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HORMONES OF THE
ENDOCRINE
SYSTEM
ENDOCRINE
THE HYPOPHYSIS
THE PITUITARY
INFUNDIBULUM
DEVELOPMENT OF PITUITARY
• NEUROHYPOPHYSIS-DOWNGROWTH
OF DIENCEPHALON
• ADENOHYPOPHYSIS--ROOF OF
MOUTH FORMS RHATHKE’S POUCH
ENTER CAPILLARIES
• REGULATORY HORMONES ENTER
CAPILLARY BED
• FENSTRATED ENDOTHELIUM
• ALLOW LARGE MOLECULES TO
ENTER
• HYPOPHYSEAL ARTERY FEEDS
HYPOPHYSEAL PORTAL
SYSTEM
• UNITE TO FORM LARGER VESSELS
• SPIRAL AROUND INFUNDIBULUM
• AS ENTERS ADENOHYPOPHYSIS
FORMS A SECOND CAPILLARY
SYSTEM
• BRANCHES SURROUND ENDOCRINE
CELLS
NEUROHYPOPHYSIS VS
ADENOHYPOPHYIS
• POSTERIOR VS ANTERIOR PITUITARY
• PRODUCES 9 HORMONES TOTAL
– 2 FROM POSTERIOR
– 7 FROM ANTERIOR
• ALL BIND TO MEMBRANE
RECEPTORS
• ALL ACTIVATE c AMP
THE NEUROHYPOPHYSIS
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PARS NERVOSA
CONTAINS AXONS OF HYPOTHALMIC NEURONS
SUPRAOPTIC NUCLEI -- ADH
PARAVENTRICULAR NUCLEI-OXYTOCIN
AXOPLASMIC TRANSPORT
– MOVEMENT OF MATERIALS BETWEEN SOMA AND
SYNAPTIC TERMINALS
– ANTEGRADE FLOW
– RELEASED TO BASMENT MEMBANES OF CAPILLARIES
NEUROHYPOPHYSIS
• COMPOSED PRIMARILY OF UNMYELINATED
NERVE FIBERS
• RELEASE ADH AND OXYTOCIN INTO BLOOD
STREAM
– ADH AND OXYTOCIN ARE PRODUCED BY THE NERVE
CELL BODIES FOUND IN THE HYPOTHALAMUS
• HERRING BODIES
– ARE ACCUMULATIONS OF ADH AND OXYTOCIN
– HERRING BODIES ARE ONLY FOUND IN THE POSTERIOR
PITUITARY
THE POSTERIOR PITUITARY
IS NOT A TRUE ENDOCRINE
GLAND
IT IS A SPECIALIZATION OF THE THAT
ALLOWS THE BRAIN TO MAINTAIN THE
BLOOD BRAIN BARRIER WHILE
ALLOWING THE SECRETION OF
HORMONES INTO THE BLOODSTEAM
THE ADENOHYPOPHYSIS
• PARS DISTALIS
• PARS TUBERALIS
• PARS INTERMEDIUS
– PROMINENT IN ANIMALS
• SECRETES MSH
– FOUND IN HUMAN FETUS
– INCORPORATED INTO PARS DISTALIS IN
THE ADULT HUMAN
HISTOLOGY OF THE
ADENOHYPOPHYSIS
CLASSIFICATION OF
ADENOHYPOPHYSEAL CELLS BY
STAINING CHARACTERISTICS
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ACIDOPHILES
BASOPHILES
CHROMOPHOBES
ROUND TO POLYGONAL SHAPE CELLS
FOUND IN CORDS AND NESTS
CLASSIFICATION BY
SECRETION
• SOMATOTROPHS--GH
• ADRENOCORTICOLIPOTROPES/
CORTICOTROPES--ACTH & MSH
• THYROTROPES--TSH
• LACTOTROPES/MAMMOTROPES--PRL
• GONADOTROPHS--LH & FSH
ADRENOCORTICOLIPOTROPES
SOMATOTROPES
SOMATOTROPE
LACTOTROPES
MAMMOTROPES
THE PARS DISTALIS
• MAJOR PORTION OF THE
ADENOHYPHYSIS
• TINY CLEFT SEPARATES IT FROM
PARS INTERMEDIA
PARS INTERMEDIA
• PRESENT IN ANIMALS
• CAUSES SEASONAL COLOR
CHANGES IN FUR
• PRESENT IN HUMAN FETUS
• PRESENT IN HUMAN CHILD
• INTEGRATES INTO PARS DISTALIS IN
HUMAN ADULT
HORMONES OF THE
PITUITARY
• NEUROHYPOPHYSIS--POSTERIOR
PITUITARY
• ADENOHYPOPHYSIS--ANTERIOR
PITUITARY
HORMONES OF THE
NEUROHYPOPHYSIS
• STORES AND SECRETES
NEUROHORMONES
– ANTIDIURETIC HORMONE
– OXYTOCIN
ANTIDIURETIC HORMONE
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ADH
VASOPRESSIN/ARGININE VASOPRESSIN
PREVENTS DIURESIS (LOSS OF URINE)
CONSTRICTS ARTERIOLES AND RAISES BLOOD
PRESSURE
• SYNTHESIZED IN SUPRAOPTIC NUCLEI OF
HYPOTHALAMUS
• CARRIED IN HYPOTHALAMOHYPOPYSEAL TRACT
• STORED IN AXON TERMINALS IN PITUITARY
ANTIDIURETIC EFFECT
• AFFERENT VAGAL NERVES
• DROP IN PRESSURE STIMULATES
ADH SECRETION
• INCREASE IN PRESSURE INHIBITS
SECRETION
FACTORS THAT INCREASE ADH
SECRETION
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EMOTIONAL STRESS
PHYSICAL STRESS
BLOOD VOLUME
INCREASED PLASMA OSMOTIC PRESSURE
DECREASED EXTRACELLULAR FLUID
VOLUME
• STRENUOUS EXERCISE
• NICOTINE AND BARBITUATES
FACTORS THAT DECREASE
ADH SECRETION
• DROP IN PLASMA OSMOTIC
PRESSURE
• INCREASED EXTRACELLULAR FLUID
VOLUME
• ALCOHOL
ANTIDIURETIC HORMONE IS ONE OF
THE HORMONES THAT HELPS TO
MAINTAIN BLOOD PRESSURE
• BECAUSE URINE IS DERIVED FROM
THE BLOOD—ADH SLOWS
REDUCTIONS IN BLOOD VOLUME
DIABETES INSIPIDUS
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POLYURIA
POLYDYSIA
LOSS OF ADH RELEASE
IMPAIRED WATER CONSERVATION
EXCESSIVE WATER LOSS IN URINE
OXYTOCIN
• WOMEN
• MEN
OXYTOCIN IN WOMEN
• STIMULATES SMOOTH MUSCLE IN
UTERUS
• PROMOTES LABOR AND DELIVER
• STIMULATES MYOEPITHELIAL CELLS
OF MAMMARY GLANDS
OTHER SOURCES OF
OXYTOCIN
• FETUS
• UTERUS
NEUROENDOCRINE REFLEXES CONTROL
OXYTOCIN IN MALES
• UNCERTAIN
• STIMULATES SMOOTH MUSCLE
CONTRACTIONS IN DUCTUS
DEFERENS AND PROSTATE
OXYTOCIN AND SEX
• AROUSAL AND ORGASM
• EMISSION
• CONTRACTIONS THAT PROMOTE
SPERM TRANSPORT
HORMONES OF THE
HYPOTHALAMUS & ADENOHYPOPHYSIS
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TSH
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ACTH
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FSH
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LH
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PRL
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GH
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MSH
LIPOTROPIN
TRH
CRH
GnRH
GnRH
PRH/PIH
GH-RH/SOMATOSTATIN
THYROID STIMULATING
HORMONE
• THYROTROPIN
• RELEASE REGULATED BY THYROTROIN
RELEASING HORMONE (TRH)
• TARGET CELLS IN THRYOID
• TRIGGERS RELEASE OF THYROID HORMONE
THYROID STIMULATING
HORMONE EFFECTS ON THE
THRYOID
• MAIN EFFECT IS TO STIMULATE THE
SECRETION OF THYROID HORONE
ADRENOCORTICOTROPIC
HORMONE
• ALSO CALLED CORTICOTROPIN
• DERIVED FROM
PROOPIMELANOCORTIN
• INCREASES SECRETION OF ADRENAL
HORMONES
• BINDS TO MELANOCYTES AND
INCREASE PIGMENTATION OF SKIN
– IS THE MAJOR FACTOR CONTROLLING
MELANIN PRODUCTION IN THE SKIN
OTHER SUBSTANCES DERIVED
FROM PROOPIMELANOCORTIN
• LIPOTROPINS
• BETA ENDORPHINS
• MELANOCYTE STIMULATING
HORMONE
LIPOTROPINS
• SECRETED FROM SAME CELLS AS
ACTH
• BIND TO MEMBRANE RECEPTORS OF
ADIPOSE CELLS
• CAUSE FAT BREAKDOWN & RELEASE
OF FAT TO CIRCULATION
BETA ENDORPHINS
• SAME EFFECT AS OPIATES
• IMPORTANT FOR ANALGESIA IN RESPONSE
TO STRESS AND EXERCISE
• MAY BE INVOLVED IN
BODY TEMPERATURE
FOOD INTAKE
WATER BALANCE
• STRESS INCREASES SECRETION ALONG
WITH ACTH
MELANOCYTE STIMULATING
HORMONE
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BINDS TO MELANOCYTES
STIMULATES DEPOSITION OF MELANIN
NOT WELL UNDERSTOOD IN HUMANS
IMPORTANT REGULATOR IN OTHER
VERTEBRATES
• PRODUCED IN PARS INTERMEDIA
IN HUMANS PARS INTERMEDIA MERGES
WITH PARS DISTALIS
RELATIONSHIP BETWEEN
MELANOCYTE STIMULATING
HORMONE AND ACTH
• MSH IS SECRETED ALONG WITH
ACTH
• USUALLY NOT IN QUANTITIES
LARGE ENOUGH TO HAVE A
SIGNIFICANT EFFECT
• MAY BE SIGNIFICANT IN ADDISON’S
DISEASE
GONADOTROPINS
• HORMONES PROMOTE GROWTH AND
FUNCTION OF GONADS
• LUTEINIZING HORMONE
• FOLLICLE STIMULATING HORMONE
• REGULATED BY TYPICAL NEGATIVE
FEEDBACK SYSTEM
– INVOLVES LEVELS OF PROGESTERONE,
ESTROGENS AND TESTOSTERONE.
PROLACTIN IN FEMALES
• STIMULATES THE
DEVELOPMENT OF
DUCT SYTEM IN
MAMMARY GLANDS
WITH OTHER
HORMONES
– ESTROGEN,
PROGESTERONE,
GLUCOCORTICOIDS,
PANCREATIC
HORMONES AND
PLACENTAL HORONES.
• RELEASING
HORMONE
• STIMULATES MILK
PRODUCTION
• USUALLY
INHIBITED BY
PROLACTIN
INHIBITING
HORMONE
• STIMULATED BY
PROLACTIN
PROLACTIN IN MALES
• MAKES INTERSTITIAL CELLS MORE
RESPONSIVE TO LUTEINIZING
HORMONE
PROLACTIN IS ALSO SECRETED BY A
VARIETY OF OTHER CELLS IN THE
BODY
• A VARIETY OF IMMUNE CELLS
• BRAIN
• DECIDUA OF PREGNANT UTERUS
CONTROL OF PROLACTIN
SECRETION
• HYPOTHALAMUS CONTINUALLY
SUPPRESSES PROLACTIN SECRETION
– IF YOU LOSE SECRETIONS FROM
HYPOTHALAMUS PROLACTIN
SECRETION INCREASES
– THIS IS DIFFERENT FROM OTHER
ADENOHYPOPHYSEAL HORMONES
DOPAMINE IS THE MAJOR
PROLACTIN INHIBITING
FACTOR
• SECRETED INTO PORTAL SYSTEM BY
NUCLEI IN HYPOTHALAMUS
• INHIBITS BOTH THE SYNTHESIS AND
SECRETION OF PROLACTIN
• THIS IS OF IMPORTANCE BECAUSE
ANYTHING THAT CHANGES
DOPAMINE SECRETION CAN HAVE
EFFECTS ON PROLACTIN SECRETION
HORMONES THAT CAN INCREASE
PROLACTIN SECRETION
• THYROID RELEASING HORMONE
• GONADOTROPIN RELEASING
HORMONE AND VASOACTIVE
INTESTINAL PEPTIDE
STIMULATION OF NIPPLES AND
MAMMARY GLANDS
• DURING NURSING
GROWTH HORMONE
• SECRETION STIMULATED BY
GROWTH HORMONE
RELEASING HORMONE
• SECRETION INHIBITED BY
GROWTH HORMONE
INHIBITING
HORMONE/SOMATOSTATIN
GROWTH HORMONE
• STIMULATES GROWTH OF
CARTILAGE AND BONE
– INDIRECT EFFECTS
– DIRECT EFFECTS
INDIRECT EFFECTS
• SOMATOMEDINS
/INSULIN-LIKE
GROWTH FACTORS
• PEPTIDE HORMONES
• BIND TO MEMBRANE
RECEPTORS
• SKELETAL MUSCLE,
CARTILAGE AND
OTHER TARGET CELLS
EFFECTS ON SKELETAL
MUSCLE FIBERS, CARTILAGE
CELLS AND OTHER TARGETS
• INCREASES RATE OF AMINO ACID UPTAKE
• INCREASE THEIR INCORPORATION INTO
NEW PROTEINS
• EFFECTS SEEN ALMOST IMMEDIATELY
AFTER A MEAL
– MOST IMPORTANT WHEN HIGH
CONCENTRATIONS OF GLUCOSE AND AMINO
ACIDS ARE IN THE BLOOD
FATES OF GLUCOSE AND AMINO
ACIDS
• GLUCOSE
– PRODUCTION OF ATP INCREASES
DURING AEROBIC RESPIRATION
• AMINO ACIDS
– AVAILABLE FOR PROTEIN SYNTHESIS
GROWTH HORMONE IS INDIRECTLY
PROMOTING PROTEIN SYNTHESIS
AND CELL GROWTH
THROUGH THE USE OF
SOMATOMEDIANS
WITHOUT SOMATOMEDIANS
THERE WILL BE NO
DEPOSITION OF CHONDROITIN
SULFATE AND COLLAGE
DIRECT EFFECTS OF GROWTH
HORMONE
• ARE MORE SELECTIVE THAN THE INDIRECT
EFFECTS
• DO NOT SEE THEM UNTIL BLOOD GLUCOSE
AND AMINO ACID LEVELS FALL
• STIMULATES STEM CELL DIVISION AND
GROWTH OF DAUGHTER CELLS
– THESE WILL ULTIMATELY COME UNDER THE
CONTROL OF SOMATOMEDIANS
GROWTH HORMONE ALSO HAS
EFFECTS ON ADIPOSE TISSUE
AND THE LIVER
EFFECTS OF GROWTH HORMONE
ON METABOLISM
• INCREASED PROTEIN SYTHESIS
• INCREASED MOBILIZATION OF FATTY
ACIDS FROM ADIPOSE TISSUE
• INCREASED USE OF FATTY ACIDS
FOR ENERGY
• DECREASED USE OF GLUCOSE
THROUGHOUT BODY
EFFECTS OF GROWTH HORMONE
ON PROTEIN SYNTHESIS
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AMINO ACID TRANSPORT AT THE CELL
PROTEIN SYNTHESIS BY RIBOSOMES
INCREASED LEVELS OF RNA
DECREASED CATABOLISM OF PROTEINS
AND AMINO ACIDS
AMINO ACID TRANSPORT AT
THE CELL
• ENHANCES TRANSPORT INTO CELL
– WORKS WITH INSULIN
• INCREASED AMINO ACID LEVELS
LEAD TO INCREASED PROTEIN
SYNTHESIS
PROTEIN SYNTHESIS BY
RIBOSOMES
• DIRECT EFFECT ON RIBOSOMES
INCREASED LEVELS OF RNA
• INCREASES TRANSCRIPTION RATE
• OVER TIME INCREASES LEVELS OF
RNA
• INCREASED RNA MEANS INCREASE
PROTEIN SYNTHESIS
DECREASED CATABOLISM OF
PROTEINS AND AMINO ACIDS
• DECREASE IN BREAKDOWN OF
PROTEINS TO AMINO ACIDS
• DECREASE OF USE OF AMINO ACIDS
FOR ENERGY SOURCE
• MAY BE DUE TO MOBILIZATION OF
FATTY ACIDS SPARING PROTEIN
EFFECTS OF GROWTH HORMONE
ON FAT METABOLISM
• CAUSE LIPOLYSIS AND THE RELEASE OF
FATTY ACIDS INTO BODY FLUIDS AND
CIRUCLATION
• ENHANCES CONVERSION OF FATTY ACIDS
TO ACETYL CO A
• INCREASES USE OF ACETYL CO A FOR
ENERGY
• FAT METABOLISM FAVORED OVER
CARBOHYDRATE AND PROTEIN
METABOLISM
GROWTH HORMONE
STIMULATES FATTY ACID
METABOLISM
SPARES GLUCOSE AND
AMINO ACIDS
EFFECTS OF GROWTH HORMONE
ON CARBOHYDRATE
METABOLISM
• DECREASES USE OF GLUCOSE FOR
ENERGY
• ENHANCES GLYGOGENESIS
• DIMINISHES GLUCOSE UPTAKE BY
CELLS
DECREASED USE OF
GLUCOSE FOR ENERGY
• PERHAPS DUE TO INCREASED
MOBILIZATION AND UTILIZATION OF
FATS
– THIS LEADS TO LARGE QUANTITIES OF
ACETYL COA
• CAUSES NEGATIVE FEEDBACK ON
GLYCOLYTIC BREAKDOWN OF GLUCOSE
• CAUSES NEGATIVE FEED BACK ON
GLYCOGENOLYSIS
ENHANCES
GLYCOGENOGENESIS
• GLUCOSE NOT USED
• GLUCOSE WILL BE STORED AS
GLYCOGEN
• RESERVES RAPIDLY FILL UP
DIMINISHED GLUCOSE
UPTAKE BY CELLS
• INITIAL INCREASED GLUCOSE
UPTAKE BY
– UNTIL GLYCOGEN RESERVES ARE
FILLED
• THEN UPTAKE DIMINISHES
• GREATLY INCREASED BLOOD
GLUCOSE LEVELS
– 50 TO 100 PERCENT OF NORMAL
SECRETION OF GROWTH
HORMONE
• 3 NANOGRAMS IN ADULT
• 5 NANOGRAMS IN CHILD
• CAN INCREASE TO AS HIGH AS 50
NANOGRAMS
– IF BODY STORES OF PROTEINS OR
CARBOHYDRATES ARE DEPLETED
• IN ACUTE CONDITIONS HYPOGLYCEMIA IS A MORE
POTENT STIMULATOR THAN LOW AMENO ACIDS
• IN STARVATION HIGH LEVELS OF GROWTH HORMONE
ARE CLOSELY RELATED TO PROTEIN DEPLETION
FEEDBACK CONTROL OF GROWTH
HORMONE SECRETION
• STIMULATES RELEASE
– GROWTH HORMONE RELEASING
HORMONE
• INHIBITS RELEASE
• SOMATOSTATIN
• BLOOD LEVELS OF GROWTH
HORMONE
• INSULIN LIKE GROWTH FACTORS
THYROID
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ANTERIOR TO TRACHEA
TWO LOBES
CONNECTED BY ISTHMUS
MAY HAVE PYRAMIDAL LOBE
WELL DEVELOPED NERVOUS
SYSTEM
THYROID FOLLICLES
• HUNDREDS OF THOUSANDS OF
FOLLICLES
• FILLED WITH GELATINOUS COLLOID
• EXTRACELLULAR STORAGE SITE
FOR THYROID HORMONE
PARENCHYME CELLS
• FOLLICULAR CELLS
– MOST PREVELENT
– LINE FOLLICLES
– PRODUCE THYROID HORMONE
• PARAFOLLICULAR CELLS/CLEAR CELLS
– USUALLY LARGER THAN FOLLICULAR
– BETWEEN FOLLICLES
– PRODUCE CALCITONIN
THYROID FOLLICLE
HORMONES OF THE
THYROID GLAND
THYROID HORMONE AND
CALCITONIN
THYROID HORMONE
• THYROXINE (T4 )
• TRIIODOTHRYONINE (T3 )
IMPORTANCE OF
THYROGLOBULIN
• GLYCOPROTEIN
• CONTAINS 140 TYROSINE AMINO
ACIDS
• SUBSTRATE IODINE BINDS WITH
• HORMONES FORM WITHIN
THYROGLOBULIN MOLECULE
IMPORTANCE OF IODINE
• USED ONLY TO MAKE THYROID
HORMONES
• STORED IN THYROID
• IDODIDE PUMP TRAPS IODIDE
THE WEDDING OF
THYROGLOBULIN AND IODIDE
IONS
• OCCURS AT THE COLLOID-CELL INTERFACE
AS THYROGLOBULIN IS SECRETED
• PROCESS IS CALLED ORGANIFICATION OF
THE THYROGLOBULIN
– IODINASE ENZYME
– IODINE BINDS WITH ABOUT 1/6 OF TYROSINE
RESIDUES IN THRYOGLOBULIN MOLECULE
MIT AND DIT
• MONOIODTYROSINE
– ONE IODINE
• DIIODOTYROSINE
– TWO IODINES
• THYROXINE
– MIT PLUS DIT
• TRIIODOTHRYRONINE
– DIT PLUS DIT
THYROGLOBULIN STORAGE
• IN COLLOID OF FOLLICLE
• ONLY HORMONE STORED
EXTRACELLULARLY
• 1-3 MONTH SUPPLY IN COLLOID
RELEASE OF THYROID
HORMONE INTO THE BLOOD
• THYROGLOBULIN IS PICKED UP BY
FOLLICULAR CELLS
• LYSOSOMES FUSE WITH PINOCYTIC
VESICLES
• THYROXINE AND TRIIODOTHYRONINE
ARE CLEAVED FROM THRYOGLOBULIN
AND RELEASED
TRANSPORT IN THE BLOOD
• THRYOXINE BINDING GLOBULIN
• ALBUMINS
THYROID HORMONES AT
THE CELLS
• ENTERS CELLS
• BINDS WITH INTRACELLULAR
PROTEIN RECEPTOR
• THYROXINE HAS GREATER AFFINITY
IMPORTANCE OF LATENCY
AND DURATION OF ACTION
• T4 -- TWO OR THREE DAY LATENT
PERIOD
• MAXIMUM ACTIVITY IN 10-12 DAYS
• T3 --- 6 TO 12 HOURS LATENT PERIOD
• MAXIMUM ACTIVITY IN 2-3 DAYS
MAJOR EFFECTS OF
THYROID HOROMONE
• GROWTH IN CHILDREN
• INCREASE IN METABOLIC RATE
EFFECTS ON GROWTH
• LACK OF THYROID HORMONE
RETARDS GROWTH
• EXCESS OF THYROID HORMONE
ENHANCES GROWTH IN CHILD
• CAUSES EPIPHYSEAL PLATES TO
CLOSE PREMATURELY SO FINAL
HEIGHT MAY BE SHORTENED
GENERALIZED EFFECTS ON
METABOLISM
• AFFECT METABOLISM OF ALMOST
ALL CELLS OF BODY
• CALORIGENIC EFFECT
EFFECT OF THYROID HORMONE
ON PROTEIN SYNTHESIS
• PHASE ONE--INCREASED
TRANSLATION
• PHASE TWO--INCREASED
TRANSCRIPTION
EFFECT OF THYROID
HORMONE ON CELLULAR
ENZYME SYSTEMS
• INCREASED PROTEIN SYNTHEIS
RESULTS IN INCREASED CELLULAR
ENZYMES
• AS MUCH AS 6 TIMES NORMAL
EFFECTS ON CELLULAR
ORGANELLES
• INCREASED ACTIVITY OF
MITOCHONDRIA
• INCREASED NUMBER OF
MITOCHONDRIA
EFFECTS ON ACTIVE
TRANSPORT
• Na-K ATPase PUMPS INCREASE
• INCREAED TRANSPORT OF SODIUM
AND POTASSIUM
EFFECTS ON CARBOHYDRATE
METABOLISM
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RAPID UPTAKE OF GLUCOSE
INCREASED GLYCOLYSIS
INCREASED GLUCONEOGENESIS
INCREASED GI ABSORPTION
INCREASED INSULIN SECRETION
EFFECT ON FAT METABOLISM
• LIPOGENESIS
• LIPOLYSIS
• MOBILIZATION OF LIPIDS
EFFECTS ON BODY MASS
• INCREASED THYROID HORMONE
DECREASES
• DECREASED THYROID HORMONE
INCREASES
EFFECTS ON CARDIOVASCULAR
SYSTEM
• INCREASED OXYGEN DEMAND
• INCREASED METABOLIC WASTE
PRODUCTS
• CAUSE VASODILATION
• NEED FOR HEAT ELIMINATION ALSO
CAUSES VASODILATION
• CARDIAC OUTPUT CAN INCREASE BY
50%
EFFECTS ON RESPIRATION
• INCREASED OXYGEN DEMAND
• INCREASED CARBON DIOXIDE
LEVELS
• ACTIVATE MECHANISMS THAT
INCREASE THE RATE AND DEPTH OF
RESPIRATION
EFFECT ON
GASTROINTESTINAL TRACT
• INCREASE ABSORPTION RATE
• INCREASES SECRETION OF DIGESTION
JUICES
• INCREASES MOTILITY OF
GASTROINTESTINAL TRACT
• TO MUCH MAY LEAD TO DIARRHEA
• TO LITTLE CONSTIPATION
EFFECT ON THE CENTRAL
NERVOUS SYSTEM
• NORMAL AMOUNTS INCREASE CEREBRATION
• TO LITTLE DECREASES CEREBRATION
• TO MUCH -- EXTREME NERVOUSNESS,
PSYCHONEUROTIC TENDENCIES, MUSLE TREMOR,
TIREDNESS BUT INABILITY TO SLEEP
• TO LITTLE -- MENTAL SLUGGISHNESS EXTREME
SOMNOLENCE
SECRETION OF THYROID
HORMONE
• TSH FROM ADENOHYPOPHYSIS
STIMULATES ITS SECRTION
TRH STIMULATES TSH SECRETION
NEGATIVE FEEDBACK
CONTROLS OF THYROID
HORMONE RELEASE
• LONG FEED BACK LOOPS
• SHORT FEEDBACK LOOPS
LONG FEEDBACK LOOP
• INHIBITORY EFFECTS OF TARGET ORGANS
ON ADENOHYPOPHYSIS
• THYROID HORMONES COULD ACT ON
HYPOTHALAMUS AND INHIBIT SECRETION
OF TRH
• THYROID HORMONE COULD ACT ON
ADENOHYPOPHYSIS AND INHIBIT ITS
RESPONSE TO RELEASING HORMONES
SHORT FEEDBACK LOOPS
• PITUITARY HORMONES THEMSELVES
INFLUENCE SECRETION OF
RELEASING OR INHIBITING
HORMONES
THYROID STIMULATING
HORMONE
• HIGH SECRETION OF TSH MAY
INHIBIT SECRETION OF TRH
SPECIFIC EFFECTS OF TSH
• INCREASED PROTEOLYTIC ACTIVITY IN
FOLLICLES
• INCREASED RELEASE OF THYROID HORMONE
INTO BLOOD STREAM
• INCREASED TRAPPING OF IODIDE IONS
• INCREASED IODINATION OF TYROSINE
• INCREAS`E IN SIZE AND ACTIVITY OF FOLLICULAR
CELLS
• INCREASED NUMBER OF FOLLICULAR CELLS
REGULATION OF THRYOID
HORMONE SECRETION
• TSH FROM PITUITARY STIMULATES
SYNTHESIS AND RELEASE
• TRH PROMOTES TSH RELEASE
• NEGATIVE FEED BACK
CALCITONIN
• POLYPEPTIDE
• PRODUCED BY PARAFOLLICULAR
CELLS
• LOWERS BLOOD CALCIUM AND
PHOSPHATE LEVELS
• SUPRESSES BONE RESORPTION
• INCREASES BONE FORMATION
• IMPORTANT IN BONE REMODELING
HOW CALCITONIN REDUCES
BLOOD CALCIUM LEVELS
• DECREASES OSTEOLYTIC EFFECT
FAVORS DEPOSITION RATHER
THAN RESORPTION
• INCREASES ACTIVITY OF
OSTEOBLASTS
• PREVENTS FORMATION OF NEW
OSTEOCLASTS FROM PROGENITOR
CELLS
CHILDREN VS ADULTS
• MAJOR ROLE IN HUMANS
• MINOR ROLE IN ADULTS
REGULATION OF
CALCITONIN SECRETION
• 10% RISE IN PLASMA CALCIUM
LEVELS LEADS TO 3-6 TIMES MORE
CALCITONIN
OTHER IMPORTANT
EFFECTS OF CALCITONIN
• REDUCES LOSS OF BONE MASS
DURING
PROLONGED STARVATION
LATE STAGES OF PREGNANCY
DIFFERENCES BETWEEN
CALCITONIN AND
PARATHYROID HORMONE
• CALCITONIN MORE RAPID
• SHORT TERM REGULATOR
REGULATION OF
SECRETION
• PLASMA LEVELS OF CALCIUM
• HIGH CONCENTRATION -- INCREASED
SECRETION
• LOW CONCENTRTION -- DECREASED
SECRETION
• GASTRIN AND OTHER INTESTINAL
HORMONES EFFECT SECRETION
PARATHYROID GLANDS
•
•
•
•
TINY
LENTIL SIZED
FOUND IN POSTERIOR OF THYROID
USUALLY TWO IN EACH LOBE
CELLS OF THE PARATHYROID
• PRINCIPAL CELLS/CHIEF CELLS
– MOST ABUNDANT
– SECRETE PARATHYROID HORMONE
• OXYPHIL CELLS
– SEEM TO STORE RESERVE OF
PARATHYROID HORMONE
PARATHYROID GLAND
• SMALL FLATTENED GLANDS
• POSTERIOR SURFACE OF THYROID
GLAND
CELLS OF PARATHYROID
• CHIEF CELLS
• OXYPHIL CELLS
PARATHYROID HORMONE
•
•
•
•
PTH
POLYPEPTIDE
TWO OR THREE FORMS
PRINCIPAL CONTOLLER OF CALCIUM AND
PHOSPHATE IN BLOOD
• INCREASES PLASMA CONCENTRATION OF
CALCIUM
• DECREASES CALCIUM CONCENTRATION
OF PHOSPHORUS
ORGANS AFFECTED BY
PARATHYROID HORMONE
• BONES
• KIDNEY
PTH EFFECTS ON BONE
• OSTEOLYTIC EFFECT (BONE
RESORPTION)
• PROLIFERATION OF OSTEOCLASTS
PTH EFFECT ON
OSTEOCLASTS
• IMMEDIATE ACTIVATION OF
OSTEOCLASTS
• PRODUCTION OF NEW OSTEOCLASTS
FROM PROGENITOR CELLS
EFFECT OF PTH ON THE
KIDNEYS
• EXCRETION AND REABSORPTION
• ACTIVATION OF VITAMIN D
EXRETION AND REABSORPTION
• IMMEDIATE AND RAPID LOSS OF
PHOSPHATE IN KIDNEYS
DUE TO DECREASED
REABSORPTION OF PHOSPHATES
• INCREASED REABSORPTION OF
CALCIUM IN KIDNEYS
ACTIVATION OF VITAMIN D
• CALCITRIOL
• IMPORTANT FOR
DEPOSITION IN
BONES
PROMOTES
CALCIFICATION
• IMPORTANT FOR
ABSORPTION OF
CALCIUM IN GI
TRACT
REGULATION OF PARATHYROID
HORMONE RELEASE
• DECREASE IN CALCIUM ION
CONCENTRATION INCREASES
SECRETION
• INCREASED CALCIUM ION
CONCENTRATION DECREASES
SECRETION
THYMUS
•
•
•
•
•
DOUBLE LOBED LYMPHOID ORGAN
ANTERIOR MEDIASTINUM
BEHIND STERNUM
CORTEX
MEDULLA
CORTEX
• MANY LYMPHOCYTES
MEDULLA
•
•
•
•
FEWER LYMPHOCYTES
HASSAL’S CORPUSCLES
UNKNOWN FUNCTION
PRODUCES THYMOSINS
THYMUS
• LOCATED UNDER MEDIASTINUM
• RELATIVELY LARGE IN CHILDREN
• REACHES GREATEST SIZE IN PUBERTY -- 40
g
• BEGINS TO INVOLUTE ON ITSELF AFTER
PUBERTY TO 0.3 g AT 50
• ACCELERATED BY GLUCOCORTICOIDS
AND SEX HORMONES
THYMIC HORMONES
•
•
•
•
•
•
THYMOSIN ALPHA
THYMOSIN BETA
THYMOSIN V
THYMOPOIETIN
THYMULIN
AND SOME OTHERS
OTHER SITES OF THYMOSIN
SYNTHESIS
• MACROPHAGES
EFFECTS OF THYMOSIN
• DEVELOPMENT OF B AND T
LYMPHOCYTES
• INFLUENCES HORMONES OF
REPRODUCTIVE SYSTEM
ADRENAL GLAND
• CORTEX
• MEDULLA
PARTS OF ADRENAL GLAND
• CORTEX
• MEDULLA
ADRENAL CORTEX
• ACCOUNTS FOR ABOUT 90% OF
WEIGHT OF GLAND
• 5-7g
• DERIVED FROM MESODERM
• PRODUCTS ARE STEROIDS
ZONES OF THE CORTEX
• ZONA GLOMERULOSA
• ZONA FASCICULATA
• ZONA RETICULARIS
ZONA GLOMERULOSA
• JUST BELOW CAPSULE
• SUPPLIES CELLS FOR
REGENERATION IF NECESSARY
• PRODUCES MINERALOCORTICOIDS
– ALDOSTERONE
ZONA FASCICULATA
•
•
•
•
DEEP TO GLOMERULOSA
MAKES UP BULK OF CORTEX
PRODUCES GLUCOCORTICOIDS
MORE CHOLESTEROL HERE THAN
ANYWHERE ELSE
• ALSO LOTS OF VITAMIN C
ZONA RETICULARIS
• DEEPEST LAYER OF CORTEX
• SECRETE GONADOCORTICOIDS
ADRENAL MEDULLA
• INNER MOST PORTION OF ADRENAL
GLAND
• DERIVED FROM NEURAL CREST CELLS
– SAME AS SYMPATHETIC GANGLIA
• COMPLETELY DIFFERENT FROM CORTEX
• MAY EXTEND INTO ZONA RETICULARIS
CELLS OF THE MEDULLA
• CELLS ARE GROUPED IN CLUMPS
AROUND BLOOD VESSELS
• CHROMAFFIN CELLS
– SYTHESIZE
– STORE
– SECRETE EPINEPHRINE AND
NOREPINEPHRINE
HORMONES OF THE
ADRENAL GLAND
CORTICAL VS MEDULLARY
HORMONES
HORMONES OF THE
ADRENAL MEDULLA
• EPINEPHRINE
• NOREPINEPHRINE
• SIMILAR TO SYMPATHETIC
GANGLION
• INNERVATED BY PREGANGLIONIC
NERVE FIBERS FROM THE
SYMPATHETIC NERVOUS SYSTEM
HORMONE SECRETION
• EPINEPHRINE MAKES UP 75-80 % OF
SECRETION
• NOREPINEPHRINE MAKES UP 20-25 % OF
SECRETION
• METABOLIC CHANGES REACHE PEAK AT
ABOUT 30 SECONDS AFTER HORMONE
RELEASE
• EFFECTS MAY LAST AS LONG AS SEVERAL
MINUTES
ANDRENERGIC RECEPTORS
•
•
•
•
ALPHA
BETA
ALL ARE G LINKED RECEPTORS
NON CHANNEL LINKED RECEPTORS
NOREPINEPHRINE
• BINDS WITH
–
–
–
–
ALPHA 1-- EFFECTIVELY
ALPHA 2 -- EFFECTIVELY
BETA 1-- EFFECTIVELY
BETA 2 --WEAKLY IF AT ALL
EPINEPHRINE
• BINDS EFFECTIVELY WITH
–
–
–
–
ALPHA 1– EFFECTIVELY
ALPHA 2 -EFFECTIVELY
BETA 1-- EFFECTIVELY
BETA 2 --EFFECTIVELY
ALPHA RECEPTORS
• MOST COMMON ALPHA RECEPTOR
• ACTIVATES Gp PROTEINS
• G PROTEINS ACTIVATE ENZYMES
– ALPHA 2 -- EFFECTIVELY
ALPHA 2 RECEPTORS
• LESS COMMON THAN ALPHA 1
• ACTIVATES INHIBITORY GI PROTEINS
• REDUCE THE FORMATION OF cyclic AMP
ALPHA RECEPTORS
•
•
•
•
VASOCONSTRICTION
IRIS DILATION
INTESTINAL RELAXATION
INTESTINAL SPHINCTER
CONTRACTION
• PILOMOTOR CONTRACTION
• BLADDER SPHINCTER
CONTRACTION
BETA 1 RECEPTORS
• HEART AND KIDNEYS
• ACTIVATES G PROTEINS
• STIMULATES PRODUCTION OF cyclic AMP
BETA 2 RECEPTOR
• MOST COMMON BETA RECEPTOR
• ACTIVATES STIMULATORY G
PROTEINS
BETA RECEPTORS
•
•
•
•
•
•
•
•
•
•
VASODILATION
CARDIOACCELERATION
INCREASED MYOCARDIAL STRENGTH
INTESTINAL RELAXATION
UTERUS RELAXATION
BRONCHIOLE DILATION
CALORIGENESIS
GLYCOGENOLYSIS
LIPOLYSIS
BLADDER RELAXATION
IMPORTANCE OF DIFFERENT
RECEPTORS
• AT LEAST PARTIALLY RESPONSIBLE
FOR DIFFENCE IN ACTIVITY OF
EPINEPHRINE AND NOREPINEPHRINE
GENERALIZED EFFECTS OF
EPINEPHRINE AND
NOREPINEPHRINE
• MOBILIZATION OF GLYCOGEN
• INCREASES CATABOLISM OF GLUCOSE
• RESERVES IN SKELETAL MUSCLE AND
LIVER
• LIPOLYSIS AND MOBILIZATION OF FAT
RESERVES
• INCREASE IN RATE AND FORCE OF CARDIAC
MUSCLE CONTRACTION
SOME SPECIFIC EFFECTS OF
CATECHOLAMINES
VASOCONSTRICTION DUE TO
CATECHOLAMINE HORMONES
• VASOCONSTRICTOR MECHANISM
• WORKS WITH SYMPATHETIC
NERVOUS SYSTEM
• CONSTRICT MOST BLOOD VESSELS
• CONSTRICT VEINS
• REACH AREAS SYMPATHETIC
NERVOUS SYSTEM DOES NOT
VASODILATION BY
EPINEPHRINE
• CAUSES MILD VASODILATION
• IN SKELETAL
• IN CARDIAC
DILATION OF BRONCHIOLES BY
CATECHOLAMINE HORMONES
• SECRETED IN RESPONSE TO
SYMPATHETIC INNERVATION
• RELAX BRONCHIOLES
EFFECT OF EPINEPHRNE ON
GLYCOGENOLYSIS
• SECRETED IN RESPONSE TO
SYMPATHETIC INNERVATION
• ACTIVATES PHOSPHORYLASE
• IN LIVER AND IN MUSCLES
• BREAKS DOWN GLYCOGEN TO
GLUCOSE
EFFECTS OF CATECHOLAMINE
HORMONES ON CARDIAC
MUSCLE
• INCREASE RATE OF SINOATRIAL
NODE DISCHARGE
• INCREASES RATE OF CONDUCTION
• INCREASES EXCITABILITY OF HEART
MUSCLE
• INCREASES PERMEABILITY TO
CALCIUM AND SODIUM
EFFECTS OF CATECHOLAMINE
HORMONES ON FAT UTILIZATION
• HEAVY EXERCISE BRINGS ABOUT DRAMATIC
INCREASE IN FAT UTILILZATION
• DUE TO RAPID RELEASE OF NOREPINEPHRINE AND
EPINEPHRINE
• DUE TO SYMPATHETIC INNERVATION OF ADRENAL
MEDULLA
• ACTIVATE HORMONE-SENSITIVE LIPASE
• LYPOLYSIS AND MOBILIZATION OF FATTY ACIDS
EFFECTS OF CATECHOLAMINE
HORMONES ON SMOOTH MUSCLE
• MOST HORMONES AFFECT SMOOTH
MUSCLE
• VARYING DEGREES
• EFFECT WILL DEPEND ON TYPE OF
RECEPTOR (INHIBITORY VS
EXCITATORY)
THE RELATIONSHIP
BETWEEN MEDULLARY
HORMONES AND THE ANS
• ACTIVATION OF THE SYMPATHETIC
NERVOUS SYSTEM USUALLY LEADS
TO RELEASE OF CATECHOLAMINES
BY ADRENAL MEDULLA
• SYMPATHETIC NERVOUS SYSTEM
AND ADRENAL MEDULLA SUPPORT
ONE ANOTHER
HORMONES OF THE
ADRENAL CORTEX
MINERALOCORTICOIDS,
GLUCOCORTICOIDS, &
ANDROGENIC HROMONES
ALL ADRENOCORTICOIDS
ARE STEROIDS
ALL ADRENOCORTICOIDS
ARE STEROIDS
ALDOSTERONE
• VERY POTENT
• 95% OF MINERALOCORTICOID
SECRETION
• PRODUCED BY ZONA GLOMERULOSA
GENERALIZED EFFECTS OF
ALDOSTERONE SECRETION
• STIMULATES CONSERVATION OF SODIUM IONS
• STIMULATES ELIMINATION OF POTASSIUM
IONS
• REABSORPTION OF SODIUM IONS HAS
SECODARY EFFECT OF ENHANCING OSMOTIC
REABSORPTION
• INCREASES SENSITIVITY OF TASTE BUDS IN
TONGUE TO SALT
TARGET CELLS OF
ALDOSTERONE
•
•
•
•
KIDNEYS
SWEAT GALNDS
SALIVARY GLANDS
PANCREAS
EFFECT OF ALDOSTERONE
ON THE KIDNEYS
• MOST IMPORTANT FUNCTION
• CAUSES TRANSPORT OF SODIUM
AND POTASSIUM THROUGH RENAL
TUBULES
• CAUSES TRANSPORT OF HYDROGEN
IONS THROUGH RENAL TUBULES
EFFECT OF ALDOSTERONE ON
+
TUBULAR REABSORPTION OF Na
AND TUBULAR SECRETION OF K+
• TUBULAR EPITHELIAL CELLS
• EXCHANGE TRANSPORT
• DISTAL TUBULES AND COLLECTING
TUBULES
• CONSERVES Na+ --ELIMINATES K+
EFFECTS OF HIGH CONCENTRATIONS
OF ALDOSTERONE
• DECREASE SODIUM LOSS TO A FEW
MILLIGRAMS PER DAY
• GREAT INCREASE IN POTASSIUM
LOSS IN URINE
EFFECTS OF TOTAL LACK OF
ALDOSTERONE
• CAN INCREASE SODIUM LOSS UP TO
20 GRAMS PER DAY
• POTASSIUM IS CONSERVED AND
LITTLE IS LOST
EFFECTS OF HIGH ALDOSTERONE
ON EXTRACELLULAR WATER
VOLUME
• CAN INCREASE EXTRACELLULAR
FLUID VOLUME
• UP TO 10 TO 20% OVER NORMAL
EFFECTS OF ALDOSTERONE LOSS
ON EXTRAFLUID VOLUME
• CAN DECREASE EXTRACELLULAR
FLUID VOLUME
• UP TO 20 TO 25% BELOW NORMAL
EFFECTS OF EXESSIVE
POTASSIUM LOSS
• CAN CAUSE A SERIOUS DECREASE
OF POTASSIUM
• HYPOKALEMIA
EFFECTS OF HYPOKALEMIA
• SEVERE MUSCLE WEAKNESS
• MUSCLE PARALYSIS
• DUE TO EFFECTS ON NERVE AND
MUSCLE FIBER MEMBRANES
EFFECTS OF HYPERKALEMIA
• CARDIAC TOXICITY OCCURS WHEN
POTASSIUM LEVELS DOUBLE
• SYMPTOMS
WEAKNESS OF CONTRACTION
ARRHYTHMIA
IF LEVELS RISE FURTHER CAN LEAD
TO DEATH
EFFECTS OF ALDOSTERONE ON
TUBULAR SECRETION OF
HYDROGEN IONS
• ALSO CAUSES HYDROGEN IONS TO BE
EXCHANGED FOR SODIUM IONS
– TO LESSER EXTENT
• DECREASES HYDROGEN ION
CONCENTRTION IN EXTRACELLULAR
FLUID
• NOT STRONG EFFECT
• CAUSES MILD DEGREE OF ALKALOSIS
EFFECTS OF ALDOSTERONE
LACK ON THE CIRCULATORY
SYSTEM
• CAN CAUSE A 20-25% DECREASE OF
BLOOD VOLUME & EXTRACELLULAR
FLUIDS
CAN CAUSE CIRCULATORY SHOCK
• WITHOUT TREATMENT MAY DIE WITH
4-8 DAYS
EFFECT OF HYPERSECRETION OF
ALDOSTERONE ON THE
CIRCULATORY SYSTEM
• EXTRACELLULAR FLUID VOLUME
INCREASES
• BLOOD VOLUME INCREASES
• CARDIAC OUTPUT INCREASES
• TO AS MUCH AS 20 TO 30% ABOVE
NORMAL AT FIRST
• COMPENSATORY MECHANISMS
RETURN IT DOWN TO 5-10 %
FACTORS THAT AFFECT THE
REGULATION OF ALDOSTERONE
SECRETION
• POTASSIUM ION CONCENTRATION OF
THE EXTRACELLULAR FLUID
• RENIN-ANGIOTENSIN SYSTEM
• QUANTITY OF BODY SODIUM
• ADENOCORTICOTROPIC HORMONE
ALDOSTERONE IS NOT AS
DEPENDENT ON CRH AND
ACTH
ANGIOTENSIN AND POTASSIUM
LEVELS ARE THE MAJOR
REGULATORS
IMPORTANCE OF POTASSIUM
IONS IN ALDOSTERONE
SECRETION
• INCREASE IN POTASSIUM IONS
CAUSES INCREASED SECRETION OF
ALDOSTERONE
• ALDOSTERONE CAUSES ENHANCED
EXCRETION OF POTASSIUM
• POTASSIUM LEVELS RETURN TO
NORMAL
EFFECT OF RENIN-ANGIOTENSIN
SYSTEM ON ALDOSTERONE
SECRETION
RENIN
• KEY IN RENIN-ANGIOTENSIN SYSTEM
• RELEASED BY JUXTAGLOMERULAR
COMPLEX OF KIDNEYS
• SECRETED AS PRORENIN
• CONVERTED TO RENIN BEFORE ENTERING
BLOODSTREAM
FACTORS THAT INCREASE
RENIN SECRETION
• SYMPATHETIC INNERVATION
• DECLINE IN RENAL BLOOD FLOW
EFFECTS OF RENIN
• CATALYZES CONVERSION OF
ANGIOTENSINOGEN TO ANGIOTENSIN I
• ANGIOTENSIN I CONVERTED TO
ANGIOTENSIN II AS PASSES THROUGH
LUNGS
• ANGIOTENSIN CONVERTING ENZYME
(ACE)
EFFECTS OF ANGIOTENSIN II
• STIMULATES SECRETION OF ADH
STIMULATES WATER REABSORPTION
COMPLEMENTS ALDOSTERONE
• STIMULATES SECRETION OF ALDOSTERONE BY
ADRENAL GLANDS
INCREASES RETENTION OF SODIUM
INCREASES LOSS OF POTASSIUM
• STIMULATES THIRST
INCREASES FLUID CONSUMPTION
INCREASES BLOOD VOLUME
• INCREASES CONSTRICTION OF ARTERIOLES
ELEVATES SYSTEMIC BLOOD PRESSURE
EFFECTS OF ALDOSTERONE
AT THE CELLULAR LEVEL
CORTISOL
GENERALIZED EFFECTS OF
CORTISOL
•
•
•
•
•
CARBOHYDRATE METABOLISM
PROTEINS METABOLISM
FAT METABOLISM
STRESS MANAGEMENT
ANTI-INFLAMMATORY EFFECTS
EFFECTS OF CORTISOL ON
CARBOHYDRATE
METABOLISM
EFFECT OF CORTISOL ON
GLUCONEOGENESIS
• INCREASE 6 TO 10 TIMES
• INCREASES ENZYMES NEEDED TO CONVERT
AMINO ACIDS TO GLUCOSE
DUE TO INCREASED TRANSCRIPTION
• INCREASES MOBILILIZATION OF AMINO ACIDS
FROM TISSUES
MUSCLE MAIN SOURCE
• INCREASES AMINO ACID CONENTRATON IN
BLOOD
EFFECTS OF CORTISOL ON GLUCOSE
UTILIZATION BY CELLS
• MODERATE DECREASE IN GLUCOSE
USE
• INCREASE OCCURS SOMEWHERE
BETWEEN POINT OF ENTRY AND
FINAL DEGRADATION
• COULD ALSO INVOLVE TRANSPORT
MECHANISMS
EFFECTS OF CORTISOL ON BLOOD
GLUCOSE CONCENTRATIONS
• INCREASED GLUCONEOGENESIS
• DECREASED GLUCOSE USE
• RAISES BLOOD GLUCOSE LEVELS
•
ADRENAL DIABETES
• INCREASE COULD BE AS LARGE AS
50 % ABOVE NORMAL
• SIMILAR TO PITUITARY DIABETES
BUT DIFFERENT FROM INSULIN
DEFICIENCY
EFFECT OF CORTISOL ON
PROTEIN METABOLISM
EFFECTS OF CORTISOL ON
CELLULAR PROTEINS STORES
• REDUCES PROTEIN STORES
EXCEPT IN LIVER
• DECREASED PROTEIN SYNTHESIS
• DECREASE IN FORMATION OF RNA
• INCREASED CATABOLISM OF PROTEIN
• DECREASED TRANSPORT OF AMINO ACIDS
INTO TISSUES OTHER THAN LIVER
EFFECTS OF CORTISOL ON
THE LIVER AND PLASMA
PROTEIN CONCENTRATIONS
• SYNTHESIS OF PROTEINS IN LIVER
INCREASES
– INCREASED ACTIVITY OF LIVER
ENZYMES
• PLASMA PROTEINS PRODUCED ARE
RELEASED INTO BLOOD
EFFECTS OF CORTISOL ON
MOVEMENTS OF AMINO ACIDS
INTO AND OUT OF THE BLOOD
AND BLOOD AMINO ACID
CONCENTRATIONS
• DEPRESSES UPTAKE BY MUSCLE AND
OTHER CELLS
• INCREASED UPTAKE BY LIVER
• INCREASES PLASMA
CONCENTRATIONS OF AMINO ACIDS
EFFECTS OF INCREASED PLASMA
CONCENTRATIONS OF AMINO ACIDS ON
LIVER UTILIZATION OF AMINO ACIDS
• INCREASED DEAMINATION OF
AMINO ACIDS
• INCREASED PROTEIN SYNTHESIS
• INCREASED SYNTHESIS OF PLASMA
PROTEINS
• INCREASED GLUCONEOGENESIS
EFFECTS OF CORTISOL ON
FAT METABOLISM
EFFECT OF CORTISOL ON THE
MOBILIZATION OF FATS
• INCREASES MOBILIZATION OF FATTY ACIDS FROM
ADIPOSE TISSUE
• INCREASES PLASMA FATTY ACID
CONCENTRATIONS
• MODERATELY INCREASES OXIDATION OF FATTY
ACIDS
• SHIFTS BODY TO FAT METABOLISM IN STARVATION
OR STRESS
• EFFECT DEVELOPS OVER SEVERAL HOURS
• GLYCOGEN AND GLUCOSE SPARER
OTHER EFFECTS OF
CORTISOL
EFFECTS OF CORTISOL IN
STRESSFUL SITUATION
• ANY KIND OF STRESS INCREASES
ACTH SECRETION
• INCREASED SECRETIONS OF
CORTISOL
IN MINUTES
EFFECTS OF CORTISOL ON THE
INFLAMMATORY RESPONSE
• INFLAMMATION IS TRIGGERED BY
TRAUMA, INFECTION OR A VARIETY
OF OTHER MECHANISMS
• CORTISOL CAN BLOCK
INFLAMMATION
• CAN EVEN REVERSE MANY OF ITS
EFFECTS
SPECIFIC EFFECTS OF CORTISOL ON THE
INFLAMMATORY RESPONSE
• STABILIZES LYSOSOMAL
MEMBRANES
• BLOCKS MOST OF THE FACTORS
CAUSING INFLAMMATION
• INCREASES HEALING PROCESS
IMPORTANCE OF CORTISOL
IN FIGHTING DISEASE
• RHEUMATOID ARTHRITIS
• RHEUMATIC FEVER
• ACUTE GLOMERULONEPHRITIS
CONTROL OF CORTISOL
SECRETION
• ACTH IS THE MAJOR FACTOR
CAUSING CORTISOL SECRETION
EFFECT OF CORTICOTROPIN
RELEASING HORMONE IN
ACTH SECRETION
• SMALL PEPTIDE FROM
HYPOTHALAMUS
• LITTLE ACTH IS SECRETED IN THE
ABSENCE OF CRH
EFFECTS OF
PHYSIOLOGICAL STRESS
ON ACTH SECRETION
• CAN LEAD TO INCREASE ACTH
• CAN RESULT IN INCREASED LEVELS
OF CORTISOL WITHIN A FEW
MINUTES
• REGULATED BY HYPOTHALAMUS
AND THE RELEASE OF CRH
FEEDBACK CONTROLS ON
ACTH SECRETION
• CORTISOL HAS A DIRECT NEGATIVE
FEEDBACK EFFECT
– ON HYPOTHALAMUS DECREASING CRH
– ON ANTERIOR PITUITARY DECREASING
ACTH
THYMUS
•
•
•
•
•
DOUBLE LOBED LYMPHOID ORGAN
ANTERIOR MEDIASTINUM
BEHIND STERNUM
CORTEX
MEDULLA
CORTEX
• MANY LYMPHOCYTES
MEDULLA
•
•
•
•
FEWER LYMPHOCYTES
HASSAL’S CORPUSCLES
UNKNOWN FUNCTION
PRODUCES THYMOSINS
PINEAL GLAND
•
•
•
•
PEA SIZED
EPITHALAMUS
ROOF OF DIENCEPHALON
NEUROENDOCRINE TRANSDUCER
NEUROENDOCRINE
TRANSDUCER
• CONVERTS SIGNALS RECEIVED
THROUGH NERVOUS SYSTEM INTO
AN ENDOCRINE SIGNAL
RELATIONSHIP TO
HYPOTHALAMUS
• INFORMATION ABOUT LIGHT AND
DARK CYCLES CARRIED FROM EYES
TO HYPOTHALAMUS
• SYMPATHETIC NERVES CARRY
ACTION POTENTIALS TO PINEAL
GLAND
HORMONES OF THE PINEAL
GLAND
• MELATONIN
• OTHERS HAVE BEEN FOUND BUT
THEY DO NOT KNOW THEIR
FUNCTIONS
ARGININE VASOTOCIN
MELATONIN
• DERIVED FROM SERATONIN
• PRODUCTION LOWEST IN DAYLIGHT
• PRODUCTION HIGHEST AT NIGHT
EFFECTS OF MELATONIN
• SLOWS MATURATION OF SPERM, EGGS
AND REPRODUCTIVE ORGANS
REDUCES RATE OF GnRH
SECRETION
• EFFECTIVE ANTIOXIDANT
• MAY BE INVOLVED IN CIRCADIAN
RHYTHM
• INCREASED SECRETION MAY CAUSE
SEASONAL AFFECTIVE DISORDER
PANCREAS
•
•
•
•
•
•
•
•
ELONGATED
FLESHY
HEAD, BODY AND TAIL
TUCKED BEHIND STOMACH
HEAD TUCKED INTO DUODENUM CURVE
BODY AND TAIL EXTEND TO LEFT
TAIL CONTACTS SPLEEN
MIXED GLAND
– EXOCRINE AND ENDOCRINE
CELLS OF THE PANCREAS
• ACINAR CELLS--EXOCRINE
SECRETION
• ALPHA CELLS--GLUCAGON
• BETA CELLS--INSULIN
• DELTA CELLS--SOMATOSTATIN
• F CELLS--PANCREATIC POLYPEPTIDE
INSULIN IN BETA CELLS
NORMAL PANCREAS
DIABETIC PANCREAS
DIABETIC PANCREAS
CHANGES IN KIDNEY IN
DIABETES
CHANGES IN KIDNEYS IN
DIABETES
EFFECTS OF DIABETES ON
LIVER
HORMONES OF THE
PANCREAS
PANCREATIC HORMONES
•
•
•
•
GLUCAGON
INSULIN
SOMATOSTATIN
PANCREATIC POLYPEPTIDE
SOMATOSTATIN
• PRODUCED BY DELTA CELLS
• IDENTICAL TO BRAIN FORM
• SUPPRESSES RELEASE OF GLUCAGON
AND INSULIN
• SLOWS RATE OF FOOD ABSORPTION
• SLOWS RATE OF ENZYME SECRETION
PANCREATIC POLYPEPTIDE
• INHIBITS GALLBLADDER
CONTRACTIONS
• REGULATES PRODUCTION OF SOME
PANCREATIC ENZYMES
• MAY HELP IN CONTOLLING RATE OF
ABSORPTION IN GI TRACT
INSULIN
• POLYPEPTIDE HORMONE
• SECRETED BY BETA CELLS
• WHEN GLUCOSE LEVELS RISE ABOVE
NORMAL LEVELS
OR
• WHEN ELEVATED LEVELS OF ARGININE,
LEUCINE AND OTHER HORMONES ARE
PRESENT IN THE BLOOD
INSULIN DEPENDENT CELLS
• MOST ALL THE CELL IN BODY
INSULIN INDEPENDENT
CELLS
•
•
•
•
BRAIN
KIDNEYS
LINING OF GI TRACT
RED BLOOD CELLS
GENERALIZED EFFECTS OF INSULIN
• ACCELERATION OF GLUCOSE UPTAKE IN ALL TARGET
CELLS
• ACCELERATION OF GLUCOSE UTILIZATION IN ALL
TARGET CELLS
• ENHANCED ATP PRODUCTION IN ALL TARGET CELLS
• STIMULATION OF GLYCOGENESIS IN SKELETAL AND
LIVER CELLS
• STIMULATION OF AMINO ACID ABSORPTION IN ALL
TARGET TISSUES
• STIMULATION OF PROTEIN SYNTHESIS IN ALL TARGET
TISSUES
• STIMULATION OF LIPOGENESIS IN ALL TARGET
TISSUES
INSULIN REDUCES THE
BLOOD GLUCOSE LEVEL
INSULIN IS A PROTEIN AND
FAT SPARER
SPECIFIC EFFECTS OF
INSULIN`
EFFECTS OF INSULIN ON
CARBOHYDRATE METABOLISM
• RAPID UPTAKE OF GLUCOSE
• STORAGE OF GLUCOSE AS
GLYCOGEN
• CATABOLISM OF GLUCOSE
• ESPECIALLY IN ADIPOSE, LIVER AND
SKELETAL TISSUES
EFFECTS OF INSULIN ON THE
UPTAKE, STORAGE AND USE OF
GLUCOSE BY THE LIVER
• MOST OF GLUCOSE ABSORBED
AFTER MEAL IS STORED IN LIVER AS
GLYCOGEN
• ACTS AS A RESERVE TO SUPPLY
GLUCOSE BETWEEN MEALS
MECHANISMS OF GLUCOSE UPTAKE
• INSULIN INHIBITS PHOSPHORYLASE
• ENHANCES UPTAKE OF GLUCOSE BY
HEPATOCYTES
– INCREASES ACTIVITY OF GLUCOKINASE
• ENZYME PHOSPHORYLATES GLUCOSE TRAPPING IT INSIDE
CELL
• INCREASES ACTIVITY OF ENZYMES PROMOTING
GLYCOGENESIS
• NET EFFECT IS TO INCREASE GLYOGEN LEVELS IN
LIVER
GLYCOGEN STORAGE IN
LIVER
• ABOUT 5-6 PERCENT OF LIVER MASS
• USUALLY 100 GRAMS
OTHER EFFECTS OF INSULIN ON
CARBOHYDRATE METABOLISM
IN THE LIVER
• PROMOTES CONVERSION OF LIVER
GLUCOSE INTO FATTY ACIDS
• FATTY ACIDS ARE THEN
TRANSPORTED TO ADIPOSE TISSUES
AND DEPOSITED
• INHIBITS GLUCONEOGENESIS
– DECREASES ACTIVITIES OF ENZYMES
EFFECTS OF INSULIN ON GLUCOSE
METABOLISM IN MUSCLE CELLS
• MUSCLES GENERALLY USE FATTY
ACIDS AS THEIR ENERGY SOURCE
• RESTING MEMBRANE IS ALMOST
IMPERMEABLE TO GLUCOSE
• UNTIL STIMULATED BY INSULIN
CONDITIONS WHERE MUSCLES
USE CONSIDERABLE GLUCOSE
• DURING PERIODS OF HEAVY
EXERCISE
• DURING THE FIRST FEW HOURS
AFTER A MEAL WHEN INSULIN
LEVELS ARE HIGH
EFFECTS OF HEAVY EXERCISE ON
MUSCLE CELLS
• DOES NOT REQUIRE LARGE
AMOUNTS OF INSULIN
• MEMBRANE PERMEABILITY
CHANGES DUE TO CONTRACTILE
PROCESS
EFFECTS OF INSULIN
• CAUSES RAPID TRANSPORT OF
GLUCOSE INTO THE CELLS
EFFECT OF INSULIN ON THE
STORAGE OF GLYCOGEN IN
MUSCLE CELLS
• IN RESTING MUSCLES AFTER MEAL
• GLUCOSE IS STORED AS MUSCLE
GLYCOGEN
• CONCENTRATION CAN BE AS MUCH
AS 1-2 % OF CELL MASS
• CAN BE USED AS ENERGY RESERVE
DIFFERENCES BETWEEN
LIVER GLYCOGEN AND
MUSCLE GLYCOGEN
• MUSCLE GLYCOGEN CANNOT BE
RECONVERTED TO GLUCOSE AND
RELEASED INTO BLOOD STREAM
WHILE LIVER CELLS CAN
• MUSCLE CELLS DO NOT HAVE
GLUCOSE PHOSPHATASE
• LIVER CELLS HAVE GLUCOSE
PHOSPHATASE
MECHANISM BY WHICH
INSULIN INCREASES GLUCOSE
TRANSPORT IN MUSCLE CELLS
• SOME GLUCOSE TRAPPING BY
GLUCOKINASE
• ENHANCES FACILITATED DIFFUSION
OF GLUCOSE THROUGH MEMBRANE
• TAKES ONLY A FEW SECONDS
EFFECTS OF GLUCOSE ON
THE BRAIN
• INSULIN INDEPENDENT
• PERMEABLE TO GLUCOSE WITH OR
WITHOUT INSULIN
• BRAIN DEPENDENT ON GLUCOSE
BLOOD GLUCOSE LEVELS ARE
MAINTAINED DUE TO THE
BRAINS NEED FOR GLUCOSE
• BLOOD GLUCOSE LEVELS MUST
ALWAYS MAINTAIN A CRITICAL
LEVEL
• LEVELS IN A RANGE OF 20-50 mg/100
ml CAUSES HYPOGLYCEMIC SHOCK
SYMPTOMS OF
HYPOGLYCEMIC SHOCK
•
•
•
•
•
PROGESSIVE IRRITABILITY
FAINTING
CONVULSIONS
COMA
DEATH
EFFECT OF INSULIN ON FAT
METABOLISM
• MAY NOT BE AS DRAMATIC AS
CARBOHYDRATE
• BUT IS MORE IMPORTANT
• INSULIN IS A PROTEIN SPARER
• EFFECTS OF INSULIN ARE BEST SEEN
WHEN THERE IS A LACK OF INSULIN
EFFECTS OF INSULIN ON EXCESS
FAT SYNTHESIS AND STORAGE
• SEVERAL EFFECTS LEAD TO AN INCREASE IN FAT
STORAGE
• INCREASE IN GLUCOSE UTILIZATION BY MANY OF
BODY’S CELLS
• INSULIN ALSO PROMOTES FATTYACID SYNTHESIS
IN LIVER
• INSULIN PROMOTES A SMALL AMOUNT OF FATTY
ACID SYNTHESIS IN THE ADIPOSE CELLS
FACTORS THAT LEAD TO AN
INCREASE IN FATTY ACID
SYNTHESIS IN THE LIVER
• INCREASED TRANSPORT OF
GLUCOSE INTO HEPATOCYTES
• EXCESS CITRATE AND ISOCITRATE
IONS ARE FORMED BY CITRIC ACID
CYCLE
• TRANSPORT OF FATTY ACIDS TO THE
ADIPOSE TISSUES
INCREASED TRANSPORT OF
GLUCOSE INTO THE LIVER
•
•
•
•
PHOSPHORYLATION
CONVERSION OF GLUCOSE TO PYRUVATE
CONVERSION OF PYRUVATE TO ACETYL-coA
SYTHESIS OF FATTY ACIDS FROM ACETYL coA
EXCESS CITRATE AND
ISOCITRATE IONS FROM THE
CITRIC ACID CYCLE
• FORMED WHEN EXCESSIVE
AMOUNTS OF GLUCOSE ARE BEING
USED FOR ENERGY
• DIRECTLY ACTIVATE ACETYL-coA
CARBOXYLASE
– CATALYZES FIRST STAGE OF FATTY
ACID SYNTHESIS
FATTY ACIDS ARE THEN
TRANSPORTED TO THE ADIPOSE
TISSUES
• REMOVES THEM AND PREVENTS A
NEGATIVE FEEDBACK EFFECT ON
ACETYL-co CARBOXYLASE
EFFECTS OF INSULIN OF FAT
STORAGE AT THE ADIPOSE
TISSUES
• SAME EFFECT AS IN THE KIDNEYS
BUT SMALLER
• ONE TENTH AS MUCH GLUCOSE IS
TRANSPORTED INTO ADIPOSE CELLS
ESSENTIAL EFFECTS OF
INSULIN ON FAT STORAGE
IN THE ADIPOSE TISSUES
• INHIBITS THE ACTIVITY OF
HORMONE SENSITVE LIPASE
– CATALYZES LIPOLYSIS
• PROMOTES TRANSPORT OF GLUCOSE
INTO CELLS
SAME AS IN MUSCLE CELLS
USED TO FORM GLYCEROL
WHEN INSULIN IS NOT
AVAILABLE FAT STORAGE IS
GREATLY INHIBITED IF NOT
BLOCKED
EFFECTS OF INSULIN ON
PROTEIN METABOLSISM
• WITH GH PROMOTES UPTAKE OF AMINO
ACIDS INTO CELLS
• DIRECTLY AFFECTS RIBOSOME TO CAUSE
TRANSLATION
• INCREASES (OVER TIME) TRANSCRIPTION
• INHIIBITS CATABOLISM OF PROTEINS
• INHIBITS GLUCONEOGENESIS ENZYMES IN
LIVER
INSULIN GREATLY
ENHANCES PROTEIN
SYNTHESIS AND
DECREASES DEGRADATION
OF PROTEINS
EFFECT OF INSULIN ON
GROWTH
• INSULIN WORKS WITH GROWTH
HORMONE
– SYNERGISTIC EFFECT
• ANIMALS DEPRIVED OF EITHER
PITUITARY OR PANCREAS DISPLAY
STUNTED GROWTH
• BOTH NEED TO BE PROVIDED FOR
NORMAL GROWTH
CONTOL OF INSULIN
SECRETION
• BY BLOOD GLUCOSE LEVELS IN THE
BLOOD
• BY AMINO ACID LEVELS IN THE
BLOOD
• BY GASTROINTESTINAL HORMONES
EFFECTS OF BLOOD GLUCOSE
LEVELS ON INSULIN SECRETION
• 80-90 mg/100ML--MINIMAL INSULIN SECRETION
• ABOVE 100mg/100ML --INSULIN SECRETION
RISES QUICKLY
• CAN REACH AS MUCH AS 400 - 600 mg/100ML
• SECRETION DECREASES RAPIDLY AS BLOOD
GLUCOSE LEVELS RETURN TO FASTING LEVEL
EFFECT OF AMINO ACIDS
ON INSULIN SECRETION
• SOME OF THE AMINO ACIDS CAUSE INCREASED
SECRETION
– IE ARGININE AND LEUCINE
• AMINO ACIDS ADMINISTERED WITHOUT AN
ACCOMPANYING RISE IN BLOOD GLUCOSE WILL
CAUSE ONLY A SMALL RISE IN SECRETION
• IF BOTH ARE PRESENT INSULIN SECRETION MAY
BE DOUBLED
•
•
•
•
•
•
EFFECT OF GASTROINTESTINAL
HORMONES ON INSULIN
SECRETION
GASTRIN
SECRETIN
CCK
GASTRIC INHIBITORY PEPTIDE
RELEASED AFTER EATING
SEEM TO CAUSE AN ANTICIPITORY RISE IN
INSULIN SECRETION
• ALMOST DOUBLE SECRETION OF INSULIN AFTER
A MEAL
CARBOHYDRATE VS FATTY
ACID (LIPID) METABOLISM
INSULIN DETERMINES WHICH
WILL OCCUR
GLUCAGON
• PRODUCED BY ALPHA CELLS
GENERALIZED EFFECTS OF
GLUCAGON
• GLYCOGENOLYSIS IN SKELETAL AND
LIVER CELLS
• LIPOLYSIS AND FATTY ACID
MOBILIZATION IN ADIPOSE TISSUES
• GLUCONEOGENESIS AT THE LIVER
• REDUCTION OF GLUCOSE UTILIZATION
• INCREASE IN BLOOD GLUCOSE LEVELS
GLUCAGON IS A GLUCOSE
SPARER
GLYCOGENOLYSIS AND
INCREASED BLOOD GLUCOSE
LEVELS CAUSED BY GLUCAGON
• MOST DRAMATIC EFFECTG
• INCREASES BLOOD GLUCOSE
LEVELS IN MINUTES
MECHANISMS OF ACTIVATING
GLYCOGENOLYSIS IN THE LIVER
•
•
•
•
•
•
ACTIVATES ADENYLATE CYCLASE
FORMS c AMP
ACTIVATES PROTEIN KINASE REGULATOR PROTEIN
ACTIVATES PROTEIN KINASE
ACTIVATES PHOSPHORYLASE b KINASE
CONVERTS PHOSPHORYLASE b INTO PHOSPHORYLASE
a
• PROMOTES THE PHOSPHORLYSIS OF GLYCOGEN INTO
GLUCOSE 1 PHOSPHATE
• GLUCOSE 1 PHOSPHATE IS DEPHOSPHORYLATED AND
LEAVES THE HEPATOCYTE BY FACILITATED DIFFUSION
EFFECT OF GLUCAGON ON
GLUCONEOGENESIS IN THE LIVER
• NONCARBOHYDRATE SUBSTRATES ARE
CONVERTED TO PYRUVATE OR AN INTERMEDIATE
IN THE CITRIC ACID CYCLE
• AMINO ACIDS ARE CONVERTED TO PYRUVATE OR
PHOSPHOPHENOLPYRUVATE
• LIPIDS CAN BE CONVERTED TO PGA, PGAL OR
ANOTHER 3 CARBON INTERMEDIATE
• GLUCONEOGENESIS HAS SAME INTERMEDIATES AS
GLYCOLYSIS
• BUT ITS ENZYMES RUN IT FROM PYRUVATE TO
GLUCOSE
REGULATION OF
GLUCAGON SECRETION
• BLOOD GLUCOSE CONCENTRATIONS
• OPPOSITE EFFECT THAN IT HAS ON
INSULIN
• WHEN BLOOD GLUCOSE FALLS AS LOW AS
70mg/100ML LARGE AMOUNTS OF
GLUCAGON ARE SECRETED
• PROTECTS THE BODY AGAINST
HYPOGLYCEMIA
EFFECTS OF AMINO ACIDS
ON GLUCAGON SECRETION
• EXACTLY THE OPPOSITE OF ITS
EFFECT ON INSULIN
• HELPS PREVENT HYPOGLYCEMIA
THAT WOULD OCCUR IF YOU ATE A
MEAL OF PURE PROTEIN
IMPORTANCE OF BLOOD
GLUCOSE REGULATION
ITS ALL FOR THE BRAIN
IN NORMAL INDIVIDUAL
• BLOOD GLUCOSE LEVELS ARE
TIGHTLY REGULATED
• BETWEEN 80-90 IN THE MORNING
• 120 TO 140 AFTER BREAKFAST
• RETURN TO NORMAL IN ABOUT 2
HOURS AFTER MEAL
MAINTENANCE OF BLOOD
GLUCOSE BETWEEN MEALS
• LIVER ACTS AS A BLOOD GLUCOSE BUFFER
– STORES GLUCOSE AFTER MEALS
• AS MUCH AS 2/3 OF GLUCOSE ABSORBED IS STORED IN
LIVER AS GLYCOGEN
– RELEASES GLUCOSE BETWEEN MEAL
• INSULIN AND GLUCAGON FUNCTION AS SEPARATE CONTROL
SYSTEMS
• IN HYPOGLYCEMIA SYMPATHETIC INNERVATION INCREASES
AND STIMULATES RELEASE OF EPINEPHRINE WHICH
INCREASES GLUCOSE RELEASE
• OVER HOURS OR DAYS--GH AND CORTISOL ARE RELEASED
– DECREASE GLUCOSE UTILIZATION
THEY DO IT ALL FOR THE
BRAIN
ALSO THE RETINA, GERMINAL
EPITHELIA OF GONADS,
KIDNEYS, AND OTHER INSULIN
INDEPENDENT CELLS
HORMONES OF THE
REPRODUCTIVE TISSUES
• MALE
• FEMALE
• REGULATED BY FSH AND LH
TESTES
SEMINIFEROUS TUBULES
LEYDIG CELLS
EPIDIDYMIS
DUCTUS DEFRENS
THE HORMONES OF THE TESTES
• TESTOSTERONE
• INHIBIN
OVARIES
MATURE GRAAFIAN
FOLLICLE
CORPUS LUTEUM
CORPUS LUTEUM
HORMONES OF THE
OVARIES
• ESTROGENS
ESTRADIOL, ESTRIN ESTRONE
• PROGESTINS
PROGESTERONE
• INHIBIN
• RELAXIN
HORMONES OF THE
PLACENTA
•
•
•
•
•
TEMPORARY ORGAN
ESTROGEN
PROGESTERONE
HUMAN CHORIONIC GONADOTROPIN
HUMAN PLACENTAL LACTOGEN
HORMONE OF THE UTERUS
• RELAXIN
THE ENDOCRINE FUNCTION
OF THE HEART
• ATRIOPEPTIN/ATRIAL NATRIURETIC
PEPTIDE
• PRODUCED BY ATRIA CARDIAC
MUSCLES
EFFECTS OF ATRIAL
NATRIURETIC PEPTIDE
• PROMOTES LOSS OF SODIUM IONS AND
WATER AT KIDNEYS
• INHIBITS RENIN RELEASE
• INHIBITS SECRETION OF ADH AND
ALDOSTERONE
• SUPPRESSES THIRST
• BLOCKS ACTION OF ANGIOTENSIN II AND
NOREPINEPHRINE ON ARTERIOLES
ENDOCRINE FUNCTION OF
THE DIGESTIVE SYSTEM
HORMONES OF THE
DIGESTIVE SYSTEM
• GASTRIN
• SECRETIN
• CHOLECYSTOKININ
GASTRIN
• POLYPEPTIDE
• SECRETED BY MUCOSAL LINING
• STIMULATES PRODUCTION OF HCL
AND PEPSIN
SECRETIN
• POLYPEPTIDE
• FIRST HORMONE
• SECRETED BY THE MUCOSA OF THE
DUODENUM
• STIMULATES A BICARBONATE RICH
SECRETION FROM THE PANCREAS
• CAN INHIBIT GASTRIC SECRETIONS
UNDER CERTAIN CONDITIONS
• STIMULATES SECRETION OF BILE
CHOLECYSTOKININ
• SECRETED BY WALL OF DUODENUM
• STIMULATES CONTRACTION OF
GALL BLADDER
• INHIBITS GASTRIC ACID SECRETIONS
UNDER CERTAIN CONDITIONS
• STIMULATES THE RELEASE OF
ENZYMES FROM THE PANCREAS
HORMONES OF THE KIDNEYS
CALCITROL
• STEROID HORMONE
• SECRETED IN RESPONSE TO PTH
• DEPENDENT ON CHOLECALCIFEROL
FROM SKIN OR DIET
CARRIED BY TRANSCALCIFERIN
• VITAMIN D REFERS TO ALL FORMS
OF THE VITAQMINS
EFFECT OF CALCITROL
• STIMULATION OF CALCIUM AND POSPHATE
ABSORPTION BY GI TRACT
• STIMULATE FORMATION AND DIIFFERNTIATION
OF OSTEOPROGENITOR CELLS AND OSTEOCLASTS
• STIMULATING CALCUM REABSORPTION AT THE
KIDNEYS
• SUPPRESSES PARATHYROID HORMONE
SECRETION
ERYTHROPOIETIN
• PEPTIDE HORMONE
• RELEASED BY KIDNEY IN RESPONSE
TO HYPOXIA IN KIDNEY TISSUES
POSSIBLE CAUSES OF
HYPOXIA
• REDUCTION IN RENAL BLOOD FLOW
• REDUCTION IN NUMBER OF RED BLOOD
CELLS
• REDUCTION IN ABILITY OF RED BLOOD
CELLS TO CARRY OXYGEN
• REDUCTION IN OXYGEN CONTENT OF AIR
• PROBLEMS WITH THE RESPIRATORY
MEMBRANE
EFFECT OF
ERYTHROPOIETIN
• STIMULATES HEMATOPOIESIS
• ELEVATES BLOOD VOLUME
SLIGHTLY DUE TO INCREASE IN RED
BLOOD CELLS
• IMPROVES OXYGEN DELIVERY TO
PERIPHERAL TISSUES
LEPTIN
A NEW HORMONE
EFFECTS OF AGING
• FEW FUNCTIONAL CHANGES
• DECLINE IN LEVELS OF
REPRODUCTIVE HORMONES
• ENDOCRINE TISSUES MAY BECOME
LESS RESPONSIVE
• SOME TARGET CELLS IN TISSUES
MAY BECOME LESS RESPONSIVE