Background and Aims: Galectin-3, a member of the multifunctional galectin family, is ubiquitously expressed and acts a broad-spectrum biological response modifier. It is involved in tissue fibrosis, tumorigenesis, immunity and inflammatory response. It can also act as a receptor for advanced glycation end products. Recent evidence suggests that galectin-3 is associated with heart failure and with progression of nephropathy in type 2 diabetes. We have therefore evaluated whether serum galectin-3 level is associated with all-cause mortality in patients with type 2 diabetes.

Materials and Methods: Galectin-3 was measured in the baseline serum samples by ELISA in 1495 type 2 diabetic patients followed up in a teaching hospital specialist diabetes clinic. All-cause mortality was ascertained from hospital electronic medical records.

Results: The mean age of the subjects was 55.3 ± 9.9 years and 54% were male. During a median follow-up of 11 years, 169 subjects died from all causes, and baseline serum galectin-3 levels were significantly higher in subjects with a fatal outcome (9.86 ± 3.11 ng/ml vs. 8.15 ± 2.73, p<0.01). When galectin-3 was analyzed as quartiles, individuals in the third quartile [hazard ratio (HR) 2.0, 95% confidence interval (CI) 1.2-3.2, p<0.01] and the highest quartile (HR 3.9, 95% CI 2.6-6.0, p<0.01) had significantly elevated risk of a fatal outcome compared to those in the lowest quartile. Multivariable Cox regression analysis showed a significant association between serum galectin-3 level and all-cause mortality and the association remained significant even after adjustment for potential confounders including age, sex, body mass index, duration of diabetes, smoking, baseline HbA1c, systolic blood pressure, LDL and albuminuria status.

Conclusion: Elevated serum galectin-3 level was independently associated with all-cause mortality in patients with type 2 diabetes. Galectin-3 may potentially be useful as a predictor of adverse outcome.


K.C.B. Tan: None. S. Shiu: None. J.K.Y. Lam: None. A.C. Lee: None. Y. Wong: None.

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