acid, exhibits notable antioxidant and anti-inflammatory properties. It plays essential roles in glucose homeostasis, osmoregulation, mitochondrial protection, and the neutralization of reactive and toxic compounds. T2DM, the most common form of diabetes, is characterized by insulin resistance, pancreatic β-cell dysfunction, low-grade systemic inflammation, and oxidative stress—factors that aggravate glucose dysregulation and cellular damage. Although lifestyle interventions are the cornerstone of T2DM management, there is growing interest in complementary therapies that target these molecular dysfunctions.</p> Recent Findings <p>Plasma taurine concentrations have been found to be reduced in individuals with T2DM, likely due to impaired reabsorption, increased renal excretion, and elevated tissue demand caused by hyperglycemia and chronic inflammation. Experimental studies suggest that taurine supplementation can enhance insulin secretion, improve insulin signaling via the PI3K/Akt pathway, and modulate GLP-1 release. Preliminary human trials also indicate improvements in insulin sensitivity and fasting glucose levels.</p> Summary <p> Taurine is essential for metabolic and cellular homeostasis, with reduced levels observed in individuals with type 2 diabetes. Emerging evidence suggests its supplementation may help counteract diabetes-related metabolic dysfunctions, supporting its potential as a complementary therapeutic strategy.</p>

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Taurine in Type 2 Diabetes: Plasma Concentrations, Metabolic Pathways, and Potential as a Therapeutic Adjuvant

  • 期刊论文

  • 发表日期：

    2025年11月11日

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  • Caroline Fogagnolo,
  • Gabriela Ueta Ortiz,
  • Sofia Germano Travieso,
  • Ana Claudia Rossini-Venturini,
  • Gabriela Ferreira Abud,
  • Bianca Monteiro Silva,
  • Adelino Sanchez Ramos da Silva,
  • Ellen Cristini de Freitas

摘要

Purpose of Review

This narrative review aims to synthesize evidence regarding plasma taurine concentrations in individuals with type 2 diabetes mellitus (T2DM), explore the underlying mechanisms involved and evaluate the therapeutic potential of taurine as an adjuvant treatment. Finally, it highlights key knowledge gaps and perspectives for future clinical research. Taurine, a sulfur-containing amino acid, exhibits notable antioxidant and anti-inflammatory properties. It plays essential roles in glucose homeostasis, osmoregulation, mitochondrial protection, and the neutralization of reactive and toxic compounds. T2DM, the most common form of diabetes, is characterized by insulin resistance, pancreatic β-cell dysfunction, low-grade systemic inflammation, and oxidative stress—factors that aggravate glucose dysregulation and cellular damage. Although lifestyle interventions are the cornerstone of T2DM management, there is growing interest in complementary therapies that target these molecular dysfunctions.

Recent Findings

Plasma taurine concentrations have been found to be reduced in individuals with T2DM, likely due to impaired reabsorption, increased renal excretion, and elevated tissue demand caused by hyperglycemia and chronic inflammation. Experimental studies suggest that taurine supplementation can enhance insulin secretion, improve insulin signaling via the PI3K/Akt pathway, and modulate GLP-1 release. Preliminary human trials also indicate improvements in insulin sensitivity and fasting glucose levels.

Summary

Taurine is essential for metabolic and cellular homeostasis, with reduced levels observed in individuals with type 2 diabetes. Emerging evidence suggests its supplementation may help counteract diabetes-related metabolic dysfunctions, supporting its potential as a complementary therapeutic strategy.