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CONTROL OF INTERMEDIARY METABOLISM

CONTROL OF INTERMEDIARY METABOLISM. D. C. MIKULECKY Dept. Physiology. ENERGY IS CAPTURED BY PLANTS. CO2 + H2O + RADIANT (SOLAR ) ENERGY --> (CH20)n + O2. ANAEROBIC METABOLISM. SUGAR CAN BE BURNED WITHOUT OXYGEN - ANAEROBICALLY FAR MORE ENERGY RELEASED FROM BURNING SUGAR AEROBICALLY

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CONTROL OF INTERMEDIARY METABOLISM

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  1. CONTROL OF INTERMEDIARY METABOLISM D. C. MIKULECKY Dept. Physiology

  2. ENERGY IS CAPTURED BY PLANTS CO2 + H2O + RADIANT (SOLAR ) ENERGY --> (CH20)n + O2

  3. ANAEROBIC METABOLISM • SUGAR CAN BE BURNED WITHOUT OXYGEN - ANAEROBICALLY • FAR MORE ENERGY RELEASED FROM BURNING SUGAR AEROBICALLY • GLYCOLYSIS IS ANAEROBIC-CARRIED OUT IN CYTOSOL • GLUCOSE ----> 3 CARBON FRAGMENTS PLUS 2 ATP

  4. AEROBIC METABOLISM • PYRUVIC ACID (3 C FRAGMENT) ENTERS MITOCHONDRIA • COMBINES WITH COENZYME A LOOSING A CO2 AND BECOMING ACETYL COENZYME A (2 C FRAGMENT) • THIS FRAGMENT ENTERS A CYCLIC REACTION SCHEME, THE CITRIC ACID CYCLE, ATP IS PRODUCED • PRODUCTS OF THE CITRIC ACID CYCLE ENTER THE ELECTRON TRANSPORT CHAIN, MORE ATP IS PRODUCED BY OXIDATIVE PHOSPHORYLATION • ULTIMATELY, 34 MORE ATP’S ARE PRODUCED

  5. MITOCHONDRIA • Extract Energy from Food Fuels • Energy is stored in ATP • Aerobic Metabolism

  6. DIETARY PROTEIN DIETARY FATS AMINO ACIDS FATTY ACIDS OVERVIEW OF CATABOLISM DIETARY CARBOHYDRATES GLUCOSE MITOCHONDRIA ELECTRON TRANSPRT CHAIN ACETYL-COA ATP CAC

  7. OVERALL REGULATION OF BLOOD GLUCOSE (+) RELEASE FROM LIVER EPINEPHRINE AND NOREPINEPHRIN (+) (-) (+) GLUCAGON BLOOD GLUCOSE INSULIN GLUCOCORTICOIDS (-) (+) (-) GH CONSUMPTION BY MUSCLE AND FAT CELLS

  8. SYNERGISTIC EFFECTS OF CORTISOL, GLUCAGON, AND EPINEPHRINE ON BLOOD GLUCOSE • WHEN ALL THREE ARE PRESENT THE EFFECT IS FAR MORE THAN ADDITIVE • COUNTERREGULATORY HORMONES • ALSO GH AND T3

  9. HYPOGLYCEMIA(LOW BLOOD SUGAR) • HYPOPITUITARYISM • ADRENAL CORTICAL FAILURE (ADDISON’S DISEASE) • SEVERE HEPATIC DAMAGE

  10. METABOLIC ACTIONS OF GROWTH HORMONE • MOBILIZES TRIGLYCERIDE FAT STORED IN ADIPOSE TISSUE • CONSERVES GLUCOSE FOR BRAIN

  11. THYROID HORMONE’S EFFECTS • METABOLIC RATE: INCREASED BMR • CALOROGENIC: INCREASED HEAT PRODUCTION • SYMPATHOMIMETIC: FLIGHT OR FIGHT • CARDIOVASCULAR:INCREASES RESPONSIVENESS OF HEART • GROWTH: ESSENTIAL FOR NORMAL GROWTH • NERVOUS SYSTEM:DEVELOPMENT AND ADULT ACTIVITY

  12. ACTIONS OF EPINEPHRINE • MIMICS SYMPATHETIC NS • MOBILIZES STORED FAT AND CARBOHYDRATE • HEART AND BLOOD VESSELS

  13. GENERAL ADAPTATION SYNDROME • FLIGHT OR FIGHT • EPINEPHRINE • CRH-ACTH-CORTISOL • RENIN-ANGIOTENSIN-ALDOSTERONE • VASOPRESSIN • COORDINATED BY HYPOTHALAMUS • CAN BE INDUCED PSYCHOSOCIALLY

  14. FEEDING : INSULIN • CEPHALIC PHASE: INSULIN • FOOD IN SMALL INTESTINE: GIP - A SECRETAGOUGE FOR INSULIN • INCREASED GLUCOSE AND AA IN BLOOD STIMULATE INSULIN SECRETION • BLOOD INSULIN MAY SWING AS MUCH AS FROM 10 TO 50 MICROUNITS/ML • MOVES ABSORBED SUGAR AND FAT TO STORES

  15. SEVERAL HOURS AFTER EATING • ABSORPTION FROM S. I. COMPLETE • INSULIN SECRETION RETURNS TO LOW BASAL RATES • BEGIN TO DRAW UPON STORES OF FUEL • BLOOD GLUCOSE RETURNS TO ABOUT 5 MMOL/L. • GLUCAGON, GH, ADRENAL HORMONES ALSO SECRETED AT LOW BASAL RATES • ABOUT 75% GLUCOSE CONSUMED BY BRAIN, BLOOD CELLS, OTHER TISSUES NOT DEPENDENT ON INSULIN, THE OTHER 25% BY MUSCLE AND ADIPOSE TISSUE. MAY BEGIN SOME GLUCONEOGENESIS IN LIVER

  16. FASTING • AFTER 24 HOURS WITHOUT FOOD FASTING BEGINS • INSULIN DECREASES FURTHER, GLUCAGON AND GH INCREASE, CORTISOL FOLLOWS ITS USUAL DIURNAL RHYTHM • FATTY ACID MOBILIZATION IS SPED UP

  17. TURNOVER OF SUBSTRATES DURING FAST: FUEL RESERVES

  18. TURNOVER OF SUBSTRATES DURING FAST: CONSUMPTION

  19. PROLONGED FASTING (3 DAYS OR MORE) • KETONE BODIES REACH 2 TO 3 MMOL/L • BECOME SIGNIFICANT PART OF BRAIN’S FUEL ALONG WITH GLUCOSE • INHIBIT PROTEIN BREAKDOWN IN MUSCLE • URINARY NITROGEN EXCRETION DECREASES (ONLY ENOUGH GLUCONEOGENESIS FOR THE BRAIN)

  20. STARVATION • URINARY NITROGEN AGAIN INCREASES • ONCE FAT AND/OR TRIGLYCERIDE RESERVES ARE DEPLEATED

  21. FASTING BLOOD LEVELS

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