Taurine reduces the risk for metabolic syndrome: a systematic review and meta-analysis of randomized controlled trials

Metabolic syndrome (MetS) affects over one billion people and is diagnosed by abdominal obesity, elevated blood pressure, elevated fasting blood glucose (FBG), high triglycerides (TG), and low high-density lipoprotein cholesterol (HDL-C). MetS increases the risk of cardiovascular disease, stroke, and type 2 diabetes, with pathogenesis linked to insulin resistance, chronic inflammation, and neurohormonal activation. Taurine, a sulfur-containing amino acid abundant in many tissues, has roles in osmoregulation, mitochondrial function, membrane stability, antioxidative defense, and cation balance. It may modulate lipid metabolism (via bile salt conjugation), improve glycemic markers (FBG, insulin, HbA1c), and exert anti-inflammatory effects (e.g., renin-angiotensin system inhibition). Despite numerous clinical studies, findings are inconsistent. This meta-analysis of randomized controlled trials (RCTs) investigates whether taurine supplementation favorably modifies MetS diagnostic parameters (SBP, DBP, FBG, TG, HDL-C), addressing knowledge gaps regarding its efficacy and potential dose-response relationships.

Prior evidence suggests taurine may influence lipid and glucose metabolism, with animal and mechanistic studies indicating benefits via bile acid synthesis, LDL receptor activity, insulin clearance, and antioxidative pathways. Previous meta-analyses reported mixed outcomes: Guan et al. found no significant FBG difference between taurine and control groups, whereas Tao et al. (in diabetes populations) reported significant HbA1c reductions. The current work extends the literature by including broader populations, more trials involving diabetes, and conducting dose–response meta-regressions, which were not assessed comprehensively in earlier reviews.

The review followed PRISMA 2020 guidelines and was registered on Inplasy.com (INPLASY2023120081). Databases searched from inception to December 1, 2023, included Embase, PubMed, Web of Science, Cochrane CENTRAL, and ClinicalTrials.gov using terms: ("taurine" OR "taufon") AND ("metabolic syndrome" OR "diabetes mellitus" OR "obesity" OR "hypertension" OR "dyslipidemia" OR "hyperglycemia"). Titles/abstracts were screened and full texts assessed; reference lists and additional sources were checked. Inclusion criteria: RCTs using pure taurine or taurine compounds; comparator arms without taurine (e.g., placebo); data available for pre/post-intervention on at least one MetS-related outcome. Exclusion criteria: non-RCTs; trials without a comparator; follow-up <24 hours; trials using herbal treatments with unclear actives; missing endpoint data; or not investigating outcomes of interest. Quality appraisal used the Cochrane RoB 2 tool (per-protocol approach for intervention adherence). Primary outcomes: SBP, DBP, FBG, TG, HDL-C. Secondary outcomes: body weight (BW), BMI, total cholesterol (TC), LDL-C, HbA1c, HOMA, fasting insulin, and adverse effects. Data extraction was performed independently by two authors, including study design, participant characteristics, interventions, and outcomes post-intervention (using standard conversions and arm-merging per the Cochrane Handbook when needed). Statistical analysis used Comprehensive Meta-Analysis v3 with random-effects models. For continuous outcomes, weighted mean differences (WMD) with 95% CIs were calculated; for categorical adverse events, odds ratios with 95% CIs were used (continuity correction of 0.5 for zero cells). Heterogeneity was assessed with Cochran’s Q and I² (25%, 50%, 75% as low, moderate, high). Meta-regressions examined dose-response using total taurine dose (daily dose × duration) and daily dose. Sensitivity analyses removed one study at a time. Publication bias was evaluated using funnel plots and Egger’s test.

- Studies: 25 RCTs; 1,024 participants; conducted 1983–2021 across multiple countries. Taurine daily dose: 0.5–6 g/day; follow-up: 5–365 days. - Primary outcomes (Taurine vs control): • SBP: WMD −3.999 mmHg (95% CI −7.293 to −0.706), p=0.017; I²=84.949. Daily dose meta-regression significant (coefficient −1.1258 mmHg per g/day, p=0.0055); total dose not significant (coefficient −0.024 mmHg/g, p=0.113). • DBP: WMD −1.509 mmHg (95% CI −2.479 to −0.539), p=0.002; I²=14.077. Both total dose (−0.014 mmHg/g, p=0.026) and daily dose (−0.3247 mmHg per g/day, p=0.0182) significant. • FBG: WMD −5.882 mg/dL (95% CI −10.747 to −1.018), p=0.018; I²=75.457. Total dose significant (−0.495 mg/dL per g, p=0.0011); daily dose not (−1.5146 mg/dL per g/day, p=0.0703). • TG: WMD −18.315 mg/dL (95% CI −25.628 to −11.002), p<0.001; I²=35.539. Daily dose significant (−3.3600 mg/dL per g/day, p=0.0062); total dose not (−0.0522 mg/dL per g, p=0.0730). • HDL-C: WMD 0.644 mg/dL (95% CI −0.244 to 1.532), p=0.155; I²=7.655; no dose–response detected. Publication bias: none detected across primary outcomes (Egger’s p-values >0.05). - Secondary outcomes: • Body composition: BW WMD −0.642 kg (95% CI −1.494 to 0.209), p=0.139; BMI WMD −0.296 kg/m² (95% CI −0.889 to 0.296), p=0.327. • Lipids: TC WMD −8.305 mg/dL (95% CI −13.771 to −2.929), p=0.003; LDL-C WMD −6.495 mg/dL (95% CI −10.912 to −2.079), p=0.004. • Glycemic profile: HbA1c WMD −0.341% (95% CI −0.709 to −0.028), p=0.070; HOMA WMD −0.693 (95% CI −1.133 to −0.252), p=0.002; fasting insulin WMD −1.521 mU/L (95% CI −2.591 to −0.451), p=0.005. • Adverse events: no significant difference (OR 1.481, 95% CI 0.843–2.604, p=0.172).

Taurine supplementation significantly improved several MetS-related parameters: lowered SBP and DBP (with dose–response associations), reduced FBG (notably with higher total cumulative dose), and decreased TG (with daily dose response). HDL-C did not significantly change, though trends may still impact atherosclerosis risk. Mechanistically, blood pressure reductions may reflect enhanced nitric oxide availability and hydrogen sulfide production, improving vasodilation. Glycemic improvements likely involve reduced hepatic glucose output, modulation of glucagon, increased UCP1, enhanced insulin clearance via insulin-degrading enzyme, and support of beta-cell function; taurine may also increase adiponectin expression, improving insulin sensitivity. Compared with prior meta-analyses, this review found significant FBG reductions, possibly due to inclusion of more diabetes-focused studies where baseline hyperglycemia magnifies effects. Lipid improvements included reductions in TC and LDL-C, consistent with taurine’s roles in stimulating bile acid synthesis (via CYP7A1), enhancing LDL receptor activity, and facilitating cholesterol clearance. No significant changes in body weight or BMI were found, suggesting lifestyle interventions may have greater impact on weight. Safety analyses showed no increase in adverse events. Overall, findings support taurine as a complementary nutraceutical for mitigating MetS risk factors, with evidence of dose dependence for several outcomes.

Taurine supplementation favorably affects key MetS risk factors, significantly reducing SBP, DBP, FBG, and TG, and improving TC and LDL-C, with supportive dose–response relationships. While HDL-C and body composition changes were not significant, glycemic markers such as HOMA and fasting insulin improved, and safety was comparable to controls. Future research should determine optimal dosing and treatment duration, include longer follow-up, and enroll MetS-susceptible populations. Addressing variability in dosage, duration, sample size, disease severity, and participant characteristics will strengthen the evidence base and may inform clinical guideline development for taurine as an adjunct in MetS prevention and management.

- High heterogeneity for some outcomes due to varied populations (e.g., diabetes, obesity, cardiovascular disease, healthy participants) and protocols (dietary/exercise differences), potentially attenuating true effects. - Short intervention durations in most trials (often ≤2 months; few up to 1 year), limiting assessment of long-term efficacy and HbA1c changes. - Potential confounding from concurrent medications affecting lipid profiles (e.g., ACE inhibitors, diuretics, vasodilators) in cardiovascular populations. - Lack of direct waist circumference data; BMI used as a surrogate. - Variability in taurine dosage and total cumulative dose across studies; differing baseline risk levels may influence responsiveness. - Some studies lacked allocation concealment details, introducing some risk of bias. - Limited evidence in non-diabetic populations for HbA1c outcomes.