Endocrine Abstracts

Background and aims: Diabetes causes tissue fibrosis by still poorly understood mechanisms which involve glycation products. Galectin-3 (Gal-3) is an emerging key player in metabolic disorders and a powerful factor in the development and progression of the fibrotic process in target organs in diabetic patients. The plasma level of Gal-3 increases during diabetic cardiomyopathy and diabetic nephropathy. We have studied the correlation between serum Gal-3 level and anti-diabetic treatment.

Methods: We carried out a cross-sectional study with an analytical aim. This work was carried out on type 2 diabetic patients followed in our department whose age range between 35 years and 80 years.

Results: On the therapeutic level, 11 patients (4.2%) were under hygieno-dietetic rules alone, 131 patients (50.4%) on oral anti-diabetics alone, 30 patients (11.5%) on insulin therapy alone and 88 patients (33.8%) on oral anti-diabetics and insulin therapy. For the oral treatment class, 207 patients (79.8%) were on metformin, 64 patients on sulfonylureas (24.6%), 13 patients (5%) on acarbose, 2 patients (0.8%) on glinide. We found a significant negative correlation of Gal-3 with metformin treatment (r=- 0.042; P=0.028).

Conclsions: We observed a significant inverse correlation between Gal-3 and metformin treatment and this effect was independent of BMI, HbA1c and CRP. Metformin reduces oxidative stress and the formation of AGEs (advanced glycation products). This may help lower serum Gal-3 levels. Metformin has also been shown to reduce Gal-3 in human adipocytes and monocytes indicating a direct effect of metformin against fibrosis. Metformin has been argued to exert a nephroprotective effect by attenuating renal fibrosis, as well as as an effect on reducing cardiac remodeling.