Download The Peripheral Endocrine Glands

Human Physiology – From Cells to Systems | 9e
Lauralee Sherwood
19
The Peripheral Endocrine
Glands
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2016. All Rights Reserved.
19.1 Thyroid Gland
• The major cells that secrete thyroid
hormone are organized into colloid-filled
follicles
– Interspersed in the interstitial spaces between
follicles are C cells, which secrete calcitonin
• Thyroid hormone is synthesized and
stored on the thyroglobulin molecule
– Most steps of thyroid hormone synthesis take
place on the thyroglobulin molecules within
the colloid
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Thyroid
follicular cell
Blood
Colloid
Golgi
complex
Endoplasmic
reticulum
I–
MIT
Tg
DIT
I–
I–
TPO
Active I–
(Deiodinase
action)
I–
I–
Lysosome
MIT DIT T3
T4
MIT
DIT
T3 , T4
Tg
MIT
DIT
T3
T4
1 MIT
2 DITs
1 DIT
T3 T
T3
4
T4
Thyroid
follicle
KEY
= Primary active transport
= Secondary active transport
(symporter)
Tg = Thyroglobulin
I– = Iodide
TPO = Thyroperoxidase
MIT = Monoiodotyrosine
Tyrosine-containing Tg produced within the thyroid follicular cells
by the endoplasmic reticulum–Golgi complex is transported by
exocytosis into the colloid.
Iodide is carried by secondary active transport from the blood into
the colloid by symporters in the basolateral membrane of the follicular
cells.
In the follicular cell, the iodide is oxidized to active form by TPO
at the luminal membrane.
DIT = Di-iodotyrosine
T3 = Tri-iodothyronine
T4 = Tetraiodothyronine
(thyroxine)
Attachment of two iodides to tyrosine yields DIT.
Coupling of one MIT and one DIT yields T3. Coupling of two DITs
yields T4.
On appropriate stimulation, the thyroid follicular cells engulf a
portion of Tg-containing colloid by phagocytosis.
Lysosomes attack the engulfed vesicle and split the iodinated
products from Tg.
The active iodide exits the cell through a luminal channel to enter
the colloid.
T3 and T4 diffuse into the blood (secretion).
Catalyzed by TPO, attachment of one iodide to tyrosine within
the Tg molecule yields MIT.
MIT and DIT are deiodinated, and the freed iodide is
recycled for synthesizing more hormone.
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Thyroid Hormone Secretions
• To secrete thyroid hormone, the follicular
cells phagocytize thyroglobulin-laden
colloid
– Thyroxine-binding globulin: a plasma protein
that selectively binds only thyroid hormone
• Transports most circulating T4 and T3
– About 90% of the secretory product released
from the thyroid gland is in the form of T4
• Most is converted into T3
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Effects of Thyroid Hormone
• Thyroid hormone increases the basal
metabolic rate and exerts other effects
– Effect on metabolic rate and heat production
• Increases the body’s overall basal metabolic rate
• Calorigenic effect: “heat-producing”
– Sympathomimetic effect
• Any action similar to one produced by the
sympathetic nervous system
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Effects of Thyroid Hormone (cont’d.)
– Effect on the cardiovascular system
• Increased heart rate, force of contraction, and
cardiac output
– Effect on growth and the nervous system
• Stimulates GH secretion, increases production of
IGF-I by the liver, and promotes GH and IGF-I
effects on the synthesis of new structural proteins
and on bone growth
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Hypothalamus–Pituitary–Thyroid axis
• Thyroid hormone is regulated by the
hypothalamus–pituitary–thyroid axis
– Most important regulator of thyroid hormone
secretion
• Abnormalities of thyroid function include
both hypothyroidism and hyperthyroidism
– Hypothyroidism: thyroid hormone secretion
deficiency
– Hyperthyroidism: thyroid hormone secretion
excess
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© Cengage Learning 2016. All Rights Reserved.
Goiter
• A goiter develops when the thyroid gland
is overstimulated
– Enlarged thyroid gland
– Readily palpable and usually highly visible
– Occurs whenever either TSH or TSI
excessively stimulates the thyroid gland
– May accompany hypothyroidism or
hyperthyroidism
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19.2 Adrenal Glands
• Each adrenal gland consists of a steroidsecreting cortex and a catecholaminesecreting medulla
– Secrete hormones belonging to different
chemical categories
• The adrenal cortex secretes
mineralocorticoids, glucocorticoids, and
sex hormones
– Layers: zona glomerulosa, zona fasciculata,
and zona reticularis
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Mineralocorticoids
• The major effects of mineralocorticoids are
on Na+ and K+ balance and blood pressure
homeostasis
– Aldosterone promotes Na + retention and
enhances K + elimination during the formation
of urine
• Mineralocorticoids are essential for life
• Without aldosterone, a person rapidly dies from
circulatory shock
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Glucocorticoids
• Glucocorticoids exert metabolic effects
and play a key role in adaptation to stress
– Metabolic effects
– Permissive actions
– Role in adaptation to stress
– Anti-inflammatory and immunosuppressive
effects
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Cortisol Secretion
• Cortisol secretion is regulated by the
hypothalamus–pituitary–adrenal cortex
axis
– Regulated through a negative-feedback
system involving the hypothalamus and
anterior pituitary
• The adrenal cortex secretes both male
and female sex hormones in both sexes
– Androgens and estrogens
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Adrenal Cortex
• The adrenal cortex may secrete too much
or too little of any of its hormones
– Aldosterone hypersecretion
– Cortisol hypersecretion
– Adrenal androgen hypersecretion
– Adrenocortical insufficiency
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Adrenal Medulla
• The adrenal medulla consists of modified
sympathetic postganglionic neurons
– Secretion of catecholamines from the adrenal
medulla
• Catecholamines are secreted into the blood by
exocytosis of chromaffin granules
• Epinephrine and norepinephrine vary in
their affinities for different receptor types
– Norepinephrine binds predominantly with ᾳ
and β1 receptors
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Epinephrine
• Epinephrine reinforces the sympathetic
nervous system and exerts metabolic
effects
– Effects on organ systems: increases cardiac
output and dilates respiratory airways
– Metabolic effects: prompts mobilization of
stored carbohydrate and fat so extra energy is
available as needed to fuel muscular work
– Other effects: promotes arousal, increases
alertness, causes sweating, etc.
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Epinephrine (cont’d.)
• Epinephrine is released only on
sympathetic stimulation of the adrenal
medulla
– Catecholamine secretion by the adrenal
medulla is controlled entirely by sympathetic
input to the gland
– Amount of epinephrine released depends on
the type and intensity of the stressful stimulus
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19.3 Integrated Stress Response
• The stress response is a generalized
pattern of reactions to any situation that
threatens homeostasis
– Roles of the sympathetic nervous system and
epinephrine in stress
– Roles of the CRH–ACTH–cortisol system in
stress
– Role of other hormonal responses in stress
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Stressor
Specific response characteristic of
type of stressor
Body
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Nonspecific generalized response
regardless of type of stressor =
Stress response
Stressor
Hypothalamus
Posterior
pituitary
CRH
Anterior
pituitary
Sympathetic
nervous system
Vasopressin
ACTH
Conserve salt and
H2O to expand the
plasma volume;
help sustain blood
pressure when
acute loss of
plasma volume
occurs
Vasopressin and
angiotensin II
cause arteriolar
vasoconstriction
to increase blood
pressure
Adrenal cortex
Adrenal medulla
Epinephrine
Cortisol
Prepare body for
“fight or flight”
Arteriolar
smooth muscle
Glucagon-secreting cells
Insulin-secreting cells
Endocrine
pancreas
Vasoconstriction
Blood flow
through kidneys
Glucagon
Renin
Angiotensin
Aldosterone
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Insulin
Mobilize energy stores
and metabolic building
blocks for use as
needed
Integrated Stress Response
• The multifaceted stress response is
coordinated by the hypothalamus
– Receives input concerning physical and
emotional stressors from virtually all areas of
the brain and many receptors
– Directly activates sympathetic nervous system
• Activation of the stress response by
chronic psychosocial stressors may be
harmful
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19.4 Endocrine Pancreas and Control of
Fuel Metabolism
• Fuel metabolism includes anabolism,
catabolism, and interconversions among
energy-rich organic molecules
– Anabolism: buildup of large organic
macromolecules from small organic subunits
– Catabolism: breakdown of large, energy-rich
organic molecules within cells
– Interconversions among organic molecules:
most small organic molecules can be
converted into other types
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© Cengage Learning 2016. All Rights Reserved.
Endocrine Pancreas and Control of Fuel
Metabolism
• Because food intake is intermittent,
nutrients must be stored for use between
meals
– Energy storage forms: excess circulating
glucose, circulating fatty acids, and circulating
amino acids
• The brain must be continuously supplied
with glucose
– Sole source of energy
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Metabolic Fuels
• Metabolic fuels are stored during the
absorptive state and mobilized during the
postabsorptive state
– Absorptive state: occurs after a meal
– Postabsorptive state: occurs between meals
– Roles of key tissues in metabolic states: the
liver, adipose tissue, muscle, and brain
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Fuel Metabolism
• Lesser energy sources are tapped as
needed
– Glycerol, lactate, and ketone bodies
• The pancreatic hormones, insulin and
glucagon, are most important in regulating
fuel metabolism
– Islets of Langerhans: endocrine cells
scattered throughout the pancreas
– Somatostatin: inhibits the digestive system
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Insulin
• Insulin lowers blood glucose, fatty acid,
and amino acid levels and promotes their
storage
– Actions on carbohydrates
– Actions on fat
– Actions on protein
– Summary of insulin’s actions
– Role of amylin
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Factors that increase blood glucose
Factors that decrease blood glucose
Transport of glucose into cells:
––For utilization for energy production
––For storage
as glycogen through glycogenesis as
triglycerides
Glucose absorption from digestive tract
Blood
glucose
Hepatic glucose production:
––Through glycogenolysis of
stored glycogen
––Through gluconeogenesis
KEY
= Factors subject to hormonal control to maintain blood glucose level
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Urinary excretion of glucose (occurs only
abnormally, when blood glucose level
becomes so high it exceeds the
reabsorptive capacity of kidney tubules
during urine formation)
Blood Glucose
• The primary stimulus for increased insulin
secretion is an increase in blood glucose
– The primary control of insulin secretion is a
direct negative-feedback system between
pancreatic β cells and concentration of
glucose in the blood flowing to them
– Glucose stimulates insulin secretion by
means of an excitation–secretion coupling
process
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Symptoms of Diabetes M ellitus
• The symptoms of diabetes mellitus are
characteristic of an exaggerated
postabsorptive state
– Consequences related to effects on
carbohydrate metabolism
– Consequences related to effects on fat
metabolism
– Consequences related to effects on protein
metabolism
– Long-term complications
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Hypoglycemia
• Insulin excess causes brain-starving
hypoglycemia
– Low blood glucose
• Glucagon in general opposes the actions
of insulin
– Actions on carbohydrate
– Actions on fat
– Actions on protein
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Glucagon Secretion
• Glucagon secretion is increased during the
postabsorptive state
– Decreases during the absorptive state
• Insulin and glucagon work as a team to
maintain blood glucose and fatty acid
levels
– Elevated blood glucose stimulates insulin
secretion, but inhibits glucagon secretion
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Glucose Homeostasis
• Glucagon excess can aggravate the
hyperglycemia of diabetes mellitus
– Diabetics frequently have a high rate of
glucagon secretion concurrent with insulin
insufficiency
• Epinephrine, cortisol, and growth hormone
also exert direct metabolic effects
– Refer to Table 19-5
• The hypothalamus plays a role in
controlling glucose homeostasis
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© Cengage Learning 2016. All Rights Reserved.
19.5 Parathyroid Glands and Control of
Calcium Metabolism
• Plasma Ca2+ must be closely regulated to
prevent changes in neuromuscular
excitability
– Vital role in a number of essential activities
• Control of Ca2+ metabolism includes
regulation of both Ca2+ homeostasis and
Ca2+ balance
– Regulation of Ca2+ metabolism depends on
hormonal control of exchanges between the
ECF and the bone, kidneys, and intestine
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Parathyroid Glands and Control of
Calcium Metabolism
• Parathyroid hormone raises free plasma
Ca2+, a life-saving effect
– Peptide hormone secreted by the parathyroid
glands
– Essential for life
• Bone continuously undergoes remodeling
– Bone remodeling: bone deposition (formation)
and bone resorption (removal)
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PTH and Ca2+
• Mechanical stress favors bone deposition
– Causes bone mass to increase and bones to
strengthen
• PTH raises plasma Ca2+
– Withdraws Ca2+ from the bone bank
• PTH’s immediate effect is to promote
transfer of Ca2+ from bone fluid into
plasma
– See Figure 19-24
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Central
canal
Osteocyte
Lamellae
Lamella
Canaliculi
(c) Lamellae within an osteon
Location of yellow marrow
Compact bone
Trabecular
bone
Osteon
Central canal
Trabecular bone
(a) Long bone
Compact bone
Blood vessel from marrow
Canaliculi
Periosteum
Lamella
Central
canal
Osteocyte
Vessel in
central canal
(b) Osteon
Osteon
© Cengage Learning 2016. All Rights Reserved.
Source: Modified and redrawn with permission from Human Anatomy and Physiology, 3rd Edition, by A. Spence a
Copyright © 1987 by The Benjamin/Cummings Publishing Company. Reprinted by permission of Pearson Educat
photo: Biophoto Associates/Science Source
Osteocytic–
osteoblastic
bone
membrane
Osteocyte
Osteoblast
Osteoblast
Osteoclast
Blood vessel
Mineralized
bone
Outer
surface
Central canal
Bone fluid
Canaliculi
Lamellae
Gap junction
KEY
= Membrane-bound
Ca2+ pump
(a) Osteocytic–osteoblastic bone membrane
In canaliculi
Mineralized bone:
stable pool of Ca2+
In central canal
Bone fluid: labile
pool of Ca2+
Plasma
1 Fast exchange
Ca2+
2 Slow exchange
(Bone
dissolution)
Ca2+
Osteocytic–osteoblastic bone membrane
(formed by filmy cytoplasmic extensions of
interconnected osteocytes and osteoblasts)
(b) Fast and slow exchange of Ca2+
between bone and plasma
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1 In a fast
exchange, Ca2+ is
moved from the labile
pool in the bone fluid
into the plasma by
PTH-activated Ca2+
pumps located in the
osteocytic–osteoblastic
bone membrane.
2 In a slow exchange,
Ca2+ is moved from the
stable pool in the
mineralized bone into
the plasma through
PTH- induced
dissolution of the bone
by osteoclasts.
Effects of PTH
• PTH’s chronic effect is to promote
localized dissolution of bone in order to
release Ca2+ into plasma
– Acts on osteoblasts
• Causes them to secrete RANKL
• PTH acts on the kidneys
– Conserves Ca2+ and eliminates PO43-
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Effects of PTH (cont’d.)
• PTH indirectly promotes absorption of Ca2+
and PO43- by the intestine
– Helps activate vitamin D
• The primary regulator of PTH secretion is
plasma concentration of free Ca2+
– All effects of PTH raise plasma Ca2+ levels
• Calcitonin lowers plasma Ca2+
concentration
– Not important in normal Ca2+ metabolism
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Ca2+ Metabolism
• Vitamin D is actually a hormone that
increases Ca2+ absorption in the intestine
– Activation of vitamin D
– Function of vitamin D
• Phosphate metabolism is controlled by the
same mechanisms that regulate Ca2+
metabolism
– See Figure 19-27
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Relieves
Plasma PO43−
(Because of inverse relationship
3−
2+
between plasma PO4
and Ca
concentrations caused by solubility
characteristics of calcium phosphate
salt)
Plasma Ca2+
Kidneys
Parathyroid glands
Activated vitamin D
PTH
PO43− reabsorption
by kidneys
Ca2+ reabsorption
by kidneys
Ca2+ absorption
in intestine
Urinary excretion
of Ca2+
(Counteract each other)
Urinary excretion
of PO43−
No change in plasma
Plasma PO43−
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Ca2+
PO43− absorption
in intestine
Disorders in Ca2+ Metabolism
• Disorders in Ca2+ metabolism may arise
from abnormal levels of PTH or vitamin D
– PTH hypersecretion: excess PTH secretion
– PTH hyposecretion: deficient PTH secretion
(i.e., hypoparathyroidism)
– Vitamin D deficiency: major consequence is
impaired intestinal absorption of Ca2
• May lead to rickets or osteomalacia
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Points to Ponder
• What do you think causes osteoporosis?
Is it an estrogen deficiency?
• The hypothalamic-pituitary axis may be
activated under stress. How does this
process occur?
• What is the purpose of measuring fasting
blood glucose levels?
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