Galectin-3 (gal-3) has recently been shown to mediate insulin resistance in mice. Its deletion leads to insulin sensitization while its excess is associated with insulin resistance. We, thus, undertook an investigation into its role in the reversal of insulin resistance in three human models of insulin sensitization: (1) 6 months following bariatric surgery (RYGB) and weight loss in patients with morbid obesity; there was a reduction in BMI from 52.1±4.8 to 40.4±4.0 kg/m2 (p<0.001) and HOMA-IR fell from 7.1±1.1 to 2.1± 0.3 (p<0.001); (2) 12 weeks of pioglitazone (45mg/day) treatment in obese patients with type 2 diabetes, when HOMA-IR fell from 3.5±0.7 to 2.1±0.4; and (3) following 6 months of testosterone replacement in obese patients with type 2 diabetes and hypogonadotropic hypogonadism, when HOMA-IR fell from 4.2±0.9 to 2.7±0.4. Gal-3 levels at baseline were 7.6±1.1, 5.7±0.9 and 4.4±0.7ng/ml, respectively in the 3 groups. In all three models, there was no significant change plasma concentrations of gal-3 (8.0±1.2, 5.9±0.9 and 5.8±0.9ng/ml, respectively) following interventions. There was no change in the expression of gal-3 in peripheral blood mononuclear cells either. Thus, insulin sensitization in all three human models is not associated with any significant alteration in either plasma concentrations or cellular expression of gal-3. Our data do not support a key role for gal-3 in the pathogenesis of insulin resistance or its reversal.


P. Dandona: Advisory Panel; Self; AstraZeneca. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca. H. Ghanim: None. M.S. Shah: None. K. Green: None. A. Makdissi: Speaker's Bureau; Self; Eli Lilly and Company. A. Chaudhuri: Speaker's Bureau; Self; AstraZeneca, Eli Lilly and Company, Boehringer Ingelheim Pharmaceuticals, Inc., Merck & Co., Inc., Novo Nordisk Inc..

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