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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
GLYCOLYSIS IS ANAEROBIC-CARRIED
OUT IN CYTOSOL
GLUCOSE ----> 3 CARBON FRAGMENTS
PLUS 2 ATP
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
MITOCHONDRIA
Extract Energy from Food Fuels
Energy is stored in ATP
Aerobic Metabolism
OVERVIEW OF CATABOLISM
DIETARY
PROTEIN
DIETARY
CARBOHYDRATES
DIETARY
FATS
AMINO ACIDS
GLUCOSE
FATTY ACIDS
MITOCHONDRIA
ACETYLCOA
CAC
ELECTRON
TRANSPRT
CHAIN
ATP
OVERALL REGULATION OF
BLOOD GLUCOSE
(+)
RELEASE
FROM LIVER
-
( )
BLOOD
GLUCOSE
INSULIN
(+)
EPINEPHRINE
AND
NOREPINEPHRIN
(+)
GLUCAGON
(+)
GLUCOCORTICOIDS
-
( )
-
( )
CONSUMPTION
BY
MUSCLE AND FAT CELLS
GH
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
HYPOGLYCEMIA
(LOW BLOOD SUGAR)
HYPOPITUITARYISM
ADRENAL CORTICAL FAILURE
(ADDISON’S DISEASE)
SEVERE HEPATIC DAMAGE
METABOLIC ACTIONS OF
GROWTH HORMONE
MOBILIZES TRIGLYCERIDE FAT STORED
IN ADIPOSE TISSUE
CONSERVES GLUCOSE FOR BRAIN
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
ACTIONS OF EPINEPHRINE
MIMICS SYMPATHETIC NS
MOBILIZES STORED FAT AND
CARBOHYDRATE
HEART AND BLOOD VESSELS
GENERAL ADAPTATION
SYNDROME
FLIGHT OR FIGHT
EPINEPHRINE
CRH-ACTH-CORTISOL
RENIN-ANGIOTENSIN-ALDOSTERONE
VASOPRESSIN
COORDINATED BY HYPOTHALAMUS
CAN BE INDUCED PSYCHOSOCIALLY
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
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





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
TURNOVER OF SUBSTRATES
DURING FAST: FUEL RESERVES
MUSCLE: PROTEIN
75 g
ADIPOSE TISSUE :
FA + GLYCEROL
LIVER: GLYCOGEN
160 g + 16 g
180 g
TURNOVER OF SUBSTRATES
DURING FAST: CONSUMPTION
NERVE
144 g
RBC, WBC, ETC.
36 G
HEART, KIDNEY,
MUSCLE, ETC.
180 g
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)
STARVATION
URINARY NITROGEN AGAIN
INCREASES
ONCE FAT AND/OR TRIGLYCERIDE
RESERVES ARE DEPLEATED
FASTING BLOOD LEVELS
SAMPLING
TIME
GLUCOSE
Mg/dL
POSTPRANDIAL
INSULIN
Mu/mL
GLUCAGON
pg/Ml
CORTISOL
ng/mL
GH
ng/mL
T3
ng/mL
150
50
120
<1
1.2
POSTABSORPTIVE
90
15
100
120
2
1.15
DAY 1
80
10-12
120
120
2
1.15
DAY 2
70
8
150
110
6
0.70
DAY 3
70
7
150
110
10
0.60