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HORMONES. ‛ Ormh ( hormae), an impetus or stimulus. outline. • OVERVIEW (NOT QUITE THE BIG PICTURE) • CLASSIFICATIONS & CHEMICAL TYPES • CHARACTERISTICS • SYNTHESIS/ DESTRUCTION (RATES) • ASSAYS • GENERAL MECHANISMS • THE ENDOCRINE SYSTEM • MISCELLANEOUS DETAILS (JUST WHAT

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hormones

HORMONES

‛Ormh (hormae), an impetus or stimulus

outline
outline

• OVERVIEW (NOT QUITE THE BIG PICTURE)

• CLASSIFICATIONS & CHEMICAL TYPES

• CHARACTERISTICS

• SYNTHESIS/ DESTRUCTION (RATES)

• ASSAYS

• GENERAL MECHANISMS

• THE ENDOCRINE SYSTEM

• MISCELLANEOUS DETAILS (JUST WHAT

YOU WERE WAITING FOR)

• SUMMARY (THE END AT LAST)

slide3

HORMONESARE ESSENTIALLY MESSENGER

MOLECULES THAT ARE MEANT TO COORDINATE

THE OPERATIONS OF BIOLOGICAL ORGANISMS.

THIS IS DONE BY INCREASING AND DECREASING

THE FUNCTIONS OF CELLS. AN EXAMPLE OF TWO

RELATED HORMONES ARE:

THESE HORMONES

ARE SECRETED BY

THE THYROID GLAND.

THEY AFFECT GENERAL

METABOLIC RATES 

slide4

THE FIRST HORMONE TO BE DISCOVERED “WAS ANTI-

DIABETIC FACTOR”IN 1921 BY BANTING, BEST AND

THEN COLLIP (in MacLeod’s lab in Toronto, Canada).

TO SHOW YOU HOW DISCOVERIES ARE GENERATED,

THE DIABETIC FACTOR IDEA CAME FROM OSKAR

MINKOWSKI AND JOSEF von MERING IN 1889 WHEN THEY

PRODUCED A DIABETIC DOG BY REMOVING ITS PANCREAS

BUT ACTUALLY THEY WERE STUDYING FAT DIGESTION!

types classifications of hormones
TYPES (CLASSIFICATIONS) OF HORMONES

EXTERNAL CELL HORMONES: ENDOCRINE, PARACRINE, AND

AUTOCRINE

slide6

ENDOCRINE HORMONES ARE MADE AND SECRETED BY

ENDOCRINE GLANDS (HYPOTHALMIC/PITUITARY SYSTEM

AND SEMI-INDEPENDENT SYSTEMS). THEY TRAVEL

THROUGH THE BLOOD STREAM TO TARGET TISSUES (CELLS).

THESE WERE THE ORIGINAL HORMONES TO BE STUDIED.

PARACRINE HORMONES ARE MADE BY A LOCAL GROUP OF

CELLS IN A SPECIFIED TISSUE. THE HORMONES ARE

SECRETED INTO THE INTERSTITIAL FLUID SURROUNDING

THE CELLS. CHOLECYSTOKININ-8 (GI TRACT HORMONE)

NH3-Asp-Tyr-Met-Gly-Trp-Met-Asp-Phe-CONH2

AUTOCRINE HORMONES ARE HORMONES MADE BY THE

CELLS THAT USE THEM; SELF-MODULATING HORMONES.

ESTRADIOL (SUPPORTS WOMB CELLS)

slide7

INTERNAL CELL HORMONES THESE ARE HORMONES

THAT ARE MADE AND FUNCTION ENTIRELY WITHIN THE

CONFINES OF A CELL. THEY ARE ALSO CALLED 2ND

MESSENGERS. THEY ARE TO BE DISTINGUISHED

FROM SOME EXTERNAL HORMONES (SUCH AS STEROIDS)

THAT ENTER A CELL FROM THE OUTSIDE.

cAMP TRANSFERS THE SIGNAL FROM A

CELL SURFACE RECEPTOR TO A SERIES OF

MOLECULES (OFTEN ENZYMES) THAT WILL

AMPLIFY THE ORIGINAL SIGNAL MANY FOLD

OVER. THIS IS CALLED A CASCADE MECHANISM.

cGMP PRODUCES OPPOSING EFFECTS. CALCIUM AND CALMODULIN WORK AS A PAIR IN ANOTHER INTERNAL SYSTEM. NITRIC OXIDE (THE GAS) IS STILL ANOTHER

INTERNAL CELL HORMONE.

hormone characteristics
HORMONE CHARACTERISTICS

● SIZE (MOLECULAR WEIGHT) TYPICALLY SMALL

MOLECULES (EXCEPTIONS INCLUDE POLYPEPTIDE

HORMONES SUCH AS GROWTH HORMONE).

OXYTOCIN IS A CYCLIC PEPTIDE WITH A MOLECULAR WEIGHT

OF 1007. IT IS MADE IN THE POSTERIOR PITUITARY GLAND

AND STIMULATES UTERINE CONTRACTION AT BIRTH.

slide9

DURATION OF EXISTENCE HORMONES GENERALLY

  • HAVE SHORT ½ LIVES* THAT CAN BE MEASURED BY THE
  • AMOUNT OF ACTIVE HORMONE THAT SURVIVES
  • AFTER A GIVEN TIME OR NUMBER OF PASSAGES
  • THROUGH THE CIRCULATION. THIS CONCEPT IS SOME-
  • WHAT DECEIVING SINCE THERE ARE OTHER FACTORS
  • THAT CONTRIBUTE TO HORMONE AVAILABILITY
  • TO CAUSE A CELLULAR RESPONSE:
  • BIOAVAILABILITY – IS THE HORMONE FREE OR BOUND?
  • RATE OF SYNTHESIS – IS IT MAXIMAL, MINIMAL?
  • RATE OF DEGRADATION – TISSUE CONTRIBUTION?

* ½ LIFE = THE AMOUNT OF TIME THAT A SUBSTANCE EXISTS UNTIL IT

IS REDUCED BY 1/2. THE REDUCTION OF HORMONE (ACTIVITY)

OFTEN FOLLOWS EXPONENTIAL DECAY N(t) = No x 2-t/t1/2

AFTER 3 HALF-LIVES ONLY 1/8 OF AN ACTIVE HORMONE SURVIVES.

slide10

MORE INFORMATION ABOUT ½ LIVES:

CONSIDER THE HORMONE T4 (THYROXINE) AS AN EXAMPLE – IT HAS A ½ LIFE OF 7 DAYS WITH A NORMAL BLOOD LEVEL OF 7.5 mg PER 100 mL OF BLOOD.

AFTER 21 DAYS (THREE - ½ LIVES), THE AMOUNT WOULD BE REDUCED TO ~0.94 mg PER 100 Ml OF BLOOD EXCEPT THAT THE SUPPLY IS CONSTANTLY BEING RENEWED BY THE THYROID GLAND.

SOME TYPICAL ½ LIVES OF HORMONES:

THYROID RELEASING HORMONE……………..2 MIN

INSULIN……………………………………………..6 MIN

GLUCAGON………………………………………. 7 MIN

GROWTH HORMONE……………………………25 MIN

CORTISOL…………………………………………90 MIN

THE VALUE OF KNOWING ½ LIVES – EVEN THOUGH CELLULAR METABOLISM RENEWS MANY HORMONES QUICKLY - IS AS AN INDICATOR OF HOW TIGHTLY THEIR LEVELS AND EFFECTS ARE CONTROLLED. THE SHORTER THE ½ LIFE, THE TIGHTER THE CONTROL.

slide11

OVERALLIT CAN BE REASONABLY STATED THAT

MOST HORMONES, ONCE SYNTHESIZED, ONLY

REMAIN FOR MINUTES BEFORE INACTIVATION AND/OR REMOVAL BY TISSUES SUCH AS LIVER,

KIDNEYS & LUNGS. THE REASON -- IS TO RETAIN

TIGHT CONTROL OVER BODILY/ CELLULAR FUNCTIONS IS ONE OF NECESSITY ESPECIALLY WITH FUNCTIONS SUCH AS BLOOD SUGAR LEVELS AND UPTAKE. THEREFORE, BOTH SYNTHESIS AND RELEASE OF HORMONES ARE EQUALLY IMPORTANT. ENDOCRINE HORMONES ARE RELEASED IN THE BLOOD RAPIDLY ONCE SIGNALLED.

AS PART OF THE SYSTEM OF CHECKS & BALANCES -SOME HORMONES HAVE COUNTERPARTS THAT

PRODUCE OPPOSING EFFECTS:INSULIN PROMOTES GLUCOSE UPTAKE INTO CELLS WHILE GLUCAGON PROMOTES GLUCOSE RELEASE FROM LIVER.

how fast can hormones cause effects
HOW FAST CAN HORMONES CAUSE EFFECTS?

THIS TEST DESIGNED TO TEST INSULIN LEVELS & FUNCTION. NOTE THE NORMAL (GOLD)

CURVE. GLUCOSE LEVEL RETURNS TO NORMAL VALUE IN 3 HRS. THEN NOTE THE DIABETIC

CURVE (RED). AFTER 5 HRS GLUCOSE REMAINS WELL ABOVE NORMAL -- INSUFFICIENT

INSULIN TO CAUSE CELL UPTAKE OF GLUCOSE. HYPOGLYCEMIA (PURPLE) HAS MANY

CAUSES, ONE BEING A TUMOR CAUSING EXCESSIVE INSULIN OUTPUT. FASTING IS

ANOTHER.

slide14

THE PRINCIPLE OF RADIOIMMUNOASSAYS

  • THESE ASSAYS WORK SO WELL SINCE THEY COMBINE
  • RADIOACTIVE LABELLING WITH ANTIGEN-ANTIBODY
  • REACTIONS:
  • RADIOACTIVE AND NON-RADIOACTIVE COMPOUNDS OF THE SAME
  • CHEMICAL COMPETE FOR REACTION WITH AN ANTIBODY (COMPLEX).
  • THE COMPLEX IS ISOLATED & MEASURED FOR RADIOACTIVTY.
  • THE SAMPLE IS NON-RADIOACTIVE WHILE A REFERENCE CHEMICAL
  • IS RADIOACTIVE.

VERY LOW LOW INTERMEDIATE HIGH VERY HIGH

SAMPLE SAMPLE SAMPLE SAMPLE SAMPLE

VERY HIGH HIGH INTERMEDIATE LOW VERY LOW

RADIOACTIVITY RADIOACTIVITY RADIOACTIVITY RADIOACTIVTY RADIOACTIVTY

how are hormones assayed
HOW ARE HORMONES ASSAYED?

HORMONE BLOOD LEVELS ARE QUITE SMALL:

1x10-6to 1x10-15 M

IN THE ASSAY, NON RADIOACTIVE

HORMONE (FROM THE PATIENT)

COMPETES WITH A STANDARD

AMOUNT OF RADIOACTIVE

HORMONE FOR BINDING TO AN

ANTIBODY. THE AMOUNT OF

NON-RADIOACTIVE HORMONE

(BOUND TO THE ANTIBODY) IS

READ FROM A STANDARD CURVE

THAT IS SHOWN TO THE RIGHT

(SEE ARROW).

chemical classes of hormones examples
CHEMICAL CLASSES OF HORMONES(EXAMPLES)

AMINO ACID DERIVED: THYROXINE

PEPTIDE HORMONES: GROWTH HORMONE &

OXYTOCIN

Growth hormone:

22, 124 daltons

slide17

LIPID DERIVED:

  • CHOLESTEROL 2) FATTY ACID DERIVED –
  • DERIVED --PROSTAGLANDIN F2a

THE STEROIDS ARE DERIVED

FROM CHOLESTEROL WHERE

CORTISOL IS ANTI-INFLAMMATORY

AND ESTRADIOL SUPPORTS

UTERINE FUNCTIONS. PGF2aCAUSES

THE CONTRACTION OF SMOOTH

MUSCLES.

general hormone mechanisms endocrine types
GENERAL HORMONE MECHANISMS:(ENDOCRINE TYPES)
  • AT THE CELL SURFACE 2. AT THE CELL NUCLEUS
  • (to a receptor protein) (through a receptor protein)

1

2

the endocrine hormone system
THE ENDOCRINE HORMONE SYSTEM

HORMONES OF THE ENDOCRINE (endokrinein - to

separate inside) SYSTEM ARE SECRETED (RELEASED)

DIRECTLY INTO THE BLOOD STREAM. THAT IS TO BE

DISTINGUISHED FROM EXOCRINE GLANDS THAT SECRETE

MOLECULAR PRODUCTS INTO A DUCT. e. g. A SWEAT GLAND.

THESE HORMONES ARE MADE IN A PECKING ORDER –

STARTING FROM THE BRAIN’S HYPOTHALAMUS. BUT,

YOU MAY HAVE GUESSED, THERE ARE INDEPENDENT

OPERATORS SUCH AS THE PANCREAS. GENERAL OBJECTIVE:

TO COORDINATE BODILY FUNCTIONS.

slide20

MAJOR ENDOCRINE

ORGANS/ GLANDS

THE PANCREAS IS

AUTONOMOUS FROM

THE BRAIN AS WELL

AS ADIPOSE TISSUE

(THAT MAY BE A SUR-

PRISE).

slide22

PAIN, FEAR,

INFECTION,

HEMORRHAGE,

HUNGER

THE INITIATION OF HORMONAL

ACTION MAY BEGIN WITH

AFFERENT NERVE SIGNALS TO THE HYPOTHALAMUS.

THIS CAUSES THE DUMPING OF RELEASING FACTORS

INTO THE PORTAL ARTERIAL SYSTEM THAT, IN TURN,

GO TO THE ANTERIOR PITUITARY. IN SOME CASES

NERVE SIGNALS GO TO THE POSTERIOR PITUITARY.

BOTH PITUITARY SECTIONS RELEASE THEIR

OWN HORMONES.

slide23

RELEASING FACTORS (WHICH ARE HORMONES)

MIGRATE TO A PRIMARY TARGET (THE ANTERIOR

PITUITARY) WHICH RELEASES ITS OWN

HORMONE (HORMONE B). B TRAVELS IN THE

CIRCULATORY SYSTEM TO A SECONDARY

TARGET TISSUE. THIS CAUSES THE RELEASE

OF HORMONE C. HORMONE C, IN TURN, TRAVELS

TO ITS ULTIMATE TARGET TISSUE, BINDS TO IT,

AND BRINGS ABOUT A PHYSIOLOGICAL EFFECT(S).

REMEMBER THAT EACH STAGE OF BINDING AND

RELEASE AMPLIFIES THE ORIGINAL SIGNAL

MANY FOLD.

slide25

WE CAN FOLLOW A TYPICAL SEQUENCE OF

  • EVENTS TO SIGNAL AN INCREASE IN METABOLIC
  • RATE:
  • A CONFLICT PRESENTS ITSELF TO THE CNS – e. g.
  • A TASK MUST BE COMPLETED IN A WEEK.
  • THE CNS SIGNALS THIS TO THE HYPOTHALAMUS
  • CAUSING THE RELEASE OF THYROTROPIN-
  • RELEASING HORMONE (TRH).
  • THIS HORMONE TRAVELS TO THE ANTERIOR PITUI-
  • TARY GLAND (via portal vein) CAUSING THE RELEASE
  • OF THYROID STIMULATING HORMONE (TSH).
  • TSH, IN TURN, IS CARRIED TO THE THYROID GLAND
  • (via the blood) WHERE IT CAUSES THE RELEASE OF
  • THYROXINE AND TRIIODOTHYRINE (T4 AND T3).
  • T4 AND T3 BIND TO MOST CELLS IN THE NUCLEUS AND
  • STIMULATE AN INCREASE IN METABOLIC RATE.
slide26

ALTHOUGH THIS MAY BE AN OVERSIMPLIFICATION – SINCE

  • HORMONES AND THEIR OPERATION ARES COMPLICATED –
  • STILL WE CAN CONSIDER SOME PRACTICAL EXAMPLES.
  • THESE ARE EASILY SEEN IN COUPLES OR EVEN SMALL GROUPS –
  • ONE LIKES TO HAVE THE THERMOSTAT SET AT 72 deg WHILE
  • THE OTHER WANTS IT AT 66 deg.
  • ONE LIKES TO HAVE HIS/HER WORK DONE IMMEDIATELY
  • WHILE THE OTHER PREFERS A LITTLE MORE TIME.
  • ONE CAN WALK THROUGH THE WOODS AND LEAVE THE
  • OTHER BEHIND IN A FEW MINUTES.
  • THESE ARE EXAMPLES OF SMALL DIFFERENCES IN METABOLIC
  • SET POINTS OF THE THYROID GLAND AND ITS HORMONE OUTPUTS
  • – SOME PEOPLE WOULD DEFINE THEM AS TYPE A AND TYPE B
  • PERSONALITIES.
slide27

SOME THINGS NOT PREVIOUSLY EXPLAINED:

1. MANY HORMONES HAVE FEEDBACK

AND SHUTDOWN MECHANISMS

(e. g., thyroid hormones affect TSH release by TRH)

2. THERE MAY BE A LAG BEFORE AN EFFECT

CAN OCCUR (AND THE REVERSE).

(e. g., growth hormone’s effects are especially slow)

3. HORMONE EXCESSES AND DIMINUTIONS

MAY BE PATHOLOGICAL.

(e. g., excess cortisol levels may cause kidney stones)

slide28

4. SPECIFIC HORMONE ACTIONS ARE

DETERMINED BY THE KIND OF

RECEPTORS THAT THEY BIND TO.

5. SOME HORMONES MAY FUNCTION AS

EITHER HORMONES OR NEURO-

TRANSMITTERS (LOCATION, LOCATION,

LOCATION), e. g., epinephrine and nor-

epinephrine.

summary
SUMMARY
  • HORMONES ARE CHEMICAL MESSENGERS
  • MEANT TO COORDINATE THE PHYSIOLOGICAL
  • SURVIVAL & FUNCTIONS OF AN ORGANISM.
  • TO SAY THAT HORMONES BELONG TO A
  • CHEMICAL CLASS WOULD BE ERRONEOUS –
  • THEY INCLUDE: PEPTIDES, POLYPEPTIDES,
  • AMINO ACID DERIVITIVES, STEROIDS,
  • FATTY ACID DERIVITIVES, cNUCLEOTIDES
  • AND OTHER TYPES.
slide30

3. THE CONCENTRATIONS OF HORMONES

ARE VERY SMALL, BUT THEIR SIGNALS

ARE AMPLIFIED GREATLY. THEY CAN BE

ASSAYED BY RIA.

4. THE ENDOCRINE SYSTEM WAS THE 1ST TO

BE STUDIED. IT ORIGINATES (FOR THE

MOST PART) IN THE HYPOTHALAMIC AND

PITUITARY TISSUES FROM CNS SIGNALS.

5. IN THE ENDOCRINE SYSTEM, HORMONES

BIND AT EITHER A CELL MEMBRANE

RECEPTOR OR AT THE NUCLEUS (via

an intracellular cell protein receptor)