{Reference Type}: Journal Article
{Title}: Vitamin K-dependent carboxylation in β-cells and diabetes.
{Author}: Lacombe J;Ferron M;
{Journal}: Trends Endocrinol Metab
{Volume}: 35
{Issue}: 7
{Year}: 2024 Jul 29
{Factor}: 10.586
{DOI}: 10.1016/j.tem.2024.02.006
{Abstract}: Vitamin K is an essential micronutrient and a cofactor for the enzyme γ-glutamyl carboxylase, which adds a carboxyl group to specific glutamic acid residues in proteins transiting through the secretory pathway. Higher vitamin K intake has been linked to a reduced incidence of type 2 diabetes (T2D) in humans. Preclinical work suggests that this effect depends on the γ-carboxylation of specific proteins in β-cells, including endoplasmic reticulum Gla protein (ERGP), implicated in the control of intracellular Ca2+ levels. In this review we discuss these recent advances linking vitamin K and glucose metabolism, and argue that identification of γ-carboxylated proteins in β-cells is pivotal to better understand how vitamin K protects from T2D and to design targeted therapies for this disease.