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HORMONES

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

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  1. HORMONES ‛Ormh (hormae), an impetus or stimulus

  2. 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)

  3. 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 

  4. 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!

  5. TYPES (CLASSIFICATIONS) OF HORMONES EXTERNAL CELL HORMONES: ENDOCRINE, PARACRINE, AND AUTOCRINE

  6. 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)

  7. 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.

  8. 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.

  9. 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.

  10. 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.

  11. 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.

  12. EXAMPLE OF VARYING LEVELS OF HORMONES DURING THE MENSTRUAL CYCLE

  13. 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.

  14. 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

  15. 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).

  16. CHEMICAL CLASSES OF HORMONES(EXAMPLES) AMINO ACID DERIVED: THYROXINE PEPTIDE HORMONES: GROWTH HORMONE & OXYTOCIN Growth hormone: 22, 124 daltons

  17. 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.

  18. GENERAL HORMONE MECHANISMS:(ENDOCRINE TYPES) • AT THE CELL SURFACE 2. AT THE CELL NUCLEUS • (to a receptor protein) (through a receptor protein) 1 2

  19. 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.

  20. MAJOR ENDOCRINE ORGANS/ GLANDS THE PANCREAS IS AUTONOMOUS FROM THE BRAIN AS WELL AS ADIPOSE TISSUE (THAT MAY BE A SUR- PRISE).

  21. THE ENDOCRINE “PECKING ORDER” NEURAL

  22. 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.

  23. 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.

  24. THE ENDOCRINE “PECKING ORDER” NEURAL

  25. 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.

  26. 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.

  27. 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)

  28. 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.

  29. 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.

  30. 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)

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