Endocrine System Review
Two major regulatory systems in the body: neural and endocrine
Endocrine functions:
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Regulating water-electrolyte balance and organic metabolism
Helping body cope with stress
Promoting growth/development
Controlling reproduction
Regulate RBC production
Working with autonomic NS to control circulation, digestion and absorption
Tropic hormone – primary function is to regulate hormone secretion by another endocrine gland
Remember:
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One endocrine gland may produce many hormones
The same hormone may be produced by two different glands
One hormone may have various target cells
Some hormone release is cyclic in pattern
One target cell may be influenced by multiple hormones
The same messenger may be a hormone or neurotransmitter depending on source/delivery
Some organs/glands may have endocrine and non-endocrine functions
General Mechanisms for Hormone Secretion control:
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Negative-feedback
o Output counteracts a change in input
Neuroendocrine
o Sudden increase in hormone secretion by neural and hormonal control
Diurnal (circadian)
o Rhythmically fluctuate up and down with time
Pituitary Gland
Located in the bone cavity at base of brain below hypothalamus, connected to hypothalamus by stalk
Anterior lobe – glandular epithelial tissue, secretes peptide hormones
Thyroid Stimulating (TSH)
Adrenocorticotropic (ACTH)
Growth Hormone (GH)
Follicle-Stimulating (FSH)
Thyroid follicular cells
Zona fasciculata/reticularis of
adrenal cortex
Bone/soft tissue, liver
Ovarian follicles
Stimulate T3/T4 production (thyroid)
Stimulate cortisol secretion (adrenal cortex)
Growth, anabolism
Follicular growth/development (ovary)
Estrogen secretion
Seminiferous tubules
Sperm production (testes)
Luteinizing (LH)
Ovarian follicle/corpus luteum
Ovulation, corpus luteum development, estrogen
and progesterone secretion (ovary)
Prolactin
Mammary glands
Breast development
Milk secretion
Corticotropin-releasing hormone  ACTH, Thyroid-releasing hormone  TSH, Gonadotropin-releasing hormone (GnRH) 
LH/FSH, Growth-releasing/inhibiting hormone  GH, Prolactin-releasing/inhibiting hormone  PRL
Hypothalamic-Hypophyseal portal system – vascular connection between the hypothalamus and anterior pituitary used for
pickup/delivery of hypophysiotropic hormones
TSH, ACTH, FSH and LH are tropic – regulate secretion of another endocrine gland
FSH and LH are collectively called Gonadotropins, TSH called Thyrotropin, GH called Somatotropin
Posterior lobe – nervous tissue, forms neuroendocrine system with hypothalamus using neurosecretory neurons, does not
produce hormones but releases them when stimulated by the hypothalamus
Vasopressin/ADH (Supraoptic)
Oxytocin (Paraventricular)
Kidney tubules
Arterioles
Uterus
Mammary glands
Increase water reabsorption
Vasoconstriction
Increases contractility
Milk ejection
Stress Response
Stress  Hypothalamus  Corticotropin-releasing H  anterior pituitary  ACTH  adrenal cortex  cortisol
Growth Hormone (GH)
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Simulates liver to make somatomedins, primary is insulin-like growth factor (IGF-1)
o Acts directly on bone/soft tissue
o Stimulates protein synthesis, cell division, lengthening/strengthening of bones
Metabolic effects
o Increases triglyceride breakdown
o Decreases glucose uptake by muscles
GH hyposecretion
o Pituitary or hypothalamic defect
o Can cause dwarfism in children and little effect in adults
GH hypersecretion
o Tumor of anterior pituitary
o Can cause gigantism before epiphyseal plates close
o Acromegaly or thickening of bones in extremities/face
Other hormones are essential for growth
o Thyroid hormone – hyposecretion causes stunted growth in children
o Insulin – decreased/excessive growth
o Androgens – pubertal growth spurt, protein synthesis
o Estrogens
Pineal Gland
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Secretes the hormone melatonin – keep body’s circadian rhythms in synchrony, increased secretion during the night
(light-dark cues)
Suprachiasmatic nucleus (SCN) serves as pacemaker for rhythms
Jet lag – not maintaining the internal clock with external environment
Photoreceptors in the eye transmit signals to SCN to maintain this clock
Thyroid Gland
Located on the trachea below the larynx consisting of two lobes joined by narrow tissue, largest endocrine gland, involved in
production, storage and release of thyroid hormone
Follicular cells:
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Surround a hollow sphere of colloid to form function unit - follicle
o Extracellular storage site for TH
Produce iodine-containing hormones derived from tyrosine
o T4/thyroxine/tetraiodothyronine
o T3/triiodothyronine
C-cell secrete calcitonin
TH Synthesis
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Requires tyrosine (made by body) and iodine (diet)
Thyroglobulin (contains tyrosine) is excreted by follicular cells into colloid
Thyroid gland transfers iodine in colloid via iodine-pump
Tyrosine and iodine bind and T3/T4 formed
TH Storage – remain in colloid until secretion, supply is enough to last body several months
TH Secretion – follicular cells thyroglobulin colloid freeing T3 and T4 (lipophilic) to diffuse across plasma membrane, T3>T4
Thyroid Gland Follicular Cells
T3/T4
Most cells
Thyroid Gland C Cells
Calcitonin
Bone
Increased metabolic rate
Improves cardiac and muscle contractility
Increases target cell response to catecholamines
Increases GH secretion
Required for proper neural growth
Increases bowel motility
Decreases LDL (bad) cholesterol
Decreases plasma [Ca2+]
Hypothyroidism
Causes – failure of the thyroid, deficiency of TRH, TSH or both, too little dietary iodine intake
Symptoms - overall reduction in metabolic activity, sensitive to cold, weight gain, easily fatigued, weak pulse, slow reflexes, slow
speech, poor memory
Myxedema – water-retaining carbohydrate molecules enter skin resulting in puffy appearance on face/extremities
Cretinism – from birth, dwarfism, mental retardation
Treatment – replacement therapy, add iodine to diet
Hyperthyroidism
Causes - Grave’s disease – most common cause, autoimmune disease that targets TSH receptors on thyroid gland acting like TSH
but lacking the negative feedback regulation
Goiter – can occur with hypo/hyperthyroidism when thyroid gland is stimulated
Symptoms – high metabolic rate, sensitive to heat/sweating, low body weight, weakness, high cardiac output, irritability,
anxiousness, exophthalmos – water-retaining carbohydrates deposited behind the eye (bulging)
Treatment – surgical removal of portion of thyroid gland, give radioactive iodine which destroys thyroid tissue, antithyroid drugs
that interfere with TH synthesis
Parathyroid Gland
Four tiny glands located on the back surface of the thyroid gland
Parathyroid hormone (PTH)
Bones, kidneys, intestines
Increase plasma [Ca2+]
Decrease plasma [PO43-]
Stimulate Vitamin D activation
Remember – Calcium allows for excitation-contraction coupling in muscles, without it, death would ensue from asphyxiation
cause by hypocalcemic spasm of respiratory muscle
Also, plasma [Ca2+] affects stimulus-secretion coupling, maintaining tight junctions between cells, blood clotting
Which hormones regulate plasma [Ca2+]?
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PTH
Calcitonin
Vitamin D
Bone density peaks at age 30 and declines after that. When bone resorption (removal) exceeds bone formation, the result is
disease such as osteoporosis – reduced bone density, bones lose minerals such as calcium (99% of this mineral is in the bones)
leading to breakage, fragility and weakness
Bone cells:
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Osteoblast – secrete extracellular organic matrix (make bone)
Osteoclast – resorb bone in vicinity by releasing acid to break down matrix (break bone)
Osteocyte – retired osteoblasts that make up main structure of bone
Hypercalcemia
PTH hypersecretion, [PO34-] reduced, reduced nerve/muscle excitability, bone thinning, kidney stones
Calcitonin – produced by C cells, secreted when plasma [Ca2+] is high and acts to lower it, inhibits osteoclast activity
Hypocalcemia
PTH hyposecretion, [PO34-] increased, increased nerve/muscle excitability, irritability, paranoia
Vitamin D Deficiency
Impaired intestinal absorption of calcium because Vitamin D (must be activated by kidney and liver, also made by sunlight) is
essential for this process, PTH maintains plasma [Ca2+] level at the expense of bone health, known as rickets in children and
osteomalacia in adults
Adrenals
Located above the kidneys in a capsule of fat, external to the peritoneal sac, outer layer is adrenal cortex (steroidal hormones)
and inner layer is adrenal medulla (catecholamines) – both are separate endocrine organs
Adrenal Cortex
Zona glomerulosa (O)
Zona fasciculate (M/biggest)
Zona reticularis (I)
Aldosterone
(Mineralocorticoid)
Cortisol
(Glucocorticoid)
Kidney tubules
Androgens
(Like sex hormones)
Bone/brain (females only)
Most cells
Increase Na+ reabsorption
Increase K+ secretion
Increase blood glucose at the
expense of storage
Stress response
Pubertal growth spurt
Sex drive
Aldosterone
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Acts on distal and collecting tubules of kidney
Secretion increased by
o Activation of rennin-angiotension-aldosterone system  reduce [Na+] and BP
o Direct stimulation on cortex by increasing plasma [K+]
Independent of anterior pituitary control
Cortisol
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Stimulates gluconeogenesis in liver
Inhibits glucose uptake (not in brain)
Stimulates protein degradation and lipolysis
Stress response
Can have anti-inflammatory/immunosuppressive effects (should not use long term)
Displays diurnal rhythm
Involved in negative feedback loop involving CRH (hypothalamus) and ACTH (pituitary)
Androgens
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Dehydroepiandrosterone (DHEA) is the only adrenal sex hormone with biological importance
Overpowered by testosterone in males
Facilitates growth of pubic hair, growth spurt and sex drive in women
Disorders
Aldosterone hypersecretion – adrenal tumor (Conn’s Syndrome) or high activity of rennin-angiotensin system Symptoms – high
Na+ retention/K+ depletion, high BP
Cortisol hyposecretion – Cushing’s Syndrome, causes include excessive CRH and ACTH, cortisol-releasing or ACTH-releasing
adrenal tumor, Symptoms – hyperglycemia, glucosuria (adrenal diabetes), abnormal fat distribution
Androgen hypersecretion –
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Adult female – hirsutism: deep voice, muscular arms/legs, small breast, menstruation ceases
Newborn female – male external genitalia
Pre-pubertal male – pseudopuberty
Adult male – no effect
Adrenocorticol insufficiency –
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Addison’s Disease (primary)
Autoimmune disease (primary)
o Aldosterone deficiency
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o Cortisol deficiency
Secondary
o Hypothalamic/pituitary deficiency
Adrenal Medulla
Epinephrine/Norepinephrine
(catecholamines)
Sympathetic receptor sight throughout
body
Reinforces sympathetic response
Helps with stress response
Blood pressure regulation
Medulla is –
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Modified part of sympathetic nervous system (postganglionic)
When stressed, site of primary adrenomedullary secretion
Epinephrine/norepinephrine secreted into blood by exocytosis (chromaffin granules)
o Fight or flight response
o Maintain arterial BP
o Increase blood glucose and fatty acids
General Stress Response
SNS stimulation  Epinephrine secretion  CRH-ACTH-cortisol system activated (mobilize metabolic resources)  elevated
blood glucose/fatty acid  decrease insulin/increase glucagon  maintain blood volume/pressure  rennin-angiotensin system
activated  vasopressin secretion increased
Interconversion Among Organic Molecules
Glucose
Fatty acids
Amino acids (protein)
Liver/muscle
Adipose tissue
Muscle
Glycogen
Triglyceride
Body protein
Primary energy source
Primary reservoir
Source during fasting
Major tissues
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Liver – maintain normal blood glucose levels, site of interconversions
Adipose tissue – energy storage
Muscle – primary amino acid storage, major energy user
Brain – can only use glucose but does not store glycogen
Pancreas
Is an exocrine (secretes solution into digestive tract through duct) and endocrine organ
Islet of Langerhans
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Cluster of endocrine cells between exocrine cells
Has various cell types
o Beta (B) cells – most abundant, synthesize/secrete insulin
o Alpha (a) cells – synthesize/secrete glucagon
o Delta (D) cells – synthesize/secrete somatostatin
o F cells (PP cells) – secrete pancreatic polypeptide (may deal with appetite control), least common
Insulin and glucagon regulate fuel metabolism
Somatostatin – released when blood sugar/amino acids are high during absorption, decrease secretion of insulin, glucagon, and
itself, more research needed
Insulin – anabolic, promotes uptake of glucose, fatty acids and amino acids turning them into stores, secreted during absorptive
state when blood glucose is high
Glucagon – mobilizes energy-rich molecules during postabsorptive state when blood glucose is low, opposes action of insulin, no
known clinical abnormalities with this hormone
Disorders
Diabetes Melllitus – elevated blood glucose level, “sweet” urine
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Type I – lack of insulin secretion, childhood, 10-20%, autoimmune destruction of B cells, treatment includes insulin
injections, diet management, exercise
Type II – normal/increased insulin secretion but reduced sensitivity of target cells, adulthood, 80-90%, treatment
includes diet and weight control, exercise, sometimes oral hypoglycemic drugs
Hormonal Control of Fuel Metabolism
Hormone
Insulin
Blood glucose
Glucose uptake
Make glycogen
Glucagon
Break glycogen
Make glucose
Break glycogen
Make glucose
Secrete glucagon
Make glucose
Decrease glucose
uptake by tissues
Decrease glucose
uptake by muscle
Epinephrine
Cortisol
Growth Hormone
Metabolic Effect
Blood Fatty Acid
Make triglyceride
Blood Amino Acid
AA uptake
Muscle protein
Make protein
Secretion Stimuli
Inc blood
glucose/AA
Break triglyceride
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Break triglyceride
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Break triglyceride
Break protein
Break protein
Dec blood
glucose, Inc AA
Sympathetic
during stress and
exercise
Stress
Break triglyceride
AA uptake
Make protein,
DNA and RNA
Deep sleep,
stress, exercise,
low blood sugar
Metabolic acidosis
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Severe diarrhea
Diabetes mellitus – excess fat metabolism because glucose cannot be utilized resulting in keto acids
Strenuous excersize – anaerobic glycolysis  lactic acid
Uremic acidosis
Sex Hormones
Undifferentiated reproductive system contains –
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Mullerian ducts – make female reproductive tract
Wolffian ducts – make male reproductive tract
The other duct degenerates resulting in a specific sex
Male Repro
Spermatogenesis requires:
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Leydig cells – produce testosterone stimulated by LH
Sertoli cells – produce androgen-binding protein (ABP) stimulated by FSH
Role in Metabolism
Regulator in postabs/absorptive
cycle
Same as insulin
Energy for
emergency/exercise
Move fuels in
adapting to stress
Growth
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4.
Remember – GnRH stimulates release of FSH and LH
Parts of sperm: acrosome covers head (nucleus), centricle connects head to midpiece (contains mitochondria), tail is
microtubules
Female Repro
Ovarian cycle alternates between two phases (1) follicular – presence of maturing follicle (2) – presence of corpus luteum,
interrupted if pregnancy occurs and lasts ~ 28 days
Follicle – secretes estrogen during first ½ of cycle
Corpus luteum – secretes progesterone and estrogen during second ½
Estrogen – LH/FSH convert androgens to estrogen
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Low concentrations – negative feedback inhibition of LH/FSH during follicular phase
High concentrations – anterior pituitary secretes more LH/FSH resulting in LH surge and ovulation
Essential for egg maturation/release
Stimulates granulosa cell proliferation  follicle maturation
Thins cervical mucous so sperm can penetrate
Triggers onset of parturition
Progesterone – negative feedback inhibition of LH/FSH preventing surge during luteal phase/pregnancy
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Make uterus a good environment for embryo
Forms thick mucus plug at cervix
Inhibits GnRH and Gonadotropin
Stimulates alveolar development but inhibits prolactin/uterine contraction during gestation
Inhibin – acts on the pituitary to inhibit secretion of FSH
Lactation
Prolactin – anterior pituitary hormones that stimulates breast development and milk production in females
Oxytocin – hypothalamic hormone stored in the posterior pituitary stimulating uterine contraction and milk ejection
Suckling  stimulate mechanoreceptors  hypothalamus  posterior pituitary releases Oxytocin  myoepithelial cells
surrounding alveoli contract  milk ejection
Sucking  stimulate mechanoreceptors  hypothalamus  increase Prolactin releasing hormone anterior pituitary releases
Prolactin  increases milk secretion