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Role of the Pancreas Structure and Endocrine Function

Anatomy:

1) Head of
pancreas
2) Ucinate
Process
3) Pancreatic
notch
4) Body of
pancreas
5) Anterior
surface
6) Inferior
surface
7) Superior

The pancreas is found mostly


posterior to the stomach
spanning the posterior
abdominal wall from the
duodenum (right) to the
spleen (left.) The Pancreas is
divided into a head, ucinate
process, neck, body and tail.
The pancreatic duct exists to
allow the supply of

The major pancreatic


hormones, insulin and
glucagon are
responsible for
regulating metabolism.
Together they
manipulate the
disposition of nutrients
from meals whilst also
controlling the amount
of endogenous
substrates released

Glucose
Amino Acids
Free fatty
acids
Potassium
Stimulate
uptake,
metabolism and
storage

Insulin

The insulin feedback loop:3

Stimulate
Secretion

Insulin secretion is
controlled by a feedback
loop with exogenous
nutrient supply. Release of
insulin in response to
nutrient inflow promotes
utilisation of the new
nutrients whilst inhibiting
the usage of endogenous
substrates.
When nutrient intake is
low, insulin secretion is
diminished and this allows

Insulin has several actions:

Stimulates the uptake of glucose


by cells and promotes its storage
as glycogen
Encourages fat storage
Stimulates protein storage
Regulates the concentrations of
cations and anions in the plasma
Increases thermogenesis (by
glycogen formation)

Glucagon is produced and released in


the response to diminishing plasma
glucose levels (and low insulin
[paracrine feedback loop within the
islet]).
Glucagon is inhibited by high levels of
free fatty acids, glucose and insulin.
Glucagon frees glucose by increasing
hepatic glycogenolysis and

The Glucagon feedback


loops:5
Conversi
on

Release

Amino
Acids
Glucose
FFAs
Ketoacids

Glucag
on

Suppress
es
Secretio

Increas
es

Carbohydrate Metabolism:
This begins with ingestion of food stuffs containing starches; plant starch
amylopectin is the most abundant source of carbohydrate in the human diet. 6 amylases found in the saliva and pancreatic juices begin the digestion of starch
(a polymer of glucose.) The salivary amylase can only break down the polymer
into smaller polymers such as maltose and this breakdown in incomplete. Further
hydrolysis occurs in the duodenum (as salivary amylase is denatured in the
stomach.) Here, within ten minutes all starch is broken down into, maltose,
maltortoise and -limit dextrins.
After this, enzymes in the brush border of the duodenum and jejunem are
utilised. This enzymes include lactase, sucrase, and isomaltase. The duodenum
and upper jejunem have the highest capacity for absorption of sugars.
As you are aware, sugars are essential for the generation of adenosine
triphosphate. This involves the Embden-Meyerhof pathway (glycolysis) where
Pyruvate is formed in addition to two ATP and two NADH. The Pyruvate molecules
are then utilised in the Krebs cycle within the mitochondria.

The Physiological Changes in Diabetes:


In type one diabetes, abnormal insulin production is the result of genetics. The
disease belongs to a family of HLA associated autoimmune diseases including,
coeliac, Addisons and thyroid disease. The disease is polygenic and
autoantibodies are directed against pancreatic islets. The appearance of these
antibodies can predate disease onset by 10-15 years. The pancreatic islets are
infiltrated by mononuclear cells insulitis. Environmental factors such as dietary
constituents and exposure to enteroviruses such as Coxsackie B4 is suspected by
there is no definitive proof of this.7
In type two diabetes, there is a genetic component to the disease as confirmed
by twin studies. The genes suspected are those which control beta-cell
development and function. The condition develops when the body cannot secrete
enough insulin to meet demand. There is debate over whether the cause of the
disease is insulin resistance or secretory failure. Abdominal obesity and
deposition of intracellular triglyceride in the muscles and liver is thought to lead
to insulin resistance as it is known that the insulin receptor on the cell still
functions. Hyperglycaemia and excessive lipids are toxic to beta-cells and thus,
once the production/function of insulin is impaired, the will be continuous
damage to the islets and further deterioration in homeostatic glucose control. 8

References:
1) http://en.wikipedia.org/wiki/Pancreas 16/09/2011
2) Drake, R. Vogl, A. Mitchell, A. Greys Anatomy p320. Churchill Livingstone,
Elsvier 2010.
3) Berne, R. Levy, M. Principles of Physiology p508. Mosby 2000.
4) Berne, R. Levy, M. Principles of Physiology p510. Mosby 2000
5) Berne, R. Levy, M. Principles of Physiology p515. Mosby 2000
6) Berne, R. Levy, M. Principles of Physiology p515. Mosby 2000
7) Berne, R. Levy, M. Principles of Physiology p390. Mosby 2000
8) Kumar, P. Clare, M. Clinical Medicine VII Edition p1033. Saunders Elsevier
2009.
9) Kumar, P. Clare, M. Clinical Medicine VII Edition p1034. Saunders Elsevier
2009.