Fig. 7: Inhibition of Gal3 improves GSIS and glucose homeostasis in db/db mice.

a–c Effect of Gal3 (80 ng/ml, 1 h) and Gal3 inhibitors GB1107 (1 μM, 1 h), TD139 (1 μM, 1 h) (a) and Cpd47 (1 μM, 1 h) (b) and Gal3 neutralizing antibody (Ab) (1 μM, 1 h) (c) on GSIS in MIN6 cells. n = 6 (a), n = 5 (b), n = 4 (c) biologically independent cell samples). d Effects of Gal3 (80 ng/ml, 30 min) and GB1107 (1 μM, 30 min) on high glucose (16.8 mM) stimulated calcium signals in MIN6 cells. e, Peak value of cytosolic calcium transient in MIN6 with or without Gal3 (80 ng/ml, 30 min) and GB1107 (1 μM, 30 min). n = 20 cells (d, e). f–l Experimental scheme (f), body weight (g), IPGTT (h), AUC of GTTs (i), ITT (j), in vivo GSIS (k), and GSIS of isolated primary islets (l) in db/db mice treated with GB1107 (10 mg/kg). n = 10 mice (f–k), n = 5 Vehicle and n = 6 GB1107 biologically independent samples (l). m Experimental scheme of db/db mice by Gal3 antibody injection. At the age of 5 weeks, db/db mice were intravenously injected with Gal3 antibodies every 3 days for a total of 5 consecutive injections. Additional injections were administered at the 13th and 14th weeks. n–q Body weight (n, n = 10 mice), IPGTT (15 weeks of age) (o, n = 9 mice), and GSIS in primary islets (16 weeks of age) (p, n = 4 biologically independent samples) from db/db mice. q LGALS3 gene expression in primary islets from healthy persons and diabetic patients (n = 7 biologically independent samples). r, s GSIS in human primary islets from healthy persons (r) and diabetic patients (s) with hGal3 (250 ng/ml, 6 h) treatment. t GSIS in islets from healthy persons after hGal3 (250 ng/ml, 6 h) and Gal3 inhibitor Cpd47 (1 μM, 6 h) treatment. n = 5 (r–t) biologically independent samples). Data were analyzed by two-sided Student’s t-test without adjustments for multiple comparisons. All data are presented as the mean ± SEM. Source data are provided as Source Data file. Mice information (g–l) was same with (f).