Annals of medicine · 2026
Serum advanced glycation end-products as a biomarker of cumulative glycaemic burden and complications in type 2 diabetes: a pilot study.
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Lin Xiuqin, Lv Danping, Meng Weifeng, Wang Panpan, Zhang Xinyuan
Аннотация
BACKGROUND: Advanced glycation end products (AGEs) link chronic hyperglycaemia to diabetic tissue damage. Serum AGE concentrations across the metabolic disease spectrum, from prediabetes through complicated diabetes, remain incompletely characterized, including the contribution of isolated dyslipidaemia.
OBJECTIVE: To quantify serum AGEs across metabolic states and evaluate their biomarker potential for disease staging and complication risk stratification.
METHODS: Cross-sectional study of 226 adults in five groups: healthy controls, isolated hyperlipidaemia, impaired glucose tolerance, uncomplicated type 2 diabetes, and complicated type 2 diabetes. Serum AGEs were measured by ELISA. Group differences were assessed by Kruskal-Wallis tests, logistic regression, and receiver operating characteristic analysis.
RESULTS: Serum AGEs increased progressively across groups (Kruskal-Wallis H = 79.95, p < .001). Compared with healthy controls (median 5.99 AU), AGEs showed a trend in impaired glucose tolerance (7.22 AU; Cohen's d = 0.425; uncorrected p = .037, corrected p = .094), significant increases in uncomplicated diabetes (9.81 AU; d = 1.027, p < .001) and complicated diabetes (13.35 AU; d = 1.540, p < .001), with no elevation in isolated hyperlipidaemia (5.86 AU; p = .987). AGEs discriminated uncomplicated from complicated diabetes (d = 0.802, p < .001) where HbA1c (d = 0.022, p = .706) and fasting glucose (d = 0.023, p = .908) did not. ROC analysis showed excellent discrimination of complicated diabetes from controls (AUC = 0.908, 95% CI [0.834-0.970]). AGEs remained an independent predictor of complicated diabetes (adjusted OR = 4.92, p = .002) and correlated with complication burden (ρ = 0.332, p = .016).
CONCLUSION: Serum AGEs rise progressively from prediabetes to complicated diabetes, driven by hyperglycaemia. Their discriminative capacity where conventional glycaemic markers plateau supports AGEs as a complementary biomarker for complication risk stratification, pending validation.
OBJECTIVE: To quantify serum AGEs across metabolic states and evaluate their biomarker potential for disease staging and complication risk stratification.
METHODS: Cross-sectional study of 226 adults in five groups: healthy controls, isolated hyperlipidaemia, impaired glucose tolerance, uncomplicated type 2 diabetes, and complicated type 2 diabetes. Serum AGEs were measured by ELISA. Group differences were assessed by Kruskal-Wallis tests, logistic regression, and receiver operating characteristic analysis.
RESULTS: Serum AGEs increased progressively across groups (Kruskal-Wallis H = 79.95, p < .001). Compared with healthy controls (median 5.99 AU), AGEs showed a trend in impaired glucose tolerance (7.22 AU; Cohen's d = 0.425; uncorrected p = .037, corrected p = .094), significant increases in uncomplicated diabetes (9.81 AU; d = 1.027, p < .001) and complicated diabetes (13.35 AU; d = 1.540, p < .001), with no elevation in isolated hyperlipidaemia (5.86 AU; p = .987). AGEs discriminated uncomplicated from complicated diabetes (d = 0.802, p < .001) where HbA1c (d = 0.022, p = .706) and fasting glucose (d = 0.023, p = .908) did not. ROC analysis showed excellent discrimination of complicated diabetes from controls (AUC = 0.908, 95% CI [0.834-0.970]). AGEs remained an independent predictor of complicated diabetes (adjusted OR = 4.92, p = .002) and correlated with complication burden (ρ = 0.332, p = .016).
CONCLUSION: Serum AGEs rise progressively from prediabetes to complicated diabetes, driven by hyperglycaemia. Their discriminative capacity where conventional glycaemic markers plateau supports AGEs as a complementary biomarker for complication risk stratification, pending validation.