STUDY UNIT 5
Pancreas Hormones (CH 79)
OUTCOMES:
 Analyse the physiological anatomy of the pancreas
 Know and describe the structure, synthesis, regulation of secretion and
cellular effects of insulin
 Describe the structure, synthesis, regulation of secretion and cellular effects
of glucagon
 Know the regulation of secretion and effects of somatostatin
5.1 Pancreas anatomy
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12-15 cm long, 4 cm wide
J-shaped, greyish-pink, soft glandular
5.2. Insulin
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Insulin is associated with energy abundance
Plays a role in storing excess energy (glucose)
Insulin stimulates the uptake of excess carbohydrates to be
converted to fats and stored in the adipose tissue
Involved in uptake of amino acids(AA) + conversion to
proteins
Structure & Synthesis:
 Composed of 2 AA chains (disulfide linkages)
 Functional activity lost when linkage breaks
 Synthesised in Beta cells (protein synthesis) [translationribosomes (preproinsulin) - ER cleaves = (proinsulin: 3
peptide chains (A,B,C)) - Golgi cleaves more = insulin (A +
B connected by disulfide link, C peptide extra)
 C peptide has no insulin activity, It binds to G-proteincoupled membrane receptor and activates Sodiumpotassium adenosine triphosphatase and Endothelial nitric
oxide synthase.
 Insulin halflife: 6mins (NB to rapidly turn off insulin control
functions)
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Insulinasw degrades insulin mainly present in liver
Regulation
 Initiation starts when insulin binds to a membrane
receptor protein
 Insulin receptor: 4 subunits, two alpha (outside), two
beta subunits (inside), disulfide links
 Enzyme-linked receptor, coz beta subunit is
autophosphorylated
 Insulin uses IRS types to direct effects on
carbohydrates, fats and protein activities
1. As soon as insulin binds, 80% cells increase uptake of
glucose (mostly adipose and muscle cells; not neurons)
- translocation in vesicles.
Glucose is phosphorylated and becomes carbohydrates
2. Cell membranes permeable to AA, K+, PO4-3 (increase transport)
3. 10-15 min slow effects (due to phosphorylation of enzymes)
4. Slow translation, transcription and overall cell activity
Effects on Carbohydrate, Fats & Protein Metabolism
 Heavy meal - glucose uptake - insulin secreted - more glucose uptake for
storage and use
 Promotes Muscle glucose uptake (increased permeability when not at rest)
(highest during exercise and after a meal)
 Promotes liver uptake, storage & use of glucose (causes glucose to be stored
as glycogen; inactivates liver phosphorylase; enhanced uptake & trapped
(enzyme glucokinase increased activity); [phosphorylated glucose cant exit
cell]; increased glycogen synthesis
 No effect on Brain: most brain cells are permeable to glucose and don’t need
insulin to initiate usage
 Carbohydrate metabolism in other cells: glucose in adipose used for glycerol
part of fat moles (indirectly deposition of fats)
 Effect on fats is long term but still NB, promotes fat synthesis and storage;
occurs in the liver; glucose - pyruvate - acetyl coenzyme A - fatty acids
(FA)(first stage of FA synthesis); storage fat: triglycerides
 Insulin deficiency uses fat for energy; lipolysis of FA; increased plasma and
cholesterol, phospholipid concentration
 Protein metabolism: promotes protein synthesis & storage; insulin promotes
AA uptake (valine, leucine, isoleucine, tyrosine and phenylalanine); increases
translation; later increased transcription; inhibits catabolism of proteins (less
AA leaves cell);