Download Control of Blood Glucose

Endocrine System
(part 2)
Keri Muma
Bio 6
Pancreas


Located behind the stomach
Has both exocrine and endocrine functions
Pancreas


Acinar cells – exocrine cells that produce
digestive enzymes that are secreted into the
duodenum
The endocrine cells are organized into the islets
of Langerhans


Alpha () cells that produce glucagon
Beta () cells that produce insulin
Control of Blood Glucose

Insulin and glucagon act as
antagonistic hormones to
control blood glucose levels

Most of the time both of
these hormones are found
in the blood, it is the ratio of
the two that determines
which is dominant
Absorptive State

Metabolic fuels are stored during the
absorptive state (fed state). This occurs
when ingested nutrients are being
absorbed into the blood.



Circulating glucose is used for energy or is
stored as glycogen in the liver and skeletal
muscles.
Excess circulating fatty acids are stored into
triglycerides, mainly in adipose tissue.
Excess amino acids not needed for protein
synthesis and excess glucose are converted to
fatty acids and stored as triglycerides in
adipose tissue.
Postabsorptive State

When blood glucose drops during the
postabsorptive state (fasting state between
meals) glycogen is broken down into
glucose

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Many body cells will burn fatty acids to spare
glucose for the brain.
To supply the brain, amino acids can be
converted to glucose by gluconeogenesis.
Insulin


Insulin lowers blood glucose, fatty acid, and
amino acid levels and promotes their storage.
Insulin’s effects:

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Enhances transport of glucose into body cells
Stimulates glycogenesis in skeletal muscle and liver
cells
Promotes the transport of amino acids into cells for
protein synthesis.
Promotes the transport of fatty acids into adipocytes
Inhibits metabolic activity that would increase blood
glucose levels: glycogenolysis, gluconeogenisis, and
lipolysis
Glucose Transporters

Glucose transporters are plasma membrane
carriers that facilitate the passive diffusion of
glucose into cells.

Some are insulin independent – do not require
insulin for transporters to be present in the
membrane


Brain, working muscles, liver, digestive mucosa,
pancreas B-cells
Most are insulin dependent – present in the
membrane when insulin binds to cell receptors

The case in most cells especially resting muscle
and adipose tissue
Glucose Transporters

Insulin promotes up regulation of GLUT 4


Glucose transporters are contained in intracellular
vesicles and are inserted into the plasma membrane
when insulin is present
10 – 30X increase in glucose uptake
Glucagon

Glucagon secretion increases when the blood
concentration of glucose is too low.


It increases blood glucose levels
Its major target is the liver, where it promotes:



Glycogenolysis – the breakdown of glycogen to
glucose
Gluconeogenesis – synthesis of glucose from
lactic acid and noncarbohydrates
Promotes fat metabolism (lipolysis)
Summary of hormones controlling
blood glucose:


Growth hormone, cortisol, epinephrine, and
glucagon all increase blood glucose
Insulin is the only hormone that decreases
blood glucose
Diabetes Mellitus

Inadequate insulin action resulting in
hyperglycemia.

Type I diabetes mellitus is due to an insulin
deficiency


Autoimmune - destruction of Beta cells
Type II is due to the reduced sensitivity of
target cells to the presence of normal or
increased insulin

Lifestyle, diet and exercise
Consequences of Diabetes

The three cardinal signs of DM are:

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Polyuria – increased urine output due to glucosuria
and osmotic diuresis. Can lead to dehydration,
circulatory and renal failure
Polydipsia – excessive thirst
Polyphagia – excessive hunger and food
consumption
Consequences of Diabetes



Liver use of fatty acids leads to ketosis.
Acidosis develops and can depress brain
function.
Increase in protein degradation can reduce
growth and leads to the wasting of skeletal
muscles.
Long-term complications include
degenerative disorders of the vascular and
nervous systems.
Effects of Diabetes Mellitus
Blood Calcium Levels


Blood calcium levels affect many physiological
events including:
 neural and muscular excitability
 excitation-coupling in skeletal, cardiac, and
smooth muscle
 cell signaling
 blood clotting
Controlled by two hormones calcitonin and
parathyroid hormone
Parathyroid Glands


Tiny glands on the posterior side of the
thyroid
Secretes parathyroid hormone which
increase blood calcium levels
Effects of Parathyroid Hormone


PTH release:
 Stimulates osteoclasts to
digest bone matrix
 Enhances the reabsorption of
Ca2+ and the secretion of
phosphate by the kidneys
 Stimulates calcitriol synthesis
which increases absorption of
Ca2+ by intestinal mucosal
cells
Rising Ca2+ in the blood inhibits
PTH release
Interaction between PTH & Vit D
Calcitonin



Produced by the parafollicular, or C cells in the
thyroid gland
Lowers blood calcium levels
Antagonist to parathyroid hormone (PTH)
Calcitonin

Calcitonin targets the skeleton and kidneys,
where it:


Inhibits osteoclast activity thus the release of calcium
from the bone matrix
Increase renal Ca2+ excretion
Calcium disorders

Hypocalcemia - deficient PTH secretion

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Nervous system becomes hyperexcitable
Causes skeletal muscle tetany
Caused by autoimmune disease
Hypercalcemia - excess PTH secretion

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This reduces the excitability of skeletal muscle and
nervous tissue
Other effects are the thinning of bones and the
development of kidney stones.
May be caused by a tumor
Additional Endocrine Glands

Thymus
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Ovaries
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Thymosin – matures T-cells
Estrogen – female characteristics
Progesterone- works with
estrogen to maintain uterine cycle
Testes

Testosterone– male
characteristics
Additional Endocrine Glands

Adipocytes

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Leptin – decreases
food intake by acting
as a satiety factor
Stomach

Ghrenlin – increases
hunger