Alejandra Tomás

This study investigates the human Glp1r A316T variant's effects on glucose metabolism and GLP-1RA responses using mouse models and structural analyses.

This study shows that lipid droplet accumulation promotes NLRP3 inflammasome activation through glutamine-dependent metabolic reprogramming in macrophages.

The paper uses molecular dynamics simulations and FRET assays to study lipid interactions with class B1 GPCRs, revealing state-dependent and conserved lipid binding patterns.

This study shows GLP-1R agonists improve mitochondrial health in beta-cells by forming a complex with VAPB and SPHKAP at ER-mitochondria MCSs, leading to mitochondrial remodelling and improved function.

This study shows that phosphorylation of specific C-terminal serine doublets in the GLP-1R is critical for receptor signaling in β-cells, with basal phosphorylation influencing receptor dynamics and signaling outcomes.

This paper describes the synthesis and properties of a novel dual GLP-1R/GIPR agonist, HISHS-2001, showing improved pharmacological profile compared to tirzepatide in vitro and in vivo.

This study identifies and validates cholesterol binding sites on GLP-1R in pancreatic beta cells, showing their role in receptor function and potential for drug design.

This study evaluates the impact of an N-terminal Halo-tag on GIPR function in mice, finding reduced cAMP responses and impaired glucose tolerance in tagged mice.

This study identifies miR-125b-5p as a glucose-regulated miRNA that negatively regulates β-cell function by modulating organelle dynamics and insulin secretion.

This paper shows that deleting Mfn1 and Mfn2 in beta cells impairs mitochondrial structure and insulin secretion, but incretins can partially compensate through EPAC2 signaling.

This study performs a GWAS on random glucose measurements in 493,036 individuals, identifying 128 loci associated with glycaemic traits and providing insights into diabetes biology and treatment.

This study identifies DRP1-mediated mitochondrial dynamics as a regulator of apoptotic response during embryonic differentiation in mouse cells.

This study identifies miR-7-mediated repression of Brg1 as a driver of β-cell dedifferentiation through EMT, leading to fibrosis and impaired glucose tolerance in diabetes.