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Pancreas - Endocrine
Insulin
Insulin release:
Insulin effects:
Glucagon
Important enzymes and transports
Glucokinase
GLUT-2:
GLUT-4: (Insulin dependant organs)
GLUT-1 & 2: (Insulin independent organs)
Divided into Pancreatic islets (Islets of Langerhans), with
millions of islets found in the pancreas. This comprises
the endocrine portion of the pancreas
Beta cells —→ Insulin (found centrally in islets and
most abundant)
Alpha cells —→ Glucagon (found outer islets)
Delta cells —→ Somatostatin (found outer islets)
Insulin
Protein hormone synthesised by Beta cells
Synthesised as preproinsulin in rough ER, then
cleaved to proinsulin and transported to Golgi
apparatus and finally turned to insulin and c-peptide in
secretory granules
Pancreas - Endocrine 1
, C-peptide can be used as an indicator of insulin
production, as it has a higher half life than insulin
Insulin release:
Promotes glucose uptake in adipose (fat) and skeletal muscle
Promotes glycogen synthesis through glycogen synthase
Inhibits gluconeogenesis
Increased fatty acid synthesis
Stimulates protein synthesis.
Through stimulating entry of amino acids into cells
^ above important as side effect of insulin therapy is weight gain.
Lowers potassium, which is why insulin + glucose used to treat hyperkalemia
Enhanced the activity of Na-K-ATPase pump in skeletal muscle
Insulin effects:
Insulin release is glucose dependent, the
more glucose that enters beta cell, the
more insulin released.
Glucose enters beta cells via GLUT-2
ATP produced through Glucokinase and
other enzymes
ATP production closes potassium channels
Depolarisation of Beta cell as potassium
stuck in cell
voltage gated calcium channels to open
resulting influx of calcium within the cell,
causes exocytosis of stored insulin.
Pancreas - Endocrine 2
, Amino acids can trigger the release of insulin too.
Production of insulin inhibited by epinephrine (adrenaline), as it acts strongly on the
alpha-2 receptors, resulting in greater plasma glucose (fight or flight response)
Glucagon
Protein hormone which is synthesised by Alpha cells
Opposes the action of Insulin, and thus is released during low plasma glucose
levels.
Increases liver (not muscle) glycogen breakdown, which raises serum glucose
levels
Increases gluconeogenesis
Increases amino acid uptake in liver, so serum amino acid levels will fall.
Glucagon receptors found mostly in liver, most other tissue have lower densities of
glucagon receptors.
Glucagon receptors NOT found in skeletal muscles.
Important enzymes and transports
Glucokinase
Glucokinase is a Beta cell enzyme found in liver and pancreas, involved in first step
of glycolysis
Insulin activates glucokinase, and promotes transcription.
Works better with high glucose concentration (inactive when glucose levels low),
and can convert lots of glucose.
GLUT-2:
Pancreas - Endocrine 3
Pancreas - Endocrine
Insulin
Insulin release:
Insulin effects:
Glucagon
Important enzymes and transports
Glucokinase
GLUT-2:
GLUT-4: (Insulin dependant organs)
GLUT-1 & 2: (Insulin independent organs)
Divided into Pancreatic islets (Islets of Langerhans), with
millions of islets found in the pancreas. This comprises
the endocrine portion of the pancreas
Beta cells —→ Insulin (found centrally in islets and
most abundant)
Alpha cells —→ Glucagon (found outer islets)
Delta cells —→ Somatostatin (found outer islets)
Insulin
Protein hormone synthesised by Beta cells
Synthesised as preproinsulin in rough ER, then
cleaved to proinsulin and transported to Golgi
apparatus and finally turned to insulin and c-peptide in
secretory granules
Pancreas - Endocrine 1
, C-peptide can be used as an indicator of insulin
production, as it has a higher half life than insulin
Insulin release:
Promotes glucose uptake in adipose (fat) and skeletal muscle
Promotes glycogen synthesis through glycogen synthase
Inhibits gluconeogenesis
Increased fatty acid synthesis
Stimulates protein synthesis.
Through stimulating entry of amino acids into cells
^ above important as side effect of insulin therapy is weight gain.
Lowers potassium, which is why insulin + glucose used to treat hyperkalemia
Enhanced the activity of Na-K-ATPase pump in skeletal muscle
Insulin effects:
Insulin release is glucose dependent, the
more glucose that enters beta cell, the
more insulin released.
Glucose enters beta cells via GLUT-2
ATP produced through Glucokinase and
other enzymes
ATP production closes potassium channels
Depolarisation of Beta cell as potassium
stuck in cell
voltage gated calcium channels to open
resulting influx of calcium within the cell,
causes exocytosis of stored insulin.
Pancreas - Endocrine 2
, Amino acids can trigger the release of insulin too.
Production of insulin inhibited by epinephrine (adrenaline), as it acts strongly on the
alpha-2 receptors, resulting in greater plasma glucose (fight or flight response)
Glucagon
Protein hormone which is synthesised by Alpha cells
Opposes the action of Insulin, and thus is released during low plasma glucose
levels.
Increases liver (not muscle) glycogen breakdown, which raises serum glucose
levels
Increases gluconeogenesis
Increases amino acid uptake in liver, so serum amino acid levels will fall.
Glucagon receptors found mostly in liver, most other tissue have lower densities of
glucagon receptors.
Glucagon receptors NOT found in skeletal muscles.
Important enzymes and transports
Glucokinase
Glucokinase is a Beta cell enzyme found in liver and pancreas, involved in first step
of glycolysis
Insulin activates glucokinase, and promotes transcription.
Works better with high glucose concentration (inactive when glucose levels low),
and can convert lots of glucose.
GLUT-2:
Pancreas - Endocrine 3
