G-protein coupled receptor for glucagon that plays a central role in the regulation of blood glucose levels and glucose homeostasis. Regulates the rate of hepatic glucose production by promoting glycogen hydrolysis and gluconeogenesis. Plays an important role in mediating the responses to fasting. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Promotes activation of adenylate cyclase. Besides, plays a role in signaling via a phosphatidylinositol-calcium second messenger system. Is rapidly internalized after ligand-binding. Expressed predominantly in liver, kidney, adrenal, lung and stomach, while lower levels of expression are detected in brown and white adipose tissue, cerebellum, duodenum and heart. Ligand-binding promotes phosphorylation of serine residues in the C-terminal cytoplasmic domain. Phosphorylation is important for receptor endocytosis after ligand-binding (By similarity). Mice are born at the expected Mendelian rate. They display pancreas islet and alpha-cell hyperplasia and increased glucagon levels, but normal insulin levels. Mice display low blood glucose levels combined with increased hepatic glycogen levels. They develop severe hypoglycemia after prolonged fasting. Mutant mice are fertile, but the females produce only few pups; half of the embryos die before birth, and liveborn pups do not survive more than one day. These pups are much smaller than their littermates and exhibit severe hypoglycemia. Belongs to the G-protein coupled receptor 2 family.