C H A P T E R 3 8
Agents to control blood glucose levels
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release, blood glucose levels fall and insulin release
drops off. Sometimes, an insufficient amount of insulin
is released. This may occur because the pancreas cannot
produce enough insulin, the insulin receptor sites have
lost their sensitivity to insulin and they require more
insulin to lower glucose effectively or the person does
not have enough receptor sites to support his or her body
size, as in obesity.
Glucagon
Glucagon is released from the alpha cells in the islets
of Langerhans located in the pancreas in response to
low blood glucose levels. Glucagon causes an immediate
mobilisation of glycogen stored in the liver and raises
blood glucose levels.
Other factors affecting glucose control
Other factors in the body have been found to have an
impact on glucose, fat and protein metabolism. These
factors play a role in the overall energy balance in the
body.
Adipocytes, or fat cells, were once thought to just
store fat for energy. However, they have been found
to have a major impact on glucose and fat metabolism
throughout the body through the secretion of
adiponec-
tin
. This hormone acts to increase insulin sensitivity,
decrease the release of glucose from the liver and protect
the blood vessels from inflammatory changes. When adi-
ponectin levels are high, it exerts a protective effect on
the body. When adiponectin levels are low, as in cases
of intra-abdominal fat accumulation, glucose levels rise
and blood vessel injury increases.
Endocannabinoid receptors
have been identified in
the adipose tissue, muscles, liver, the satiety centre and
the GI tract. These receptors seem to be part of a sig-
nalling system within the body to keep the body in a
state of energy gain, to prepare for stressful situations.
When stimulated, these receptors promote food intake,
decrease adiponectin release, increase fat breakdown,
decrease insulin sensitivity, increase fat storage and alter
gastric emptying to promote greater nutrient absorption.
People who are obese have been shown to have increased
stimulation of these receptors.
The sympathetic nervous system, through noradren-
aline and adrenaline effects, directly causes a decrease
in insulin release, an increase in the release of stored
glucose and an increase in fat breakdown. A person
under stress will have increased glucose levels and
increased free fatty acids (FFAs) levels, which will
provide the energy needed for the immediate “fight or
flight” associated with a stress reaction. Prolonged stress
can alter the control of metabolism that regulates the
body’s energy balance.
Corticosteroids, which are released diurnally but
also during a stress reaction, decrease insulin sensitivity,
increase glucose release and decrease protein building.
All of these actions conserve energy and provide imme-
diate glucose for any stressful situation.
Growth hormone causes decreased insulin sensitiv-
ity, increase of FFAs and increase in protein building.
Fluctuating levels of growth hormone can upset the
metabolic homeostasis. Box 38.2 summarises effects of
various factors on blood glucose levels.
Loss of blood glucose control
When an insufficient amount of insulin is released or
insulin receptors are no longer responding, several
metabolic changes occur, beginning with hyperglycae-
mia, or increased blood sugar. Hyperglycaemia results
in
glycosuria
: Sugar is excreted into the urine because
the concentration of glucose in the blood is too high for
complete reabsorption. Because this sugar-rich urine is
an ideal environment for bacteria, cystitis is a common
finding. The person experiences fatigue because the
body’s cells cannot use the glucose that is there; they
need insulin to facilitate transport of the glucose into the
cells.
Polyphagia
(increased hunger) occurs because
the hypothalamic centres cannot take in glucose; thus
the cells sense that they are requiring glucose.
Polydipsia
Insulin
Decreases blood glucose; glycogen
storage; adipose tissue deposit;
synthesis of proteins to form amino
acids
Glucagon
Increases blood glucose
Somatostatin
Decreases insulin release; decreases
glucagon release; slows GI emptying
Growth hormone Decreases insulin sensitivity;
increases protein building; increases
free fatty acid formation
Incretins
Increases insulin release; decreases
glucagon release; stimulates satiety
centre; slows GI emptying
Adiponectin
Increases insulin sensitivity;
decreases glucose output from liver;
protects vessels from inflammatory
reactions
Catecholamines Decreases insulin release; increases
glucose output from liver and
muscles; increases breakdown of fat
to free fatty acids
Corticosteroids
Increases glucose output; decreases
insulin sensitivity
Endocannabinoid
system
Increases food intake by blocking
satiety signals; decreases adiponectin
release; decreases insulin sensitivity;
increases fat synthesis; alters gastric
motility
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BOX 38.2
Glucose control mechanisms
