Hindrik Mulder

This study uses hiPSC and hESC to model the MTNR1B risk variant's effect on β-cell function, finding increased MTNR1B protein and melatonin sensitivity in G-allele carriers.

This study shows lysine enhances insulin secretion through AASS-dependent catabolism, which regulates GABA content and mitochondrial function in beta cells.

The paper identifies a causal eQTL at MTIF3 associated with weight loss and shows MTIF3 deficiency affects adipocyte mitochondrial function and lipid metabolism.

The paper identifies splicing QTLs in human pancreatic islets that contribute to type 2 diabetes susceptibility by affecting gene splicing and revealing novel molecular mechanisms.

The paper introduces Islet Gene View (IGW), a platform that integrates gene expression and phenotypic data from pancreatic islets to explore T2D-related gene expression changes and their functional implications.

This study identifies DIMT1 as a regulator of ribosomal biogenesis in beta-cells, showing its role in mitochondrial function and insulin secretion, with implications for type 2 diabetes.

The paper creates TIGER, a resource integrating RNA-seq and genotyping data from human pancreatic islets to identify eQTLs and their associations with type 2 diabetes.

This study shows that mitochondrial Ca2+ clearance regulates insulin secretion by modulating plasma membrane Ca2+ entry in beta-cells.

The paper links altered mitochondrial metabolism to beta-cell dysfunction in type-2 diabetes by analyzing metabolites and gene expression in islets.