the endocrine system - warner pacific universityclasspages.warnerpacific.edu/bdupriest/bio 420/unit...
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The Endocrine
System
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THE ENDOCRINE SYSTEM
Definition of an endocrine gland
How is this different from an
exocrine gland?
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Major Endocrine Glands
See Fig. 74-1 See Table 74-1 3
Pituitary
Hypothalamus
Thyroid Parathyroids
Thymus
Adrenals
Pancreas
Ovaries
Testes
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Other “Endocrine” Tissues
Pineal gland “biological clock”
Placenta Fetal, breast development
Heart Decreases blood pressure
Increases Na+ excretion by kidneys
Stomach Secretes HCl
Small intestine Secretes of digestive enzymes
Adipose tissue (fat) Large variety of hormones, especially
leptin and adiponectin
See Fig. 74-1 4
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Types of Chemical Signals
Endocrine hormones
Secreted by specific cells into the blood; have
specific physiological effects on other body cells
Neurotransmitters
Released by axon terminals; locally acting
Neuroendocrine hormones
Neurotransmitters released into the blood
Paracrine signals
Pass through extracellular spaces to affect
nearby tissues (different cell type)
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Types of Chemical Signals
Autocrine signals
Secreted into extracellular fluids
Binds to receptors on/in the originating cell
Cytokines
Peptides – mostly related to immune system
Secreted into extracellular fluids
May function as autocrine, paracrine or
endocrine hormones
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Chemical Structures of Hormones
1) Peptide Hormones
Hydrophilic molecules – pituitary hormones, e.g.
2) Tyrosine-Derived Hormones
E.g., Hormones from thyroid or adrenal medulla
3) Steroid Hormones
Cholesterol derivatives, amphiphilic
E.g., Hormones of gonads and adrenal cortex
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Hormone Synthesis & Storage: Peptides &
Tyrosine-derived hormones
Preprohormone Prohormone Active hormone
Fig. 74-2 8
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Hormone Synthesis & Storage: Steroid
Hormones
Lipid soluble
Steroid passes through cell membranes freely
Implications for synthesis and storage?
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cholesterol
Fig. 74-3
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Which of these is most likely to be stored in
vesicles prior to release?
A) Insulin
B) Estrogen
C) Cortisol
D) Carbon dioxide
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Which of these is most likely to be reduced in
patients taking a statin drug?
A) Growth hormone
B) Testosterone
C) Thyroxine
D) Nitric oxide
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Factors Influencing Hormone Production and
Release
Hormones are released in response to
extracellular stimuli:
Hormonal stimuli
Response to other hormones
Humoral stimuli
Response to specific molecules in circulation
Neural stimuli
Response to stress (sympathetic response)
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Regulation of Hormonal Secretions
Regulation occurs primarily through
feedback mechanisms
Negative feedback
Inhibit stimulus
Direct or indirect
E.g., thyroid hormones
Hypothalamus
TRH
Pituitary
TSH
Thyroid
T3 / T4
x
x
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Regulation of Hormonal Secretions
Regulation occurs primarily through
feedback mechanisms
Negative feedback
Positive feedback
Reinforce stimulus
E.g., labor contractions
Fetal tissue
stimulus
Uterus / cervix
signal
Hypothalamus
RH
Pituitary
oxytocin 14
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Hormone Transport
Water soluble hormones
E.g., peptide & adrenal medullary hormones
Transported in plasma
Short half-life
Cholesterol-based & nonpolar hormones
E.g., steroids, thyroid hormones
Must bind to plasma proteins (i.e., “binding
proteins”) in blood
Longer half-life
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Angiotensin II is a hormone produced when
blood pressure is low. It causes sodium
retention, water retention, and vasoconstriction,
which all lead to increases in blood pressure.
This is an example of…
A) Positive feedback
B) Negative feedback
C) Feed-forward
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Cellular Response to Hormones
How are hormones recognized by cells?
What are the general responses of cells to
hormones?
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Cellular Receptors: Recognition
Peptide hormones
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Cellular Receptors
Intracellular receptors
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Cellular Receptors
Notes on receptor specificity…
Receptors are specific to a particular hormone
(with varying degrees of specificity).
A hormone may have multiple types of receptors.
Depending on the receptors present, a single
hormone may elicit varied reactions from
different cells, or from the same type of cell at
different stages of development (fetal vs. adult)
or under different conditions.
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Cellular Response to Hormones
Change in membrane permeability
Membrane potential changes
E.g., membrane depolarization
Fast action
Ligand-gated ion channels
A.k.a. Ion channel-linked receptors
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Cellular Response to Hormones
G Protein-Coupled Receptors (GPCRs)
Trimeric G protein binds receptor
G protein activates intracellular signaling
cascade once hormone binds to receptor
Second messenger systems
cAMP
Phospholipase C
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E.g., cAMP Mechanism of Hormone Action
Fig. 74-7 23
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E.g., Phospholipase C Mechanism of Hormone
Action
Fig. 74-8 24
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Cellular Response to Hormones
Enzyme-linked receptors
Directly linked
E.g., insulin
Indirectly linked
E.g., leptin
No trimeric G protein
See Fig 74-5 in textbook on Jak-Stat pathway
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Cellular Response to Hormones
Gene activation
Slow acting
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Which of these pathways is least likely to
involve gene transcription (and new protein
production?
A) GPCR (via cAMP or PLC)
B) Enzyme-linked receptors
C) Intracellular receptors
D) Nuclear receptors
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Measurement of Hormone Concentration
Radioimmunoassay
Use specific antibody to detect hormone
Mix radioactive “tracer” hormone, antibody and
sample together
Competitive assay: Tracer competes with
endogenous hormone for Ab binding sites.
The more hormone you have, the less tracer will bind.
Remove all unbound (free) mixture, leaving Ab
bound to either tracer or endogenous hormone
High [endogenous hormone] low tracer
Low [endogenous hormone] high tracer
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Measurement of Hormone Concentration
Radioimmunoassay
Measure radioactivity of remaining sample,
compare to standard curve
Fig. 74-9 29
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Measurement of Hormone Concentration
ELISA (enzyme-linked immunosorbent assay)
Coat sample wells with antibody
Add test sample
Add antibody conjugated to enzyme
Add enzyme substrate
Color development
indicates presence
of test substance;
concentration
determined by
comparison to
standard curve
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Fig. 74-10
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What kind of molecule is used as a “molecular
tool” to measure how much of a particular
substance a sample has?
A) Protein
B) Receptor
C) DNA
D) Antibody
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Survey of Endocrine Tissues
and Hormones
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Pituitary Gland
and
Hypothalamus
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Cellular Organization
Fig. 75-1
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Fig. 75-3
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Pituitary Control Mechanisms
Neural stimulation by hypothalamus
Negative feedback systems
Direct & indirect mechanisms
Positive feedback systems
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Hypothalamic Control of Anterior Pituitary
Releasing and inhibiting hormones from
hypothalamus to pituitary
Fig. 75-4 36
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Hypothalamic Releasing & Inhibiting Hormones
Examples
Thyrotropin releasing hormone (TRH)
Corticotropin releasing hormone (CRH)
Growth hormone releasing hormone (GHRH)
Growth hormone inhibiting hormone (GHIH)
Aka. somatostatin
Gonadotropin releasing hormone (GnRH)
Prolactin releasing hormone (PRH)
Prolactin inhibiting hormone (PIH)
Aka. dopamine
See Table 75-2 37
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The portal circulation carries hormones from
______________ to _____________.
A) Hypothalamus / anterior pituitary
B) Hypothalamus / posterior pituitary
C) Anterior pituitary / hypothalamus
D) Posterior pituitary / hypothalamus
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Hormones of the Anterior Pituitary
Fig. 75-2 39
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Hormones of the Anterior Pituitary
Growth Hormone (GH)
Aka. somatotropin (ST)
Regulated by GHRH, GHIH
Protein produced by somatotropes (~30-40% of
cells)
Primary effects
Stimulate cellular growth (protein synthesis,
multiplication, differentiation)
Hypertrophy
Hyperplasia
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Hormones of the Anterior Pituitary
Adrenocorticotropic Hormone (ACTH)
Polypeptide produced by corticotropes
(~20% of cells)
Regulated by CRH
Primary effects
Controls release of adrenocortical
hormones related to:
Electrolyte balance (Na+)
Tissue stress (inflammation)
Metabolism (glucose, protein, fat)
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Hormones of the Anterior Pituitary
Thyroid-stimulating Hormone (TSH)
Aka. thyrotropin
Glycoprotein produced by thyrotropes (~3-5% of
cells)
Regulated by TRH
Primary effects
Stimulates release of thyroid hormones
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Hormones of the Anterior Pituitary
Prolactin (PRL)
Protein produced by lactotropes (~3-5% of cells)
Primary effects
Stimulates lactation & mammary gland
development
Concentration of PRL is correlated with
estrogen levels and controlled by hypothalamus
[estrogen] PRH release (hyp) pituitary PRL
[estrogen] PIH release (hyp) pituitary PRL
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Hormones of the Anterior Pituitary
Gonadotropins
Produced by gonadotropes (~3-5% of cells)
Regulated by GnRH
Luteinizing Hormone (LH)
Promotes production of gonadal hormones (e.g.,
testosterone, estrogens, progesterone)
Follicle Stimulating Hormone (FSH)
Stimulates gamete production (oogenesis,
spermatogenesis)
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Which anterior pituitary hormone is responsible
for maintaining sodium balance?
A) ACTH – adrenocorticotrophic hormone
B) TSH – thyroid stimulating hormone
C) GH – growth hormone
D) FSH – follicle stimulating hormone
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Growth Hormone
Broad range of effects on cellular metabolism
Atypical for pituitary hormones
General metabolic effects
a.a. uptake & protein synthesis, transcription
protein stability
fat utilization for energy
glucose uptake, insulin secretion
Diabetogenic effect
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Growth Hormone
Effect of GH injection on body weight in
growing rats
Fig. 75-5
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Growth Hormone
Effects of exercise and sleep on GH
production
Fig. 75-6
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Growth Hormone
Factors stimulating GH secretion
Starvation (esp. protein deficiency) – Fig 75-7
Hypoglycemia or hypolipidemia
Exercise
Excitement
Trauma
Ghrelin
Deep sleep
GH secretion drops steadily decreases after
puberty
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Based on the previous slides, which of these
factors affects GH secretion most strongly on a
daily basis?
A) Sleeping
B) Waking
C) Strenuous exercise
D) Hypoglycemia
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Growth Hormone
Indirect effects on skeletal system
Stimulates production of insulin-like growth
factors (IGFs; aka somatomedins)
Stimulate bone growth (particularly IGF-I)
Promotes growth in length of long bones
Promotes growth in bone thickness
Congenital defects in IGF-I production causes
dwarfism
Lack bone growth even when given hGH
51
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Growth Hormone Abnormalities
Panhypopituitarism
Onset during childhood
Dwarfism
Proportional development but at drastically
reduced rate
Treatable with hGH injections if diagnosed
early
Onset during adulthood
Lethargy, weight gain, loss of sexual function
Due to lack of anterior pituitary hormones
Result of tumor or thrombosis
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Growth Hormone Abnormalities
Hypersecretion of GH
Onset during childhood
Gigantism
All body tissues over-
stimulated to grow
Often tumor-related
reverts to
panhypopituitarism due to
tissue destruction
Diabetogenic
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Growth Hormone Abnormalities
Hypersecretion of GH
Onset during adulthood
Acromegaly
Growth in bone width
Hands, feet, forehead, jaw, nose, vertebrae
Age 16 Age 52 See Fig. 75-8 54
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Overproduction of GH during childhood results
in…
A) Dwarfism
B) Gigantism
C) Acromegaly
D) Panhypopituitarism
55
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Hormones of the Posterior Pituitary
Antidiuretic Hormone (ADH)
Aka. (arginine) vasopressin (AVP)
Primary effects
Stimulates kidneys to reabsorb H2O
Oxytocin
Primary effects
Stimulates uterine contractions
+ feedback stimulated by fetus/uterus
Stimulates milk letdown
+ feedback stimulated by suckling
Fig. 75-9
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ADH
Primarily formed in supraoptic nuclei
Mode of action
Operates under cAMP 2nd messenger system
Increases permeability of distal tubules and
collecting ducts of kidney to H2O to promote
reabsorption
Regulation
Involves osmoreceptors in/near hypothalamus
Specialized cells associated with sensory
neurons that indirectly monitor blood
electrolyte concentrations by sensing cell
distention 57
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ADH
H2O
osmosis
[electrolytes]
Y Y cell shrinkage
signal
posterior pituitary
kidneys
ADH
reabsorb H2O [electrolytes] 58
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ADH
H2O
osmosis
[electrolytes]
Y Y cell swells
signal
kidneys
ADH H2O not
reabsorbed [electrolytes]
X 59
posterior pituitary
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Hypothalamic Control of the Post. Pituitary
Control over the posterior pituitary
See Fig. 75-9 60
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True or false: oxytocin is produced and
released by the hypothalamus
A) True
B) False
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Thyroid
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THYROID
Anatomical position
Two lobes lateral to the trachea connected by an
isthmus anterior to the trachea
anterior posterior 63
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Primary Hormones of the Thyroid
Thyroid Hormone
Thyroxine (T4) & triiodothyronine (T3)
Tyrosine derivatives
Primary effects
Increase gene transcription to increase cellular
metabolism
CH2O, fat, protein metabolism
BMR ( temp)
Body weight
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Primary Hormones of the Thyroid
Calcitonin
Release stimulated by humoral [Ca2+]
Primary effects
Inhibits osteoclast activity
Enhances activity of osteoblasts
Promotes Ca2+ uptake / deposition into bone
Deposited as hydroxyapatite crystals
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Histology of the Thyroid Gland
See Fig. 76-1 66
Thyroid hormones
Calcitonin
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Synthesis of Thyroid Hormone
Formation & storage of thyroglobulin (TG)
Glycoprotein containing 70 Tyr residues
Exocytosed into colloid
Fig. 76-2 67
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Synthesis of Thyroid Hormone
Iodide (I-) trapping & oxidation
Membrane bound I- pump
Concentrates I- to 30x humoral concentration
68 Fig. 76-2
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Synthesis of Thyroid Hormone
Iodination of TG (organification)
I0 added to Tyr residues of TG
Formation of mono- (MIT; T1) and
diiodotyrosine (DIT; T2) residues
69 Fig. 76-2
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Iodination of TG
See Fig. 76-3
70
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Synthesis of Thyroid Hormone
T1-T2 coupling
Hydrolysis reaction that binds T1 and T2 residues
between adjacent TG molecules
Stored in colloid
71 Fig. 76-2
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T1-T2 Coupling
72
See Fig. 76-3
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Synthesis of Thyroid Hormone
See Fig. 76-3 73
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Synthesis of Thyroid Hormone
TG uptake
Mature TG endocytosed (pseudopodia)
74 Fig. 76-2
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Synthesis of Thyroid Hormone
Cleavage & release of T3 / T4
Vesicles fuse with lysosomes
Proteases digest TG and release free T4 (93%)
& T3 (7%)
75 Fig. 76-2
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Which of these processes must occur before
the other processes in this list?
A) Iodine organification
B) T1-T2 coupling
C) Thyroglobulin pinocytosis
D) Proteolytic cleavage of TG
E) Synthesis of TG protein
76
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Thyroid Hormone Transport & Delivery
Transported in plasma via plasma proteins
Thyroxine-binding globulin
Slow release to tissues
High affinity for plasma proteins (>90% bound)
T4>T3 T4 released to cells slower (6x)
Uptake via diffusion or carriers
Bind nuclear receptors
Initiate/block transcription to increase metabolic
functions
77
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Thyroid Hormone Transport & Delivery
Fig. 76-5 78
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T3 vs. T4 Activity
T3 more biologically active because…
T4 binds more tightly to plasma proteins
Higher ratio of free:bound T3 vs. T4
T4 converted to T3 within tissues (iodinase)
Nuclear thyroid hormone receptors ~10x greater
affinity for T3
79
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Thyroid Hormone Regulation
Stimuli
Thyroid hormone, cold, I-
Control
Negative feedback
Signaling pathways
TRH = phospholipase C
TSH = cAMP
Stimulates all known
secretory functions of thyroid
TSH T3/T4 release in 30
min
Hypothalamus
TRH
Pituitary
TSH
Thyroid
T3 / T4
80
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TSH
Increases TG proteolysis
Increases iodide pump activity
Increases organification (iodination) activity
Increases size / activity of thyroid cells
Increases number of thyroid cells
81
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Increases or decreases in TRH causing
increases or decreases in TSH level is an
example of…
A) Hormonal regulation of TSH
B) Hormonal regulation of TRH
C) Negative feedback
D) Positive feedback
82
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Physiological Effects of Thyroid Hormone
Effects on cellular metabolism
Macromolecules
all aspects of (CH2O)n metabolism
Uptake
Glycolysis
Gluconeogenesis
lipid mobilization and oxidation to free fatty
acids
cholesterol & triglycerides in plasma
cholesterol excretion in bile
83
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Effect on Basal Metabolic Rate (BMR)
Slow onset, long duration
[high] increases BMR 60-100%
[low] decreases BMR 30-50%
84
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Effect of Large Single Dose on BMR
Fig. 76-4
85
Long latent period; prolonged effect
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Daily Effect on BMR
Fig. 76-6 86
“norm”
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Physiological Effects of Thyroid Hormone
Effect on body weight
[increase] weight decrease
However, may be offset by increased appetite
[decrease] weight increase
Effect on cardiovascular system
Increased…
Heart rate, blood pressure, cardiac output
Inotropy (contractility/strength of contraction)
87
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Physiological Effects of Thyroid Hormone
Effect on respiratory system
Increased…
Breathing rate and depth
Effect on nervous system
[increase] irritability & nervousness
[decrease] depression, lethargy
88
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Based on the previous slides, which of these is
most likely to be a symptom associated with
hyperthyroidism?
A) Lethargy / fatigue
B) Slow reaction time
C) Weight loss
D) Reduced cardiac output
89
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Hyperthyroidism
General symptoms
Excitability / nervousness
Intolerance to heat / profuse sweating
Weight loss
Fatigue / insomnia
Exophthalmos
Protrusion of the eyeballs due to edema of
orbital tissues
See Fig. 76-8 90
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Hyperthyroidism
Graves disease
Autoimmune disease
Ab bind TSH receptors on thyroid
Results in continual hormone secretion
Symptoms
Exophthalmos
Goiter
Other typical symptoms
91
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Hyperthyroidism
Treatment
Typically tumor related
Surgery
Radiation treatment (131I)
Why use this isotope?
92
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Hypothyroidism
General Symptoms
Fatigue
Mental sluggishness
Weight gain
Myxedema
General edema
Fig. 76-9 93
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Hypothyroidism
Endemic goiter
Caused by dietary iodine deficiency
Thyroid stimulated to produce thyroid hormone
but is unable to produce active hormone
Follicle cells replicate; follicles swell (10-20x)
May return to normal with dietary iodine
supplements
iodized salt
94
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Hypothyroidism
Cretinism
Severe hypothyroidism during fetal stages /
infancy / childhood
Symptoms
Mental retardation
Short / disproportionate body
Thick tongue / neck
Treatable with hormone replacement therapy but
symptoms irreversible
95
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Hypothyroidism
Hashimoto Thyroiditis
Hypothyroidism due to autoimmune attack
against thyroid peroxidase or thyroglobulin
Most common form of primary hypothyroidism
in North America
Symptoms same as other adult forms of
hypothyroidism
Treatable with hormone replacement therapy
(T4)
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Which of these diseases is a type of
hypothyroidism that is due to an autoimmune
cause?
A) Hashimoto thyroiditis
B) Grave’s disease
C) Endemic goiter
97
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Parathyroid Glands
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PARATHYROID GLANDS
Anatomy
Typically 2 pairs on posterior surface of thyroid
lobes
99
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Parathyroid Hormones
Parathyroid hormone (PTH)
Elevates blood calcium levels
10
0
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Vitamin D Conversion
Fig. 79-6 101
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Physiological Roles of Ca2+
Critical component in nerve transmission
Neurotransmitter release
Critical component in muscle contraction
Exposure of myosin binding sites on actin
filaments
Autorhythmic cycles of cardiac muscle
Exocytosis
Intracellular signaling
Homeostasis maintained by antagonistic
effects of PTH and calcitonin 102
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Parathyroid hormones has all of the following
effects EXCEPT:
A) Stimulating osteoclast activity
B) Inhibiting osteoblast activity
C) Increasing intestinal absorption of Ca2+ directly
D) Stimulating the kidney to produce more
vitamin D
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Adrenal Glands
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ADRENAL GLANDS
Anatomical considerations
Located on superior surface of kidneys (humans)
Cortex vs. medulla
See Fig. 77-1 105
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Cortex vs. Medulla
Functional differences
Adrenal cortex: produces corticosteroids
Cholesterol derivatives
Examples: aldosterone, cortisol, sex steroids
Adrenal medulla: produces catcholamines
Produce catecholamines
Examples: epinephrine & norepinephrine
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Hormones of the Adrenal Cortex
3 primary hormone groups produced by
the 3 primary cell layers
Zona glomerulosa
Produce mineralocorticoids
E.g., aldosterone
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Hormones of the Adrenal Cortex
3 primary hormone groups produced by
the 3 primary cell layers
Zona glomerulosa
Zona fasciculata
Produce glucocorticoids &
some gonadocorticoids
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Hormones of the Adrenal Cortex
3 primary hormone groups produced by
the 3 primary cell layers
Zona glomerulosa
Zona fasciculata
Zona reticularis
Produce gonadocorticoids &
some glucocorticoids
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Hormones of the
Adrenal Cortex
Fig. 77-2
Synthesis
pathways
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The primary hormone produced by the zona
glomerulosa of the adrenal cortex is…
A) Aldosterone
B) Cortisol
C) Adrenal androgens
D) All of the above
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Mineralocorticoids
Aldosterone
Primary effects
Regulation of [electrolyte] in extracellular
fluids
Na+, K+
Primary target = kidneys
Stimulates reabsorption of Na+ from urine
Na+ in plasma water follows blood
volume & blood pressure
Stimulates K+ excretion in urine
Critical for survival
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Effects of Na+ / K+ Imbalances
Sodium
Excess/deficiency of Na+ in plasma
Osmotic imbalance Δ blood volume &
pressure
Excess Na+ in urine
Water follows blood volume & bp
circulatory shock
Potassium
Excess K+ in plasma
Hypertension, heart failure
K+ deficiency in plasma
Inhibits muscle/nerve depolarization 113
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Effect of Aldosterone Infusion
sodium
retention…
arterial
pressure
extracellular
fluid
urinary Na+
output
“escape” due
to filtration
pressure
Fig. 77-3
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Aldosterone Regulation
ACTH
Required for aldosterone secretion
Does not influence rate of secretion
K+ concentration
[K+ ] stimulates zona glomerulosa cells
Aldosterone release
Na+ concentration
[Na+ ] only slightly inhibits aldosterone release
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Aldosterone Regulation
Renin-angiotensin
system
Cells in kidneys
stimulated by…
blood pressure,
blood volume,
plasma
osmolarity
Fig. 19-9
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Glucocorticoids
Cortisol (hydrocortisone) & cortisone
Primary effects
Increase blood glucose
Increase gluconeogenesis
Synthesis of glucose from amino acids
Depress inflammation & immune response
Inflammatory reaction may
overcompensate for actual problem
Increase “healing” through energy
availability and mobilization of precursors
for structural components (aa’s, fa’s)
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Regulation
Fig. 77-6
Fig. 77-7
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Gonadocorticoids
Adrenal androgens
Sex hormones
Primarily “male” hormones
Testosterone precursor, androstenedione
Can be converted to estrogens
Also progesterone and estrogens
All secreted in small amounts with weak effects
relative to hormones of gonad origin …so why do we care about this?
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Hypoadrenalism
Addison’s disease
Typically autoimmune reaction resulting in
atrophy of cortex
Mineralocorticoid & glucocorticoid deficiencies (why not adrenal androgens, too?)
Dehydration ( aldosterone)
Hypertension ( K+)
Blood glucose imbalance ( glucocorticoids)
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Hyperadrenalism
Cushing’s syndrome
Primarily due to cortisol excess (due to ACTH
excess)
Hypertension & edema
Facial edema (“moon face”) & acne
Redistribution of fat
Abdomen & posterior neck (buffalo hump)
Protein loss
Weakness
Depressed immunity
Fig. 77-9 121
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Which disease is most likely the result of an
autoimmune destruction of the adrenal cortex?
A) Cushing disease
B) Addison’s disease
C) PCOS
D) All of the above
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Hormones of the Adrenal Medulla
Catecholamines
Epinephrine (adrenaline)
Norepinephrine (noradrenaline)
General effects
Emergency response (fast / brief)
heart rate, metabolic rate, blood
pressure (vasoconstriction)
Same results; epinephrine provides stronger
response
Short term response
123
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Hormones of the Adrenal Medulla
Stimulus
Sympathetic NS response (fight / flight)
Signals adrenal medulla
Catecholamines released
Epinephrine (80%)
Norepinephrine (20%)
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Which hormone is released in the largest
quantities by the adrenal medulla?
A) Aldosterone
B) Cortisol
C) Epinephrine
D) Norepinephrine
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Pancreas
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PANCREAS
Cellular composition Mixed gland
Endocrine & exocrine activity
Islets of Langerhans
cells (60%)
Insulin
cells (25%)
Glucagon
cells (10%)
Somatostatin (GHIH)
Fig. 78-1
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Endocrine Activity of the Pancreas
Regulate blood glucose levels
Uptake / release of glucose
Fat & protein metabolism
Conditions of imbalance:
Hyperglycemia
Hypoglycemia
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In cells: insulin production
Released in response to elevated blood glucose
Fig. 78-7 129
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Insulin Processing
Fig. 78-2 130
C-Peptide
A-chain
B-chain
S S
S S
S S
S S
S S
S S
Connecting peptide
Insulin
HOOC
NH2
NH2
NH2
COOH
COOH
Proinsulin
A-chain B-chain
1
5
10 15
20
25
30
1 5 10 15
20
1 5 10 15 20 25 30
1
5 10
15
20
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In target cells: Insulin signaling
Membrane receptors consist of 4 subunits
Fig. 78-3
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If you didn’t already know that insulin is a
protein, you could assume that it is based on
the fact that…
A) it reduces blood glucose levels
B) it is released from the pancreas
C) it is released in response to increases in
intracellular calcium
D) it binds to receptors on the plasma membrane
of target cells
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Insulin
Release produces a hypoglycemic effect
Glucose uptake
Esp., muscle, liver, adipose
Fig. 78-8
133
Fig. 78-9 Fig. 78-4
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Insulin
Effect on glucose storage
[Glycogen] in liver
Convert glucose to triglycerides
Effect on fuel utilization
Increased a.a. transport
Increased mRNA translation
Inhibition of protein catabolism
Depressed gluconeogenesis (liver)
Depressed fat utilization & increased storage
(“fat sparer”)
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Insulin
Effect on nervous tissue
Essentially none
Neurons very “permeable” to glucose, don’t
require insulin for glucose uptake
Normally use only glucose as energy source
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Insulin
Synergistic effect with growth hormone
Fig. 78-6
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Glucagon
Released in response to decreased blood
glucose
Release provides hyperglycemic effect
Glycogen breakdown & release
Liver glycogen
Muscle glycogen
Enhances gluconeogenesis
Glucose production from amino acids
Activates adipose cell lipase
Release fatty acids for energy use
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Factors Affecting Insulin / Glucagon Release
See Table 78-1
Figs. 78-9, 78-10 138
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General Regulation
139
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Other Regulatory Factors
Increased aa levels enhance effect of
glucose on insulin release
Gastrointestinal hormones increase insulin
secretion
E.g., gastrin, cholecystokinin (CCK)
Severe hypoglycemia
Hypothalamus stimulates sympathetic response
Epinephrine stimulates glucose release from
liver
Release of growth hormone and cortisol
Inhibit glucose utilization; increase fat
utilization 140
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Insulin levels are increased by all of the
following except:
A) hyperglycemia
B) Severe hypoglycemia
C) Normal hypoglycemia
D) CCK
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Diabetes Mellitus
Physiological effects of hyperglycemia
Glucose in urine (glycosuria)
Dehydration
Increased diuresis (polyuria)
Excessive thirst (polydipsia)
Hunger (polyphagia) with weight loss
Ketoacidosis (not an effect; coincidental, resulting from low insulin
levels)
Shift to fat metabolism for energy fatty
acids in blood
Acetone breath
Rapid/deep breathing (CO2 buffering)
Diabetic (acidotic) coma (blood pH <7.0) 142
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Diabetes Mellitus
Type I diabetes (insulin-dependent)
Cause
Lack of insulin secretion
Predisposing factors
Heredity
Autoimmune reaction (viral related)
Early onset (< 20 yrs)
Treatment
Insulin
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Diabetes Mellitus
Type II diabetes (non-insulin-dependent) Cause
Decreased cellular sensitivity to insulin (insulin resistance)
Predisposing factors Heredity Obesity (reduction in transport proteins)
Traditionally late onset (>40 yrs), now earlier Treatment
Diet & exercise Insulin Drugs
Increase tissue insulin sensitivity (thiazolidinediones, metformin)
Increase insulin production/release (sulfonylureas)
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Diabetes Mellitus
Testing
Acetone breath
Urinary glucose
Fasting blood glucose levels
Morning blood glucose should be
~90mg/100ml
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Diabetes Testing
Glucose tolerance test
Evaluate glucose clearance rate
Ingest 1g glucose/kg body weight
Blood glucose returns to normal within 2 hr
With diabetes…
Much greater rise in blood glucose
Delay in return to normal levels
To determine Type I or Type II…
Test insulin levels
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Glucose Tolerance Test
Fig. 78-12
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Hypoglycemia
Not enough glucose available for nervous
tissue
General symptoms
Nervousness
Trembling
Sweating
Seizure
Unconsciousness
Coma
Death
glucose 50-70mg/100ml
glucose 20-50mg/100ml
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True or false: Type II diabetes only occurs in
people over 40
A) true
B) false
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Gonads
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GONADS
Testes Androgens
Testosterone,
dihydrotestosterone,
androstenedione
Conversion to estrogen
(estradiol) in other
tissues
Ovaries Estrogens,
progesterone
Hypothalamus
GnRH
Pituitary
LH
FSH
Gonads Fig. 81-6
Fig. 80-8
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Testosterone
Fetal development Responsible for initial development of male
sexual organs from genital ridge
Produced 7th week of development → 10 weeks after birth
Not produced again until 10-13 yrs
Fig. 80-9 152
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Testosterone
Puberty - adult
Development of primary & secondary sexual
characteristics
Hair distribution and baldness
Increased skin thickness & rate of sebaceous
gland secretion ( acne)
Increased muscle mass and bone thickness
Increased BMR
Spermatogenesis
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True or false: “Manopause” is when men stop
producing testosterone when they get to ~65
years old
A) true
B) false
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Estrogens
Promote development of most secondary
sex characteristics; progression of
endometrial cycle
Forms
Estradiol (-estradiol)
Primary product; most potent
Estrone
Also formed from adrenal
androgens
Estriol
Derivative of estradiol & estrone
Conversion mainly in liver
Fig. 81-6
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Estrogens
Only minute quantities secreted during
childhood
Production decreases at menopause
Fig. 81-10 156
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Estrogens
Development of primary & secondary sexual
characteristics
Increased osteoblast activity
Uniting of the epiphyses
Decreased osteoblast activity after menopause
Osteoporosis
Increases fat deposition (sc / gluteofemoral)
Thickening, softening of skin
Increased vascularization
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Progestins
Preparation of …
Uterus for pregnancy
Breasts for lactation
Progression of endometrial cycle
Primary form
Progesterone
Secreted by corpus luteum during latter half of
ovarian cycle
Secreted by placenta during pregnancy
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Endometrial Cycle
Proliferative phase
Proliferation of epithelial cells and development
of uterine endometrial layer after menstruation
Influenced by elevated estrogen levels
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Endometrial Cycle
Secretory phase
Increased secretion of estrogens and
progesterone after ovulation
Increased development of the endometrium
Secretory activity relates to nutrient storage
for implanted fertilized ovum (uterine milk)
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Endometrial Cycle
Menstruation
Sloughing of endometrium
Reduction in estrogens and progesterone (10)
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Endometrial Cycle
Fig. 81-7
Fig. 81-3 162
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Which hormone is primarily responsible for
driving the uterine cycle (menstrual cycle)?
A) -estradiol
B) Progesterone
C) Testosterone
D) Cortisol
163