Chapter 45 Chapter 45 Hormones & the Endocrine SystemHormones & the Endocrine System
Roohi RamachandranRoohi Ramachandran
Vocab.• Endocrine glands: ductless gland that secretes hormones directly
into interstitial fluid, from which they diffuse into the bloodstream
• Exocrine glands: have ducts that carry secreted substances onto body surfaces or into body cavities, e.g. salivary glands
• Hormones: one of many types of secreted chemicals that are formed in specialized cells, travel in body fluids and act on specific target cells in other parts of the body to change their functioning
• Target cells: cells that have receptors for a particular hormone
• Neurosecretory cells: specialized neurons found in the brain that secrete molecules that diffuse from nerve cell endings into the bloodstream
• Neurotransmitters: molecules released from the synaptic terminal of a neuron at a chemical synapse, diffuses across the synaptic cleft and binds to the postsynaptic cell, triggering a response
Nervous & Endocrine Systems
• Work together to maintain homeostasis, development and reproduction
• Hypothalamus: receives information from nerves throughout body and brain and initiates endocrine signalling according to environmental conditions
Insect Development
Brain
Neurosecretory cells
Corpus cardiacum
Corpus allatum
EARLYLARVA
LATERLARVA PUPA ADULT
Prothoracicgland
Ecdysone
Brainhormone (BH)
Juvenilehormone(JH)
LowJH
Brain
Neurosecretory cells
Corpus cardiacum
Corpus allatum
EARLYLARVA
LATERLARVA PUPA ADULT
EARLYLARVA
LATERLARVA PUPA ADULT
Prothoracicgland
Ecdysone
Brainhormone (BH)
Juvenilehormone(JH)
LowJH
• Neurosecretory cells produce PTTH
• PTTH signals ecdysone release
• Each ecdysone release stimulates molting
• Juveline hormone determines effect of ecdysone; high concentration suppresses metamorphosis
Types of Signalling Molecules• Local regulators: secreted
molecules that act over short distances and reach their target cells solely by diffusion
• Hormones: molecule secreted into extracellular fluid, circulates in blood/hemolymph and communicates regulatory messages throughout body
• Pheromones: small molecule released into environment that functions in communication between same species; acts like hormone in animals
Inflammation
• Interleukins: regulate lymphocytes, other immune cells
• Prostaglandins: promote inflammation & fever, intensify pain, regulate platelet aggregation (blood clotting)
• Histamines: blood vessel dilation – more permeable to inflammatory response
Local Regulators• Have varied effects because of
differences in target cells’ reception, transduction and/or response
• Prostaglandins:– Childbirth: excite muscles,
induce labor– Immune: fever, inflammation,
intensify pain• Nitric Oxide (NO)
– Neurons: neurotransmitter– White blood cells: kills bacteria
and cancer cells– Endothelial cells: dilates the
walls of blood vessels
Regulation & Communication
Figure 8.19 (b) Competitive inhibition
A competitiveinhibitor mimics the
substrate, competingfor the active site.
Competitiveinhibitor
A substrate canbind normally to the
active site of anenzyme.
Substrate
Active site
Enzyme
(a) Normal binding
Figure 8.19 (b) Competitive inhibition
A competitiveinhibitor mimics the
substrate, competingfor the active site.
Competitiveinhibitor
A substrate canbind normally to the
active site of anenzyme.
Substrate
Active site
Enzyme
(a) Normal binding
(b) Competitive inhibition
A competitiveinhibitor mimics the
substrate, competingfor the active site.
Competitiveinhibitor
(b) Competitive inhibition
A competitiveinhibitor mimics the
substrate, competingfor the active site.
Competitiveinhibitor
A competitiveinhibitor mimics the
substrate, competingfor the active site.
Competitiveinhibitor
A substrate canbind normally to the
active site of anenzyme.
Substrate
Active site
Enzyme
(a) Normal binding
Figure 8.19
A noncompetitiveinhibitor binds to theenzyme away from
the active site, alteringthe conformation of
the enzyme so that itsactive site no longer
functions.
Noncompetitive inhibitor
(c) Noncompetitive inhibitionFigure 8.19
A noncompetitiveinhibitor binds to theenzyme away from
the active site, alteringthe conformation of
the enzyme so that itsactive site no longer
functions.
Noncompetitive inhibitor
(c) Noncompetitive inhibition
A noncompetitiveinhibitor binds to theenzyme away from
the active site, alteringthe conformation of
the enzyme so that itsactive site no longer
functions.
Noncompetitive inhibitor
(c) Noncompetitive inhibition
Active siteavailable
Isoleucineused up bycell
Feedbackinhibition
Isoleucinebinds to allostericsite
Active site of enzyme 1 no longer binds threonine;pathway is switched off
Initial substrate(threonine)
Threoninein active site
Enzyme 1(threoninedeaminase)
Intermediate A
Intermediate B
Intermediate C
Intermediate D
Enzyme 2
Enzyme 3
Enzyme 4
Enzyme 5
End product(isoleucine)
Figure 8.21
Active siteavailable
Isoleucineused up bycell
Feedbackinhibition
Isoleucinebinds to allostericsite
Active site of enzyme 1 no longer binds threonine;pathway is switched off
Initial substrate(threonine)
Threoninein active site
Enzyme 1(threoninedeaminase)
Intermediate A
Intermediate B
Intermediate C
Intermediate D
Enzyme 2
Enzyme 3
Enzyme 4
Enzyme 5
End product(isoleucine)
Active siteavailable
Isoleucineused up bycell
Feedbackinhibition
Isoleucinebinds to allostericsite
Active site of enzyme 1 no longer binds threonine;pathway is switched off
Initial substrate(threonine)
Threoninein active site
Enzyme 1(threoninedeaminase)
Intermediate A
Intermediate B
Intermediate C
Intermediate D
Enzyme 2
Enzyme 3
Enzyme 4
Enzyme 5
End product(isoleucine)
Figure 8.21
EXTRACELLULARFLUID
Receptor
Signal molecule
Relay molecules in a signal transduction pathway
Plasma membraneCYTOPLASM
Activationof cellularresponse
Figure 11.5
EXTRACELLULARFLUID
Receptor
Signal molecule
Relay molecules in a signal transduction pathway
Plasma membraneCYTOPLASM
Activationof cellularresponse
EXTRACELLULARFLUID
Receptor
Signal molecule
Relay molecules in a signal transduction pathway
Plasma membraneCYTOPLASM
Activationof cellularresponse
Figure 11.5
Hormones are signalling molecules. Their receptors can be affected by (non)competitive inhibitors. Negative feedback loops (feedback inhibition) regulate them.
Hypothalamus & PituitaryTropic Effects OnlyFSH, follicle-stimulating hormoneLH, luteinizing hormoneTSH, thyroid-stimulating hormoneACTH, adrenocorticotropic hormone
Nontropic Effects OnlyProlactinMSH, melanocyte-stimulating hormoneEndorphin
Nontropic and Tropic EffectsGrowth hormone
Neurosecretory cellsof the hypothalamus
Portal vessels
Endocrine cells of theanterior pituitary
Hypothalamicreleasinghormones(red dots)
HORMONE FSH and LH TSH ACTH Prolactin MSH Endorphin Growth hormone
TARGET Testes orovaries
Thyroid Adrenalcortex
Mammaryglands
Melanocytes Pain receptorsin the brain
Liver Bones
Pituitary hormones(blue dots)
Figure 45.8
Tropic Effects OnlyFSH, follicle-stimulating hormoneLH, luteinizing hormoneTSH, thyroid-stimulating hormoneACTH, adrenocorticotropic hormone
Nontropic Effects OnlyProlactinMSH, melanocyte-stimulating hormoneEndorphin
Nontropic and Tropic EffectsGrowth hormone
Neurosecretory cellsof the hypothalamus
Portal vessels
Endocrine cells of theanterior pituitary
Hypothalamicreleasinghormones(red dots)
HORMONE FSH and LH TSH ACTH Prolactin MSH Endorphin Growth hormone
TARGET Testes orovaries
Thyroid Adrenalcortex
Mammaryglands
Melanocytes Pain receptorsin the brain
Liver Bones
Pituitary hormones(blue dots)
Tropic Effects OnlyFSH, follicle-stimulating hormoneLH, luteinizing hormoneTSH, thyroid-stimulating hormoneACTH, adrenocorticotropic hormone
Nontropic Effects OnlyProlactinMSH, melanocyte-stimulating hormoneEndorphin
Nontropic and Tropic EffectsGrowth hormone
Neurosecretory cellsof the hypothalamus
Portal vessels
Endocrine cells of theanterior pituitary
Hypothalamicreleasinghormones(red dots)
HORMONE FSH and LH TSH ACTH Prolactin MSH Endorphin Growth hormone
TARGET Testes orovaries
Thyroid Adrenalcortex
Mammaryglands
Melanocytes Pain receptorsin the brain
Liver Bones
Tropic Effects OnlyFSH, follicle-stimulating hormoneLH, luteinizing hormoneTSH, thyroid-stimulating hormoneACTH, adrenocorticotropic hormone
Nontropic Effects OnlyProlactinMSH, melanocyte-stimulating hormoneEndorphin
Nontropic and Tropic EffectsGrowth hormone
Neurosecretory cellsof the hypothalamus
Portal vessels
Endocrine cells of theanterior pituitary
Hypothalamicreleasinghormones(red dots)
HORMONE FSH and LH TSH ACTH Prolactin MSH Endorphin Growth hormone
TARGET Testes orovaries
Thyroid Adrenalcortex
Mammaryglands
Melanocytes Pain receptorsin the brain
Liver Bones
Pituitary hormones(blue dots)
Figure 45.8
Hypothalamus
Neurosecretorycells of thehypothalamus
Axon
Anteriorpituitary
Posteriorpituitary
HORMONE ADH Oxytocin
TARGET Kidney tubules Mammary glands,uterine muscles
Hypothalamus
Neurosecretorycells of thehypothalamus
Axon
Anteriorpituitary
Posteriorpituitary
HORMONE ADH Oxytocin
TARGET Kidney tubules Mammary glands,uterine muscles
• Hypothalamus: maintains homeostasis, coordinates endocrine & nervous systems
• Anterior pituitary: synthesize/secrete several tropic/nontropic hormones; regulated by hypothalamus
• Posterior pituitary: extension of hypothalamus; stores/secretes oxytocin & ADH
Pineal, Thyroid, Parathyroid• Pineal gland: in center of brain;
synthesizes/secretes melatonin• Thyroid gland: two lobes on ventral
side of trachea; secretes iodine-containing T3 and T4, which control
metabolism & development; regulated by TSH (thyroid stimulating hormone)
• Parathyroid gland: four small structures embedded in back of thyroid; regulate Ca2+ levels (PTH decomposes bone, stimulates reabsorption in kidneys, activates Vitamin D to stimulate intestines to absorb)
CalcitoninThyroid glandreleasescalcitonin.
StimulatesCa2+ depositionin bones
ReducesCa2+ uptakein kidneys
STIMULUS:Rising bloodCa2+ level
Blood Ca2+
level declinesto set point
Homeostasis:Blood Ca2+ level
(about 10 mg/100 mL)
Blood Ca2+
level risesto set point
STIMULUS:Falling bloodCa2+ level
StimulatesCa2+ releasefrom bones
Parathyroidgland
IncreasesCa2+ uptakein intestines
Activevitamin D
Stimulates Ca2+
uptake in kidneys
PTH
Figure 45.11
CalcitoninThyroid glandreleasescalcitonin.
StimulatesCa2+ depositionin bones
ReducesCa2+ uptakein kidneys
STIMULUS:Rising bloodCa2+ level
Blood Ca2+
level declinesto set point
Homeostasis:Blood Ca2+ level
(about 10 mg/100 mL)
Blood Ca2+
level risesto set point
STIMULUS:Falling bloodCa2+ level
StimulatesCa2+ releasefrom bones
Parathyroidgland
IncreasesCa2+ uptakein intestines
Activevitamin D
Stimulates Ca2+
uptake in kidneys
PTH
CalcitoninThyroid glandreleasescalcitonin.
StimulatesCa2+ depositionin bones
ReducesCa2+ uptakein kidneys
STIMULUS:Rising bloodCa2+ level
Blood Ca2+
level declinesto set point
Homeostasis:Blood Ca2+ level
(about 10 mg/100 mL)
Blood Ca2+
level risesto set point
STIMULUS:Falling bloodCa2+ level
StimulatesCa2+ releasefrom bones
Parathyroidgland
IncreasesCa2+ uptakein intestines
Activevitamin D
Stimulates Ca2+
uptake in kidneys
PTH
Figure 45.11
PancreasBeta cells ofpancreas are stimulatedto release insulininto the blood.
Insulin
Liver takesup glucoseand stores itas glycogen.
Body cellstake up moreglucose.
Blood glucose leveldeclines to set point;stimulus for insulinrelease diminishes.
STIMULUS:Rising blood glucose
level (for instance, aftereating a carbohydrate-
rich meal)
Homeostasis:Blood glucose level
(about 90 mg/100 mL)
Blood glucose levelrises to set point;
stimulus for glucagonrelease diminishes.
STIMULUS:Dropping blood glucoselevel (for instance, after
skipping a meal)
Alpha cells of pancreasare stimulated to releaseglucagon into the blood.
Liver breaksdown glycogenand releasesglucose intoblood.
GlucagonFigure 45.12
Beta cells ofpancreas are stimulatedto release insulininto the blood.
Insulin
Liver takesup glucoseand stores itas glycogen.
Body cellstake up moreglucose.
Blood glucose leveldeclines to set point;stimulus for insulinrelease diminishes.
STIMULUS:Rising blood glucose
level (for instance, aftereating a carbohydrate-
rich meal)
Homeostasis:Blood glucose level
(about 90 mg/100 mL)
Blood glucose levelrises to set point;
stimulus for glucagonrelease diminishes.
STIMULUS:Dropping blood glucoselevel (for instance, after
skipping a meal)
Alpha cells of pancreasare stimulated to releaseglucagon into the blood.
Liver breaksdown glycogenand releasesglucose intoblood.
Glucagon
Beta cells ofpancreas are stimulatedto release insulininto the blood.
Insulin
Liver takesup glucoseand stores itas glycogen.
Body cellstake up moreglucose.
Blood glucose leveldeclines to set point;stimulus for insulinrelease diminishes.
STIMULUS:Rising blood glucose
level (for instance, aftereating a carbohydrate-
rich meal)
Homeostasis:Blood glucose level
(about 90 mg/100 mL)
Blood glucose levelrises to set point;
stimulus for glucagonrelease diminishes.
STIMULUS:Dropping blood glucoselevel (for instance, after
skipping a meal)
Alpha cells of pancreasare stimulated to releaseglucagon into the blood.
Liver breaksdown glycogenand releasesglucose intoblood.
GlucagonFigure 45.12
• Islets of Langerhans: endocrine cells w/i pancreas; secrete into interstitial fluid & circulate– Alpha cells: glucagon– Beta cells: insulin
• Insulin lowers blood glucose by stimulating glucose uptake in body cells
• Glucagon signals liver to increase glycogen hydrolysis, convert aminos & glycerol to glucose & release glucose into bloodstream
Spinal cord(cross section)
Nervesignals
Nervecell
Releasinghormone
Hypothalamus
Anterior pituitary
Blood vessel
ACTH
Adrenalgland
Kidney
Adrenal medullasecretes epinephrineand norepinephrine.
Effects of epinephrine and norepinephrine:
1. Glycogen broken down to glucose; increasedblood glucose
2. Increased blood pressure
3. Increased breathing rate
4. Increased metabolic rate
Effects ofmineralocorticoids:
1. Retention of sodiumions and water bykidneys
2. Increased bloodvolume and bloodpressure
Effects ofglucocorticoids:
1. Proteins and fatsbroken down andconverted to glucose,leading to increasedblood glucose
(b) Long-term stress response(a) Short-term stress response
Nerve cell
Spinal cord(cross section)
Nervesignals
Nervecell
Releasinghormone
Hypothalamus
Anterior pituitary
Blood vessel
ACTH
Adrenalgland
Kidney
Adrenal medullasecretes epinephrineand norepinephrine.
Effects of epinephrine and norepinephrine:
1. Glycogen broken down to glucose; increasedblood glucose
2. Increased blood pressure
3. Increased breathing rate
4. Increased metabolic rate
Effects ofmineralocorticoids:
1. Retention of sodiumions and water bykidneys
2. Increased bloodvolume and bloodpressure
Effects ofglucocorticoids:
1. Proteins and fatsbroken down andconverted to glucose,leading to increasedblood glucose
(b) Long-term stress response(a) Short-term stress response
Nerve cell
Adrenal Glands• Adrenal glands: near kidneys
• Adrenal medulla: secretes epinephrine/norepinephrin in response to stress; regulates metabolism, blood pressure, etc.
• Adrenal cortex: secrete glucocorticoids (promote glucose synthesis) and mineralocorticoids (maintain salt/water balance)
Gonads• Gonads produce following hormones:
• Androgen: any steroid that stimulates development of male reproductive system
• Testosterone: major mammalian androgen
• Estrogen: any steroid that stimulates development of female reproductive system
• Estradiol: major mammalian estrogen
• Progestin: any steroid w/ progesterone-like activity
• Progesterone: steroid that prepares uterus for pregnancy; major mammalian progestin
• All are produced in both genders – proportions differ
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