A hyperglycaemic principle was demonstrated to be present in the pancreatic islets just two years after the discovery of insulin in 1921. It was named ‘glucagon’. Glucagon is a single chain polypeptide containing 29 amino acids, MW 3500.
GLUCAGON
A
hyperglycaemic principle was demonstrated to be present in the pancreatic
islets just two years after the discovery of insulin in 1921. It was named
‘glucagon’. Glucagon is a single chain polypeptide containing 29 amino acids,
MW 3500. Beef and pork glucagon are identical to human glucagon. It is secreted
by the α cells of the islets
of Langerhans.
Like
insulin, glucagon is also derived by cleavage of
a larger peptide prohormone. Its secretion is regulated by glucose levels, other
nutrients, paracrine hormones and nervous system. Glucose has opposite effects
on insulin and glucagon release, i.e. high glucose level inhibits glucagon
secretion and it is more sensitive to orally administered glucose: suggesting
that the same gastrointestinal incretins which evoke insulin release may be
inhibiting glucagon secretion. FFA and ketone bodies also inhibit glucagon
release. Amino acids, however, induce both insulin and glucagon secretion.
Insulin, amylin and somatostatin, elaborated by the neighbouring β and D cells, inhibit
glucagon secretion. Sympathetic stimulation consistently and parasympathetic
stimulation under certain conditions evokes glucagon release.
Actions
Glucagon
is hyperglycaemic; most of its actions are opposite to that
of insulin. Glucagon causes hyperglycaemia primarily by enhancing
glycogenolysis and gluconeogenesis in liver; suppression of glucose utilization
in muscle and fat contributes modestly. It is considered to be the hormone of
fuel mobilization. Its secretion is increased during fasting: this serves to
maintain energy supply by mobilizing stored fat and carbohydrate as well as by
promoting gluconeogenesis in liver. It plays an essential role in the
development of diabetic ketoacidosis. Increased secretion of glucagon has been
shown to attend all forms of severe tissue injury.
Glucagon
increases the force and rate of cardiac contraction and this is not antagonized
by β blockers. It has a
relaxant action on the gut and inhibits gastric acid production.
Glucagon,
through its own receptor and coupling Gs
protein activates adenylyl cyclase and increases cAMP in liver, fat cells,
heart and other tissues; most of its actions are mediated through this cyclic
nucleotide.
Glucagon
is inactive orally; that released from pancreas is broken down in liver,
kidney, plasma and other tissues. Its t½ is 3–6 min.
Uses
1. Hypoglycaemia due to insulin or
oral hypoglycaemics; use of glucagon is secondary to that of glucose; only an
expedient measure. It may not work if hepatic glycogen is already depleted:
0.5–1 mg i.v. or i.m.
2. Cardiogenic shock to stimulate the
heart in β adrenergic blocker
treated patients. However, action is not very marked.
3.
Diagnosis of pheochromocytoma 1 mg i.v. causes release
of catecholamines from the tumour and markedly raises BP. Phentolamine should
be at hand to counter excessive rise in BP.
GLUCAGON 1 mg inj.
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