= Glucagon
{wiki}
<Glucagon> is a <peptide hormone> made by <alpha cells> in the <pancreatic islets>. Its mature <polypeptide> has 29 <amino acid residues>. <Alpha cells> store <glucagon> in <secretory granules> and release it by <exocytosis>. <Glucagon> is a message about fuel availability; <glucose> is the <sugar> whose supply it helps regulate. A falling <blood glucose> <concentration> favors <glucagon> release, whereas a rise usually suppresses it. <Amino acids> can also stimulate release, so a meal containing <protein> need not produce the same <hormone> pattern as a meal dominated by <carbohydrates>. <Endotext/Glucagon Physiology>{ref}
The principal <blood glucose>-raising target is the <liver>. In a <hepatocyte>, the <glucagon receptor> is a <G protein-coupled receptor>: activation of a stimulatory <G protein> drives <adenylyl cyclase>, increasing the <second messenger> <cAMP> and activating <protein kinase A>. Downstream <phosphorylation>, including the <phosphorylase kinase> relay to <glycogen phosphorylase>, favors <glycogenolysis>. <Glucagon> also supports <gluconeogenesis>. These are different supplies: <glycogenolysis> draws on a finite <glycogen> reserve, whereas <gluconeogenesis> makes <glucose> from other <substrates> and depends on their availability. Longer fasting depletes the <glycogen> reserve; a stronger <hormone> signal cannot release material that is no longer there. <Endotext/Glucagon Physiology>{ref} <Anatomy and Physiology 2e by J. Gordon Betts and others/17.9 The Endocrine Pancreas>{ref}
Do not copy the <liver> pathway into every target of <insulin>. <Skeletal muscle> uses its own <glycogen> reserve locally; its <glucose> uptake and the <liver>'s <glucose> output are different flows. Nor is direct <glucagon>-stimulated <lipolysis> in human <adipose tissue> as firmly established as its action in the <liver>. <Glucagon> action depends on the tissue, other <hormones>, and available <substrates>. <Endotext/Glucagon Physiology>{ref}
There is a useful surprise inside the <pancreatic islets>: local <glucagon> can support <insulin> release from neighboring <beta cells>. The <islet perifusion experiment> distinguishes that interaction from <glucagon>'s action on the <liver>. Thus the two <hormones> can oppose each other's effects on <blood glucose> while cooperating locally. <Delta cells> supply another local brake through <somatostatin>. <Intraislet glucagon signaling is critical for maintaining glucose homeostasis by Lu Zhu and others>{ref} <Anatomy and Physiology 2e by J. Gordon Betts and others/17.9 The Endocrine Pancreas>{ref}
Back to article page
