Galectin-1 impacts on glucose homeostasis by modulating pancreatic insulin release

VICTORIA SUNDBLAD; ISABEL GARCIA-TORNADU; ANA ORSTEIN; VERONICA MARTINEZ ALLO; RODRIGO LORENZO; SABRINA GATTO; ROSA MORALES; JULIAN GAMBARTE-TUDELA; MONTANA MANSELLE COCCO; DIEGO CROCI; DAMASIA BECU-VILLALOBOS (*); GABRIEL RABINOVICH (*)

GLYCOBIOLOGY

OXFORD UNIV PRESS INC

Lugar: Oxford; Año: 2021 p. 908 - 915

0959-6658

Type-2 diabetes mellitus (T2DM) is an expanding global health problem, involving defectiveinsulin secretion by pancreatic β-cells and peripheral insulin resistance, leading to impairedglucose regulation. Galectin-1, an endogenous lectin with affinity for N-acetyllactosamine(LacNAc)-containing glycans, has emerged as a regulator of inflammatory and metabolicdisorders. However, the role of galectin-1 in glucose homeostasis and pancreatic β-cellfunction, independently of hypercaloric diets, has not been explored. Here, we identified aphenotype compatible with T2DM, involving alterations in glucose metabolism andpancreatic insulin release, in female but not male mice lacking galectin-1 (Lgals1-/-).Compared with age-matched controls, Lgals1-/ female mice exhibited higher body weightand increased food intake ad libitum as well as after fasting and acute re-feeding. Althoughfasted serum insulin levels and insulin sensitivity were similar in both genotypes, Lgals1-/-female mice presented altered glucose tolerance and higher basal glucose levels dependingon the fasting period. Insulin response to glucose overload was impaired, while pancreaticinsulin content was enhanced in the absence of galectin-1. Accordingly, recombinantgalectin-1 enhanced glucose-stimulated insulin release in vitro. Our study identifies a role forgalectin-1 in regulating glucose metabolism through modulation of pancreatic insulinsecretion, highlighting novel opportunities to control T2DM.