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Chapter 18: The Endocrine System
BIO 211 Lecture
Instructor: Dr. Gollwitzer
1
• Today in class we will:
– Compare intercellular communication in the
endocrine and nervous systems
• Learn the differences and similarities in each system’s
function(s) and how they are important with regard to
homeostasis in the body
– Talk about hormones
• The 3 major structural classes and examples of each
• The secretion, distribution, and elimination of hormones
• The mechanisms that allow hormones to affect target
cells and organs
– Identify the organs of the endocrine system
• Learn the names of the hormones that each endocrine
organ produces
2
Intercellular Communication
• Cellular activities in the body must be
coordinated to maintain homeostasis (a stable
internal environment within the body)
• Homeostasis is the key to survival in an ever
changing environment
– Failure to maintain homeostasis eventually leads to
illness or death
• Activities in the human body are coordinated
through intercellular communication
(communication between cells)
3
Table 18-1 Mechanisms of Intercellular Communication
4
Endocrine System vs. Nervous System
Differences
• Endocrine system
– Endocrine
communication
• Via hormones
• Thru circulatory system
– Affects target cells in
other tissues/organs
distant to tissue of origin
– Slow response, but lasts
much longer
• Nervous System
– Neural (synaptic)
communication
• Via neurotransmitters
• Across synaptic cleft
– Affects limited, specific
area (post-synaptic)
– Fast response, short-term
crisis management
5
Endocrine System vs. Nervous System
Similarities
• Both systems:
– Share many chemical messengers
– Use chemical messengers that must bind to
specific receptors on their target cells
– Share the common goal of maintaining
homeostasis
6
Endocrine System
• One of the body’s two
coordination/communication systems
– Nervous system is the other
• Endocrine glands are ductless glands
• Communicate with other cells/organs/
systems in the body through release of
hormones
• Endocrine cells  hormone (chemical
messenger)  interstitial fluid or
circulatory system  target cells 
effect(s)
7
Examples of Endocrine Control
•
•
•
•
Growth and maturation
Sexual development (puberty)
Reproduction
Response to environmental stress 24
hours/day for a lifetime
8
Hormone Structure
• Divided into 3 major groups based on
chemical structure
– Amino acid derivatives
– Peptide hormones
• Produced as inactive prohormones; converted to
active hormones
– Lipid derivatives
9
Hormone Structure:
Amino Acid Derivatives
• Small molecules structurally related to
amino acids
• Derivatives of tyrosine
– Thyroid hormones – T3, T4
– Catecholamines – epinephrine and
norepinephrine, dopamine
• Derivative of tryptophan
– Melatonin
10
Figure 18–2
11
Hormone Structure:
Peptide Hormones
• Chains of amino acids
• Synthesized as prohormones
– Inactive molecules converted to active
hormones before or after secretion
• 2 Groups
– Glycoproteins
– Short polypeptides and small proteins
12
Figure 18–2
13
Glycoproteins
• More than 200 amino acids long, with
carbohydrates
• Released by:
– Anterior pituitary: LH, FSH, TSH
– Reproductive organs: inhibin
– Kidneys: erythropoietin
14
Short Polypeptides and
Small Proteins
• All other hormones secreted by:
– Hypothalamus
– Anterior pituitary
– Posterior pituitary
– Pancreas
– Parathyroid gland
– Thymus, heart, and digestive tract
15
Hormone Structure:
Lipid Derivatives
• 2 Classes
– Steroid hormones
• Synthesized from cholesterol
– Eicosanoids
• Synthesized from arachidonic acid
16
Figure 18–2
17
Steroid Hormones
• Produced by:
– Male and female reproductive organs
• Testes  androgens (testosterone)
• Ovaries  estrogens and progestins (progesterone)
– Adrenal glands  corticosteroids
– Kidneys  calcitrol
• Bound to transport proteins in plasma
(albumins, globulins) so remain in circulation
longer than peptide hormones
18
Eicosanoids
• Small molecules with 5-C ring at one end
• Important local (paracrine) hormones secreted by
all cells except RBCs
• Primarily affect neighboring cells
– Coordinate cellular activities
– Affect enzymatic processes in extracellular fluid
• 2 Types
– Leukotrienes (from WBCs or leukocytes)
• Coordinate tissue response to injury or disease
– Protaglandins (produced by most tissues of the body)
• Coordinate local cellular activities
19
Hormone Distribution and Transport
• Hormones secreted/released into:
– Interstitial space
– Capillaries
• Circulate/distributed through bloodstream
as:
– Free hormones
– Bound hormones
20
Free Hormones
• Proteins, polypeptides, amino acid
derivatives
• Rapidly removed from bloodstream
– Diffuse out of bloodstream and bind to
receptors on target cells
– Absorbed by liver or kidney and broken down
– Broken down by enzymes in plasma or
interstitial fluids
• Functional for <1 hr
21
Bound Hormones
• Thyroid and steroid hormones
• Bound to transport proteins in blood, i.e.,
albumins and globulins
• Remain in circulation much longer (weeks)
22
Hormone Function and Mechanism of
Action on Target Organs
• Alter cellular operations
• Change biochemical properties or physical
structure of target cells
– Activate genes in nucleus that code for synthesis
of enzyme or structural protein
– Turn existing enzyme on or off by changing its
shape or structure
– Increase/decrease rate of synthesis of enzyme or
other protein
23
Hormone Function and Mechanism of
Action
• Hormone effect depends on:
– Type of target cell
– Type of receptor = protein molecule to which
particular hormone binds strongly
• Requires interaction of hormone with
appropriate receptor
• Presence or absence of specific receptor
determines cell’s hormonal sensitivities
– Receptor present  response
– Receptor absent  no response
24
Hormone Receptors
• On cell membrane (extracellular)
– For water-soluble hormones (can’t cross
membrane)
• Catecholamines (E and NE)
• Peptide hormones
– Hormones can’t have direct effect inside cell
– Act as first-messenger
• Causes second-messenger to appear in cytoplasm
(cAMP, cGMP, Ca++)
• Second messenger  changes in rates of metabolic
reactions
25
Figure 18–3
26
Hormone Receptors
• Inside cell (intracellular)
– For lipid-soluble hormones (can cross membrane)
• Steroid and thyroid hormones
– Cross cell membrane and bind to receptors in cytoplasm or
nucleus
– Hormone/receptor complex activates/inactivates specific
genes and changes protein/enzyme synthesis, e.g.,
• Testosterone stimulates production of enzymes and protein in
skeletal muscle, causing increased muscle mass and strength
• Thyroid hormones increase/decrease concentrations of enzymes
and bind to mitochondria and increase ATP production
27
Figure 18–4
28
Endocrine Organs
•
•
•
•
•
•
•
•
•
•
Hypothalamus
Pituitary gland
Thyroid gland
Parathyroid glands
Adrenal glands
Pineal gland
Pancreas
Kidneys
Other: heart, thymus, adipose tissue
Reproductive organs (gonads and placenta)
29
Fig 18-1
30
• Today in class we will:
– Discuss the hormones (and each hormone’s function)
along with the general effects of abnormal levels of
each hormone produced by the:
• Hypothalamus
– More in depth info on the hypothalamus:
» The structural relationship of the hypothalamus and pituitary
gland
» Learn about the hypophyseal portal system and its importance
» Learn how the hypothalamus controls endocrine function
• Pituitary gland
» Identify hormones secreted by the posterior pituitary gland
and produced and secreted by the anterior pituitary gland
• Thyroid gland
• Parathyroid glands
31
Hypothalamus:
A Neuroendocrine Organ
• Neural effects
– Controls feeding reflexes, heart rate, blood pressure,
body temp, day-night activity cycles
• Endocrine contribution
– Hormone synthesis (for release by posterior pituitary),
i.e., ADH and OT
• Transported via axons of neurosecretory cells to posterior
pituitary for release
– Hormone synthesis and release, i.e., RHs
• Transported via hypophyseal portal system to anterior
pituitary
32
Hypothalamus
Figure 14–10a
33
Hypothalamic Hormones
• Hypothalamus produces:
– ADH (antidiuretic hormone)
– OT (oxytocin)
– RHs (regulatory hormones)
34
Hypothalamic Hormones
• ADH (antidiuretic hormone)
– Produced by supraoptic nuclei (released by
posterior pituitary)
– Effects
• Decreases water lost at kidneys by increasing
reabsorption
• Elevates blood pressure through vasoconstriction
– Release inhibited by alcohol why you urinate a
lot while drinking
35
Diabetes Insipidus
• Inadequate amounts of ADH released from
posterior pituitary
• Impairs water conservation at kidneys 
watery urine
36
Hypothalamic Hormones
• OT (oxytocin)
– Produced by paraventricular nuclei (released by
posterior pituitary)
– Produced during:
• Sex, breastfeeding, and other bonding experiences
(increases trust and compassion)
• Labor
– Stimulates smooth muscle in:
• Mammary gland  milk ejection
• Uterus to promote labor and delivery
• Male and female reproductive tracts
– Plays a role in sexual function
37
Hypothalamic Hormones
• RHs (regulatory hormones)
– Produced by median eminence (tuberal area)
– Stimulate/inhibit anterior pituitary hormone
synthesis and release
38
Hypophyseal Portal System
• Prevents dilution of very small quantities of
RHs by systemic circulation
• Ensures RHs entering portal vessels will reach
target cells in anterior pituitary
39
Fig 18-7
40
Control of Endocrine Organs
• Involves endocrine reflexes, i.e., stimulus 
hormone secretion
• In most cases, controlled by negative feedback
mechanisms
• Hormones released in response to one or
more of the following stimuli:
– Humoral
– Neural
– Hormonal
41
Control of Endocrine Organs
• Humoral stimuli
– From local changes in composition of extracellular
fluid
– Hormones released continually, but rate rises and
falls in response to humoral stimulation
• e.g., pancreatic hormones
increased blood glucose  increased extracellular glucose 
increased insulin
42
Control of Endocrine Organs
• Neural stimuli
– Via arrival of neurotransmitters at neuroglandular
junctions
• e.g., hypothalamic control of adrenal medullae via
action potentials along efferent nerve fibers (also have
hormonal component)
– Hypothalamus has autonomic centers that exert direct neural
control over endocrine cells of adrenal medullae
– When sympathetic division activated, adrenal medullae
release E and NE into bloodstream
43
Control of Endocrine Organs
• Hormonal stimuli
– Via arrival/removal of hormones from other
endocrine glands
• Hypothalamus
– Highest level of endocrine control
– Secretes regulatory hormones/factors that stimulate synthesis
and secretion of anterior pituitary hormones and/or prevent
the synthesis and secretion of hormones
• Anterior pituitary
– Hormones it secretes controls activities of other endocrine
organs (thyroid, adrenal cortex, reproductive organs)
44
Hypothalamic Control of
Endocrine Function
• Involves most complex responses
• Integrates activities of nervous and endocrine
systems
• 3 mechanisms
– Secretion of AP regulatory hormones
– Production of ADH and oxytocin
– Control of sympathetic stimulation of adrenal
medullae
45
Figure 18–5
46
Hypothalamic Control of
Endocrine Function
• Secretion of AP regulatory hormones
– Neurosecretory cells in median eminence of Hth
secrete RHs
– Delivered to AP thru hypophyseal portal system
– Control release of AP hormones (e.g., TSH, ACTH,
FSH, LH) that control other endocrine organs
– Rate of RH release controlled by negative
feedback
47
Hypothalamic
Regulatory Hormones
Figure 18–8a
48
Hypothalamic Control of
Endocrine Function
• Production of ADH and oxytocin
– Hth acts as endocrine organ by producing ADH
and oxytocin that are released by PP
– Neurosecretory cells connect Hth to PP
– ADH and oxytocin packaged in vesicles and
transported along axons to PP where they are
stored in axon terminals
– When neurosecretory cells stimulated, action
potential triggers release of stored ADH and
oxytocin from PP
49
Hypothalamic Control of
Endocrine Function
• Control of sympathetic stimulation of adrenal
medullae
– Hth contains autonomic centers
– Exert direct control over adrenal medullae  E
and NE
50
Pituitary Gland (Hypophysis)
Figure 18–6
51
Pituitary Gland (Hypophysis)
• Releases 9 important peptide hormones
– 2 from posterior pituitary (produced in
hypothalamus)
– 7 from anterior pituitary (produced in anterior
pituitary)
• Peptide hormones:
– Bind to membrane receptors
– Use a second messenger (cAMP)
52
Hypothalamic/Posterior Pituitary Hormones
• ADH (antidiuretic hormone)
– Produced by supraoptic nuclei
– Released from axons of neurosecretory cells
• Oxytocin
– Produced by paraventricular nuclei
– Released from axons of neurosecretory cells
(See earlier discussion of hypothalamic
hormones.)
53
Anterior Pituitary Gland Hormones
Mnemonic:
Anatomy and physiology is tough going for many learners.
Anatomy and
Physiology is
Tough
Going
For
Many
Learners
= ACTH/adrenocorticotropic hormone
= PRL/prolactin
= TSH/thyroid-stimulating hormone
= GH/growth hormone
= FSH/follicle-stimulating hormone
= MSH/melanocyte-stimulating hormone
= LH/luteinizing hormone
54
Pituitary Gland Hormones
Fig 18-9
55
Anterior Pituitary Hormones
• ACTH (adrenocorticotropic hormone)
– Stimulates release of steroid hormones
(glucocorticoids) by adrenal cortex
• TSH (thyroid-stimulating hormone)
– Stimulates secretion of thyroid hormones
• PRL (prolactin)
– “Social bonding” hormone; increases with social
interaction, touch
– Stimulates development of mammary glands and
milk production
56
Anterior Pituitary Hormones
• GH (growth hormone or somatotropin)
– Stimulates release of somatomedins (peptide
hormones) from liver cells
• Accelerate protein synthesis and cell growth, esp.
skeletal muscle and cartilage
– Stimulates cell division
– Metabolic effects
• Glucose-sparing effect
– Stimulates adipocytes: triglycerides (TGs)  fatty acids (FA)
 ATP (vs. glu  ATP)
• Diabetogenic effect
– Stimulates liver: glycogen   glucose
57
Anterior Pituitary Hormones
• MSH (melanocyte-stimulating hormone)
– Stimulates melanocytes in stratum germinativum of skin
(Fig 5-5)  melanin (brown, black or yellow-brown
pigment)
– Not normally secreted by nonpregnant adult humans
– Secreted during:
•
•
•
•
Fetal development
Early childhood
Pregnancy
Certain diseases
– In nonhuman vertebrates  seasonal change in hair coat
color
58
Anterior Pituitary Hormones
• Gonadotropins
– Follicle-stimulating hormone (FSH)
– Luteinizing hormone (LH)
• Regulate activities of gonads (testes, ovaries)
• Stimulates release of steroid hormones by
gonads, e.g., estrogens, progestins, androgens
59
Anterior Pituitary Hormones
• Follicle-stimulating hormone (FSH)
– In females
• Stimulates follicle development and estrogen secretion
• Promotes oocyte development
– In males
• Stimulates sustentacular cells
• Promotes sperm development
– Production inhibited by inhibin (peptide hormone)
60
Anterior Pituitary Hormones
• Luteinizing hormone (LH)
– In females
• Causes ovulation and progesterone production by
corpus luteum (CL)
– In males (aka interstitial cell-stimulating hormone,
ICSH)
• Causes androgen production by interstitial cells of
testes
61
Thyroid Gland
Fig 18-10a
62
Thyroid Gland Hormones
• Follicle cells
– Simple cuboidal epithelium
– Synthesize and release “thyroid hormones”
• T3 (triiodothyronine)
• T4 (tetraiodothyronine)
• C (clear, parafollicular) cells
– Synthesize and release calcitonin
63
Fig 18-10c
64
Fig 18-11a
65
Fig 18-11b
66
Effects of Thyroid Hormones
• Many, diverse effects
• On almost every cell in the body
– Especially metabolically active tissues and organs, e.g.,
skeletal muscle, liver, kidneys
• Increase
– Cellular metabolism, e.g., energy utilization, oxygen
consumption
– RBC formation
– Growth and development
– Heart rate, contraction
– Mineral turnover in bone
• Calorigenic/thermiogenic effect
– Enables body to adapt to cold temperatures
67
Hypothyroidism
• Inadequate production of thyroid hormones
– From inadequate dietary iodide
• Effects
– In later childhood: retarded growth and mental
development; delayed puberty
– In adults: lethargy, unable to tolerate cold temperatures,
leads to myxedema (subcutaneous swelling, dry skin, hair
loss, low body temp, muscular weakness, slowed reflexes)
– Most commonly diagnosed in women >50 y.o.
• Congenital
– Cretinism (in an infant); inadequate skeletal and nervous
development; metabolic rate dec 40%
68
69
Hyperthyroidism
• Excessive quantities of thyroid hormones;
thyrotoxicosis (“poisoning”)
• Effects
– Increased metabolic rate, increased blood pressure and
heart rate, irregular heart beat, skin flushed and moist with
perspiration
– Restless, excitable, subject to shifts in moods and
emotional states
– Limited energy reserves and fatigues easily
• Graves’ Disease
– May be accompanied by exophthalmia or goiter
– Common with age (affected both George Bush Sr. and
Barbara Bush)
70
71
C Cell Hormone Production
• C cells (interspersed between follicles)
– Respond to increased calcium levels
– Produce calcitonin
• Effects of calcitonin
– Decreases calcium levels in body fluids (“tones down” Ca)
• Increases calcium excretion at kidneys
• Inhibits osteoclast activity
– Especially impt during childhood (stimulates bone
growth) and pregnancy (when maternal skeleton
competes with developing fetus for Ca++)
– Opposes action of parathyroid hormone (PTH) which
increases calcium
72
Calcitonin
Figure 6–16b
73
Parathyroid Glands
Fig 18-12a
74
Parathyroid Glands
• Principal (chief) cells
– Respond to decreased calcium levels
– Produce PTH (parathyroid hormone)
• PTH
– Increases calcium levels in body fluids
• Decreases calcium excretion at kidneys
• Stimulates osteoclasts
• Increases intestinal absorption of calcium (with
calcitriol)
– Opposes action of calcitonin (from thyroid) which
decreases calcium
– Primary regulator of blood calcium in adults
75
Parathyroid Hormone (PTH)
Figure 6–16a
76
Hypoparathyroidism
• Inadequate PTH production
• Low calcium levels in body fluids
• Nervous system more excitable; may lead to
muscle tetany (prolonged muscle spasms that
initially involve limbs and face)
77
Hyperparathyroidism
•
•
•
•
•
•
Abnormally high PTH levels
High calcium levels in body fluids
CNS function depressed
Thin, brittle bones; weak skeletal muscles
Nausea, vomiting
May become comatose
78
Functions of Calcium
• Calcium especially important to
– Membranes
– Neurons (conduction)
– Muscle cells (contraction; especially cardiac)
• Must be closely regulated
79
Review of Calcium Homeostasis
• Regulated by 2 major hormones
– Calcitonin
– PTH
• Hormones affect:
– Ca excretion (kidneys)
– Ca storage (bones)
– Ca absorption (digestive tract)
• Calcium homeostasis
– ↑Ca  ↑Calcitonin  ↓Ca
– ↓Ca  ↑PTH  ↑Ca
80
Fig 18-13
81
• Today in class we will:
– Continue our discussion of the hormones (and each
hormone’s function) along with the general effects of
abnormal levels of each hormone produced by the:
• Adrenal glands
– Identify the region of the adrenal gland in which each adrenal
hormone is produced
•
•
•
•
•
•
•
•
Pineal gland
Pancreas
Gastrointestinal tract
Kidneys
Heart
Thymus
Gonads
Adipose tissue
82
• Today in class we will:
– Describe the:
• 4 possible outcomes to exposure to multiple hormones
• Role of hormones in growth
• Hormonal responses to stress
– The 4 possible outcomes when cells are exposed to
multiple hormones
– Examples of complex hormone interactions
– The role of hormones in the growth process
– Hormonal responses to stress
– Interactions between the endocrine system and other
body systems
83
Adrenal Glands
Fig 18-14a
84
Adrenal Glands
• aka Suprarenal glands
• Location
– On superior surface of kidneys
• 2 regions
– Adrenal cortex
•  steroid hormones (adrenocortical steroids/
corticosteroids)
– Adrenal medulla
•  epinephrine and norepinephrine (E, NE)
• Under ANS control)
85
Fig 18-14b
86
Adrenal Cortex: Zona Glomerulosa
• Produces mineralocorticoids, primarily aldosterone
• Effects: primarily on electrolytes
– Increases renal (kidney) reabsorption of sodium (and
water)
– Increases urinary loss of potassium
• Stimulated by:
–
–
–
–
Decreased plasma sodium levels
Increased plasma potassium levels
Decreased blood volume or BP
Angiotensin II
• Inhibited by natriuretic peptides (e.g. atrial
natriuretic peptide, ANP)
87
Adrenal Cortex: Zona Fasciculata
• Produces glucocorticoids (cortisol/cortisone, hydrocortisone)
• Effects
– Glucose-sparing
• In liver-forms glucose and stimulates gluglycogen
• In muscle-releases amino acids for gluconeogenesis (aaglu)
• In adipose tissues-releases lipids for gluconeogenesis; promotes
lipid utilization (like GH)
– Anti-inflammatory
• Inhibits activity of WBCs (cortisone used for poison ivy, insect
bites)
• Stimulated by ACTH
88
Adrenal Cortex: Zona Reticularis
• Produces androgens (converted to estrogens)
• Effects
– Not important in adult men
– Promotes bone growth, muscle growth, and blood
formation in women and children
• Stimulated by ACTH
89
Adrenal Medullae
• Secretes epinephrine and norepinephrine
• E and NE secreted
– Continuously at low levels via exocytosis
– During ANS sympathetic activation
• Effects
– Mobilize energy stores
• Glycogen in skeletal muscle and liver  glucose 
increased muscular strength and endurance
– Accelerate energy utilization
•  breakdown of glucose and fats  ATP
– Increase heart rate and contraction
90
Pineal Gland
Figure 14–11a
91
Pineal Gland
• Has neuroendocrine (neural and endocrine) effects
(like hypothalamus)
• Pinealocytes produce melatonin
– Time-keeping hormone; released in brain in response to
darkness and tells body it’s time for sleep
– Establishes circadian rhythms = daily changes in
physiological processes that follow regular pattern (e.g.,
body temperature, hormone and enzyme levels)
– Inhibits reproductive function, e.g., maturation of sperm,
oocytes, reproductive organs; decreases at puberty
– An antioxidant; may protect CNS neurons from free
radicals (NO, H2O2) generated in active neural tissue
– Inhibits MSH (secreted by anterior pituitary)
92
Pancreas
Figure 18–15
93
Pancreas
• Exocrine
– Clusters of gland cells (pancreatic acini and ducts)
– Release enzyme-rich fluid for digestion into small
intestine
• Endocrine
– Regulates blood glucose concentrations
– 2 major cell types: alpha and beta cells
94
Pancreas
• Alpha cells
– Secrete glucagon
• Released in response to decreased blood glucose levels
• Increase blood glucose levels via:
– Glycogen breakdown  glucose (skeletal muscle and liver)
– Fats  FAs  glucose (adipose tissue)
– Glucose manufacture (liver)
95
Pancreas
• Beta cells
– Secrete insulin
• Released in response to increased blood glucose
• Receptors present in most cell membranes
– Except brain, kidneys, digestive tract epithelium, RBCs (insulinindependent)
• Decreases blood glucose levels
– Increases glucose uptake and utilization by most cells
– Increases glycogen synthesis from glucose in skeletal muscle
and liver
• Stimulates amino acid absorption and protein synthesis
• Stimulates triglyceride formation in adipose tissue
96
Pancreatic Islets
Figure 18–16
97
Review of Glucose Homeostasis
• Increased blood glucose  beta cells  increase insulin
secretion  decreased blood glucose
• Decreased blood glucose  alpha cells  increase glucagon
secretion  increased blood glucose
98
Diabetes Mellitus
• Occurs when glucose concentration so high it
overwhelms normal reabsorption capabilities of
kidneys
–  Glycosuria and polyuria
• Caused by:
– Genetic abnormalities (inadequate insulin production,
abnormal insulin, defective receptor proteins)
– Pathological conditions
– Injuries
– Immune disorders
– Hormonal imbalances
– Obesity
99
Diabetes Mellitus
• Two major types
– Type I
•
•
•
•
Insulin-dependent, juvenile-onset
May be autoimmune disease
Occurs first in childhood or young-adulthood
Body does not produce insulin, so must take daily insulin for
rest of life
– Type II
• Non insulin-dependent, adult-onset
• Develops gradually
• Most often in people over 45, but seen younger (even
children) with increasing obesity problems
• Accounts for 90-95% of diabetes in US
• Body doesn’t make enough insulin or doesn’t use insulin
effectively
100
Diabetes Mellitus
• Symptoms
–
–
–
–
–
–
–
–
Extreme fatigue
Excessive thirst
Frequent urination
Extreme hunger
Weight loss
Irritability
Blurred vision
Vaginal yeast infections
• Chronic Medical Problems
–
–
–
–
Retinopathy, cataracts
Nephropathy
Neuropathy
Degenerative changes in
cardiac circulationTIAs
and early heart attacks
– Reduced blood flow to
limbs; extreme cases
require amputation
101
Gastrointestinal (GI) Tract
• All coordinate digestive activities ( Function):
– Secretin
– Gastrin
– Cholecystokinin
NOTE: There are many hormones associated with the digestive system.
These are just a few examples.
• Primary targets are other regions and organs
of the digestive system
102
Kidneys
Figure 26–2
103
Kidneys
• Hormones produced
– Erythropoietin (EPO)
• Stimulates RBC production by bone marrow
• Secreted when oxygen is low (hypoxia) due to
– Disease
– High altitude
– Calcitriol
• UV radiation  epidermal cells  cholecalciferol (vit
D3)  liver (intermediary product)  kidneys 
calcitriol
• Stimulates calcium and phosphate ion absorption
along the digestive tract
104
Calcitriol
Figure 18–17a
105
Kidneys
• Enzyme produced = renin
– Converts prohormone angiotensinogen to hormone
angiotensin I (in liver) (“tenses blood vessels”)
– Angiotensin I converted to hormone angiotensin II (in lung
capillaries)
– Angiotensin II
• Stimulates adrenal  aldosterone  increased blood Na and volume
(blood pressure, BP)
• Stimulates posterior pituitary  ADH (produced by supraoptic
nucleus of hypothalamus)  increased blood volume (BP)
• Stimulates thirst  increased blood volume (BP)
• Constricts blood vessels  increased BP
106
The Renin–Angiotensin System
Figure 18–17b
107
Heart
• When blood volume high, cardiac muscle cells
produce natriuretic peptides (NPs)
– ANP = atrial NP
– BNP = brain NP (produced by ventricles)
• Natriuretic peptides
– Act opposite to angiotensin II
– Reduce blood volume and blood pressure
108
Thymus
• Produces thymosin hormones
– Help develop and maintain normal immune
defenses (T cell development)
109
Gonads
• Testes
– Interstitial cells  androgens
• Testosterone is most important
– Sustentacular cells  inhibin
• Supports sperm development
• Ovaries
– Follicle cells  produce estrogens
• Primarily estradiol
– After ovulation, follicle cells:
• Reorganize into corpus luteum (CL)
• Release estrogens and progestins, primarily progesterone
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Adipose Tissue Secretions
• Leptin
– Inhibits appetite
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Endocrine Disorders
• GH
– Excess production 
• Gigantism - before epiphyseal plates close
• Acromegaly - after epiphyseal plates close
– Under-production 
• Pituitary growth failure (dwarfism)
• ADH
– Inadequate productiondiabetes insipidus
(polyuria)
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Endocrine Disorders
• Thyroid Gland
– Hypothyroidism
• Cretinism
• Goiter
– Hyperthyroidism
• Graves Disease (exophthalmia)
• Adrenal
– Inadequate GC production 
• Addison’s Disease - inadequate GC production
– Excess GCs  Cushing’s Disease (due to
hypersecretion of ACTH)
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Patterns of Hormonal Interaction
• Cells never respond to only one hormone; respond to
multiple hormones simultaneously
• When cell receives instructions from 2 hormones at once 
4 possible effects:
– Antagonistic (opposing): result depends on balance between two
hormones, e.g., insulin and glucagon, PTH and calcitonin)
– Synergistic (additive): both hormones give same instructions and
effect is magnified, e.g., GH and glucocorticoids  glucose-sparing
effect
– Permissive: first hormone needed for second hormone to produce
effect, e.g., thyroid hormones must be present for epinephrine
effect on energy consumption
– Integrative (different but complementary results): important in
coordinating activities of different physiological systems, e.g.,
calcitriol and PTH effects on tissues involved in calcium metabolism
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Examples of Complex Hormone
Interactions
• Growth
– Involves GH, thyroid hormones, insulin, PTH,
calcitriol, reproductive hormones
• Behavior
– Many hormones involved
– Produce changes in mood, emotional states
and behavior
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Examples of Complex Hormone
Interactions
• Stress
– General Adaptation Syndrome (GAS) or stress
response
– Divided into 3 phases
• Alarm phase
• Resistance phase
• Exhaustion phase
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Figure 18–18
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General Adaptation Syndrome
• Alarm phase
– Immediate response
– Directed by sympathetic division of ANS
– Epinephrine is dominant hormone
– Energy reserves (glucose) mobilized from
glycogen
– “Fight or flight” responses
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General Adaptation Syndrome
• Resistance phase
– Entered if stress lasts longer than few hours
– Energy demands still high
• Glycogen reserves nearly exhausted after hours of
stress
– Glucocorticoids are dominant hormones
• Mobilize lipid and protein reserves
• Raise and stabilize blood glucose concentrations
• Conserve glucose for neural tissues
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General Adaptation Syndrome
• Exhaustion phase
– Begins when homeostatic regulation breaks
down
– Failure of 1 or more organ systems proves fatal
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Interactions between
Endocrine and Other Systems
Figure 18–19
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