Transcript CONTROL OF THE ENDOCRINE SYSTEM

CONTROL OF THE ENDOCRINE SYSTEM
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NEGATIVE FEEBACK MECHANISM
Regulates the endocrine system through a negative-feedback
mechanism to maintain homeostasis.
Occurs when an increase in a substance inhibits the process leading
to the increase.
Works like a thermostat in a house keeping the temp. constant.
TSH stimulates the thyroid and is regulated by the hypothalamus
Causes it to release thyroxine and increase metabolism
When level of thyroxine drops the cell’s metabolic activity drops
Hypothalamus is sensitive to body temp. as well as thyroxine. How
would this affect metabolic rates?
HORMONE ACTION (Polypeptide and Steroid Hormones)
Polypeptide: Large proteins composed of amino acids: thyroxine
Steroid: Lipids produced from cholesterol: progesterone
HORMONE ACTION
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Polypeptide: Don’t enter target cells; instead bind to receptors on the
cell membrane.
This activates enzymes on inner surface of membrane which convert
ATP into cAMP (cyclic AMP) 2nd mesenger (calcium ions are as well)
cAMP diffuses through membrane and activates other enzymes
Different target cells respond in different ways to the change in
cAMP levels, so cells may speed up or slow down.
Example: Adrenaline binds to liver cell membrane which
stimulates the break down of glucogen to glucose into bloodstream.
Steroid hormones: Can easily diffuse through lipid layer entering the
cytoplasm of target cells.
Attach to receptor cells of proteins forming a hormone-receptor
complex. Drifts through the cell until it reaches the cell nucleus.
Can affect gene expression by attaching tightly to gene sequences
that previously were not expressed. (dramatic changes)
PROSTAGLANDINS: LOCAL HORMONES
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Prostaglandins: Small amount of hormonelike substance produced in
other cells and tissues.
Originally found in the prostrate of males.
Fatty acids that function only within the same cells in which they are
produced. (local hormones)
Effects:
Ability to cause contractions in smooth muscles: uterus, bronchioles
Sensation of pain: Aspirin stops the synthesis of pain-causing
prostaglandins.