Genetic variation can modulate gene expression, and thereby phenotypic variation and
susceptibility to complex diseases such as type 2 diabetes (T2D). Here we harnessed the …

Genome-wide association studies have revealed >60 loci associated with type 2 diabetes (T2D),
but the underlying causal variants and functional mechanisms remain largely elusive. …

Normal glucose homeostasis is characterized by appropriate insulin secretion and low HbA1c.
Gene expression signatures associated with these two phenotypes could be essential for …

Dysregulation of gene expression in islets from patients with type 2 diabetes (T2D) might be
causally involved in the development of hyperglycemia, or it could develop as a …

Aims/hypothesis The G q -coupled 5-hydroxytryptamine 2B (5-HT 2B ) receptor is known to
regulate the proliferation of islet beta cells during pregnancy. However, the role of serotonin …

Glucose-stimulated insulin secretion is biphasic, with a rapid first phase and a slowly
developing sustained second phase; both are disturbed in type 2 diabetes (T2D). Biphasic …

Aims/hypothesis Pancreatic beta cell dysfunction is a prerequisite for the development of type
2 diabetes. Histone deacetylases (HDACs) may affect pancreatic endocrine function and …

Type 2 diabetes is triggered by reduced insulin production, caused by genetic and environmental
factors such as inflammation originating from the innate immune system. Complement …

The secretion of insulin and glucagon from the pancreas and the incretin hormones
glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) from the …

Characterization of gene expression in pancreatic islets and its alteration in type 2 diabetes (T2D)
are vital in understanding islet function and T2D pathogenesis. We leveraged RNA …