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

• 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

• 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

• 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

• 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

• 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

• TSH• ACTH• FSH• LH• PRL• GH• 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 TEMPERATUREFOOD INTAKEWATER BALANCE

• STRESS INCREASES SECRETION ALONG WITH ACTH

MELANOCYTE STIMULATING HORMONE

• 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

• 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

• 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

• 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 STARVATIONLATE 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

• SYMPTOMSWEAKNESS OF CONTRACTIONARRHYTHMIA

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 REABSORPTIONCOMPLEMENTS ALDOSTERONE

• STIMULATES SECRETION OF ALDOSTERONE BY ADRENAL GLANDS

INCREASES RETENTION OF SODIUMINCREASES LOSS OF POTASSIUM

• STIMULATES THIRSTINCREASES FLUID CONSUMPTION INCREASES BLOOD VOLUME

• INCREASES CONSTRICTION OF ARTERIOLESELEVATES 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 GLUCOSEDUE 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 STORESEXCEPT 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 ORGANSREDUCES 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 LEVELSOR

• 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 CELLSUSED 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

• ESTROGENSESTRADIOL, ESTRIN ESTRONE

• PROGESTINSPROGESTERONE

• 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 CHOLECALCIFEROLFROM SKIN OR DIETCARRIED 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