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Metabolism and Nutrition
Lecture 9: Metabolism III
Lecture Outline
• Metabolic Adaptations
– Absorptive State
– Post-Absorptive State
• Heat and Energy Balance
• Tortora: Chapter 25
Metabolic Adaptations
• During the absorptive state ingested nutrients are entering
the blood stream
– Glucose readily available for ATP production
– Typical meal requires 4 hrs for complete absorption; with 3 meals per
day, the body spends about 12 hrs in absorptive state
– Effects of insulin dominate
• During postabsorptive state absorption of nutrients from GI
tract complete
– Energy needs must be met by fuels already in the body
– Nervous system and red blood cells continue to depend on glucose
for ATP production so maintaining steady blood glucose is critical
Absorptive State
• Soon after a meal nutrients enter blood
– Glucose, amino acids, and triglycerides in chylomicrons
• 2 metabolic hallmarks
– Oxidation of glucose for ATP production in all body cells
– Storage of excess fuel molecules in hepatocytes, adipocytes, and
skeletal muscle cells
• Pancreatic beta cells release insulin
– Promotes entry of glucose and amino acids into cells
Absorptive State - Pathway
FATE OF GLUCOSE
• About 50% of glc absorbed is oxidized by cells to
produce ATP
• Most glc that enters hepatocytes is converted to
glycogen
• Some FA and triglycerides synthesized by the liver
remain there, but most are transported via VLDLs to
adipose tissue for storage
• Adipocytes take up glc not picked up by the liver and
convert it into triglycerides for storage. Overall, 40% of
glc absorbed from a meal is converted to triglycerides,
10% is stored as glycogen in skeletal muscles and
hepatocytes
Absorptive State - Pathway
FATE OF OTHER NUTRIENTS
• Most dietary lipids (mainly triglycerides and FA) are
stored in adipose tissue, only a small portion is used for
synthesis reactions
• Many absorbed amino acids that enter hepatocytes are
deaminated to keto acids, which can either enter Krebs
cycle for ATP production or be used to synthesize glc or
FA
• Some amino acids entering hepatocytes are used for
synthesis of proteins ie. plasma proteins
• Amino acids not taken up by hepatocytes are used by
body cells to produce various proteins
AMINO ACIDS GLUCOSE TRIGLYCERIDES
(in chylomicrons)
Blood
GLUCOSE
GASTROINTESTINAL
TRACT
GLUCOSE
HEPATOCYTES IN LIVER
SKELETAL
MUSCLE
Storage
+ H2O +
CO2
MOST TISSUES
Oxidation
ATP
Triglycerides
ADIPOSE TISSUE
VLDLs
Triglycerides
Fatty
acids
Triglycerides
Glyceraldehyde
3-phosphate
Glucose
Keto acids
Fatty acids
Proteins
Triglycerides
Glyceraldehyde
3-phosphate Glycogen
Glucose
Glycogen
Glycogen
Proteins
Proteins
+ H2O +
CO2 ATP
1
2
3
4 5
6
7
8
4
Postabsorptive State
• Approx. 4 hrs after absorption in small intestine
• Blood glucose levels start to fall
• Main metabolic challenge to maintain normal blood glucose
levels; this is achieved via glc production and conservation
• Glucose production
– Breakdown of liver glycogen, lipolysis (glycerol -> glc),
gluconeogenesis using lactic acid and/or amino acids
• Glucose conservation (use components other than glc to
generate ATP)
– Oxidation of fatty acids, lactic acid, amino acids, ketone bodies and
breakdown of muscle glycogen
Postabsorptive State
1
Liver
glycogen
Keto
acids
Glucos
e
Amino
acids
LIVE
R
Fatty
acids
Lactic
acid
Ketone
bodies
Glycero
l
Bloo
d
NERVOU
S
TISSUE
Keton
e
bodie
s
Glucos
e
Starvatio
n
HEAR
T
Fatty
acids
Muscle
proteins
Fatty
acids
Glycero
l
Triglyceride
s
ADIPOSE
TISSUE
Fasting
or
starvatio
n
SKELETAL MUSCLE
TISSUE
Ketone
bodies
OTHER
TISSUES
Fatty
acids
Protein
s
Amino
acids
Glucose
6-
phosphate
Pyruvic
acid
Lacti
c
acid
Muscle
glycogen
(aerobic
)
(anaerobi
c)
Amino
acids
Fatty
acids
Ketone
bodies
Lactic
acid
AT
P
O
2
AT
P
AT
P
AT
P
AT
P
AT
P
AT
P
AT
P
AT
P
AT
P
AT
P
AT
P
+ O
2
–
4
5
8
5
6
8
8
7
4
3
9
5
4
2
8
Postabsorptive State - Regulation
• As blood glucose decline, insulin secretion falls
 Glucagon – increases release of glucose into blood via
gluconeogenesis and glycogenolysis
• Sympathetic nerve endings of ANS release norepinephrine
and adrenal medulla releases epinephrine and
norepinephrine
– Stimulate lipolysis, glycogen breakdown
Metabolism – Fasting/Starvation
• Fasting – going without food for several hrs or days
• Starvation – food deprivation or deficiency for weeks or
months
• People can survive without food for 2 months if they’re not
dehydrated
– Glycogen storage depleted within few hrs
– Stored triglycerides and structural proteins can provide energy for
several weeks
Metabolism – Fasting/Starvation
• Proteins: decreased insulin/increased cortisol  stimulates
protein catabolism to generate amino acids 
gluconeogenesis
• Triglycerides undergoes lipolysis:
– Glycerol  gluconeogenesis
– FA  acetyl-Coa  Krebs cycle, ETC  ATP
Metabolism – Fasting/Starvation
• Most dramatic change is formation of KETONE BODIES by
hepatocytes:
– Only small amounts of glc undergo glycolysis to form pyruvic acid
– Oxaloacetic acid is scarce hence only some acetyl-Coa can enter
Krebs cycle
– Excess acetyl-Coa (resulting from increased catabolism of FA) is used
by the liver for ketogenesis
– Ketone bodies can be used as an alternate source for ATP production,
especially by cardiac/skeletal muscle fibres and neurons
• Presence of ketones reduces the use of glc for ATP
production  decreases demand for gluconeogenesis 
slows catabolism of proteins
HEAT AND ENERGY BALANCE
• Heat – form of energy that can be measured as
temperature and can be expressed in calories
– calorie (cal) – amount of heat required to raise 1 gram of water
1°C
– Kilocalorie (kcal) or Calorie (Cal) is 1000 calories
• Metabolic rate – overall rate at which metabolic
reactions use energy
– Some energy used to make ATP, some lost as heat
– Basal metabolic rate (BMR) – measurement with body in quiet,
resting, fasting condition (basal state)
– BMR is 1200-1800 Cal/day in adults; about 24 Cal/kg of body
mass in adult males and 22 Cal/kg of body mass in adult
females
Body Temperature Homeostasis
• Despite wide fluctuations in environmental temperatures,
homeostatic mechanisms maintain normal range for internal
body temperature
• Core temperature (37°C or 98.6°F) versus shell temperature
(1-6°C lower)
• Heat production is proportional to metabolic rate. Several
factors affect metabolic rate: exercise, some hormones (ie.
thyroid hormones, GH), sympathetic nervous system, fever,
ingestion of food, younger age, etc.
Body Temperature Homeostasis
• Heat can be lost through
– Conduction to solid materials in contact with body
– Convection is the transfer of heat by movement of a gas
or liquid
– Radiation is the transfer of heat in form of infrared rays
– Evaporation from exhaled air and skin surface (insensible
water loss)
• Hypothalamic thermostat in preoptic area (anterior part of
hypothalamus)
– Heat-losing center and heat-promoting center
Thermoregulation
• If core temperature declines
– Skin blood vessels constrict
– Release of thyroid hormones, epinephrine and
norepinephrine increases cellular metabolism
– Shivering
• If core body temperature too high
– Dilation of skin blood vessels
– Decrease metabolic rate
– Stimulate sweat glands
Hypothermia
• The lowering of core body temperature to 35-degree-Celcius
or below
• Causes: exposure to extreme coldness, metabolic diseases,
drugs, burns, malnutrition
• Characterized by the following as core body temp. falls:
sensation of cold, shivering, confusion, vasoconstriction,
muscle rigidity, bradycardia, acidosis, hypoventilation,
hypotension, loss of spontaneous movement, coma and
death (usually d/t cardiac arrhythmias)
Energy homeostasis
• Energy homeostasis: energy intake (depends only on the
amount of food consumed) = energy expenditure
• 3 components contribute to energy expenditure
– BMR (60%)
– Physical activity (30-35%)
– Food induced thermogenesis (5-10%) – heat produced
while food is digested/absorbed/stored
• Major site of stored chemical energy is adipose tissue
Regulation of food intake
No sensory receptors exist to monitor our weight or size.
Regulation of food depends on several factors
• Neural and endocrine signals
• Nutrient levels in the blood
• Psychological elements
• Signals from GI tract and special senses
• Neural connections b/w hypothalamus and other parts of the
brain
– Clusters of hypothalamic neurons (arcuate and
peraventricular nuclei) receive signals that indicate hunger
and satiety (feeling of fullness)
Emotional eating
• Eating in response to emotional drives, such as feeling
stressed, bored or tired
• Very common; if done within limits, is considered part of
normal behaviour
• Excess can lead to physical (obesity) and emotional (low-self
esteem) problems
• Emotional eaters typically overconsume carbohydrate foods
(sweets and starches), which may raise brain serotonin levels
and lead to feelings of relaxation

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AP104 - Lesson 10 - Metabolism III.pptx

  • 2. Lecture Outline • Metabolic Adaptations – Absorptive State – Post-Absorptive State • Heat and Energy Balance • Tortora: Chapter 25
  • 3. Metabolic Adaptations • During the absorptive state ingested nutrients are entering the blood stream – Glucose readily available for ATP production – Typical meal requires 4 hrs for complete absorption; with 3 meals per day, the body spends about 12 hrs in absorptive state – Effects of insulin dominate • During postabsorptive state absorption of nutrients from GI tract complete – Energy needs must be met by fuels already in the body – Nervous system and red blood cells continue to depend on glucose for ATP production so maintaining steady blood glucose is critical
  • 4. Absorptive State • Soon after a meal nutrients enter blood – Glucose, amino acids, and triglycerides in chylomicrons • 2 metabolic hallmarks – Oxidation of glucose for ATP production in all body cells – Storage of excess fuel molecules in hepatocytes, adipocytes, and skeletal muscle cells • Pancreatic beta cells release insulin – Promotes entry of glucose and amino acids into cells
  • 5. Absorptive State - Pathway FATE OF GLUCOSE • About 50% of glc absorbed is oxidized by cells to produce ATP • Most glc that enters hepatocytes is converted to glycogen • Some FA and triglycerides synthesized by the liver remain there, but most are transported via VLDLs to adipose tissue for storage • Adipocytes take up glc not picked up by the liver and convert it into triglycerides for storage. Overall, 40% of glc absorbed from a meal is converted to triglycerides, 10% is stored as glycogen in skeletal muscles and hepatocytes
  • 6. Absorptive State - Pathway FATE OF OTHER NUTRIENTS • Most dietary lipids (mainly triglycerides and FA) are stored in adipose tissue, only a small portion is used for synthesis reactions • Many absorbed amino acids that enter hepatocytes are deaminated to keto acids, which can either enter Krebs cycle for ATP production or be used to synthesize glc or FA • Some amino acids entering hepatocytes are used for synthesis of proteins ie. plasma proteins • Amino acids not taken up by hepatocytes are used by body cells to produce various proteins
  • 7. AMINO ACIDS GLUCOSE TRIGLYCERIDES (in chylomicrons) Blood GLUCOSE GASTROINTESTINAL TRACT GLUCOSE HEPATOCYTES IN LIVER SKELETAL MUSCLE Storage + H2O + CO2 MOST TISSUES Oxidation ATP Triglycerides ADIPOSE TISSUE VLDLs Triglycerides Fatty acids Triglycerides Glyceraldehyde 3-phosphate Glucose Keto acids Fatty acids Proteins Triglycerides Glyceraldehyde 3-phosphate Glycogen Glucose Glycogen Glycogen Proteins Proteins + H2O + CO2 ATP 1 2 3 4 5 6 7 8 4
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  • 9. Postabsorptive State • Approx. 4 hrs after absorption in small intestine • Blood glucose levels start to fall • Main metabolic challenge to maintain normal blood glucose levels; this is achieved via glc production and conservation • Glucose production – Breakdown of liver glycogen, lipolysis (glycerol -> glc), gluconeogenesis using lactic acid and/or amino acids • Glucose conservation (use components other than glc to generate ATP) – Oxidation of fatty acids, lactic acid, amino acids, ketone bodies and breakdown of muscle glycogen
  • 11. Postabsorptive State - Regulation • As blood glucose decline, insulin secretion falls  Glucagon – increases release of glucose into blood via gluconeogenesis and glycogenolysis • Sympathetic nerve endings of ANS release norepinephrine and adrenal medulla releases epinephrine and norepinephrine – Stimulate lipolysis, glycogen breakdown
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  • 13. Metabolism – Fasting/Starvation • Fasting – going without food for several hrs or days • Starvation – food deprivation or deficiency for weeks or months • People can survive without food for 2 months if they’re not dehydrated – Glycogen storage depleted within few hrs – Stored triglycerides and structural proteins can provide energy for several weeks
  • 14. Metabolism – Fasting/Starvation • Proteins: decreased insulin/increased cortisol  stimulates protein catabolism to generate amino acids  gluconeogenesis • Triglycerides undergoes lipolysis: – Glycerol  gluconeogenesis – FA  acetyl-Coa  Krebs cycle, ETC  ATP
  • 15. Metabolism – Fasting/Starvation • Most dramatic change is formation of KETONE BODIES by hepatocytes: – Only small amounts of glc undergo glycolysis to form pyruvic acid – Oxaloacetic acid is scarce hence only some acetyl-Coa can enter Krebs cycle – Excess acetyl-Coa (resulting from increased catabolism of FA) is used by the liver for ketogenesis – Ketone bodies can be used as an alternate source for ATP production, especially by cardiac/skeletal muscle fibres and neurons • Presence of ketones reduces the use of glc for ATP production  decreases demand for gluconeogenesis  slows catabolism of proteins
  • 16. HEAT AND ENERGY BALANCE • Heat – form of energy that can be measured as temperature and can be expressed in calories – calorie (cal) – amount of heat required to raise 1 gram of water 1°C – Kilocalorie (kcal) or Calorie (Cal) is 1000 calories • Metabolic rate – overall rate at which metabolic reactions use energy – Some energy used to make ATP, some lost as heat – Basal metabolic rate (BMR) – measurement with body in quiet, resting, fasting condition (basal state) – BMR is 1200-1800 Cal/day in adults; about 24 Cal/kg of body mass in adult males and 22 Cal/kg of body mass in adult females
  • 17. Body Temperature Homeostasis • Despite wide fluctuations in environmental temperatures, homeostatic mechanisms maintain normal range for internal body temperature • Core temperature (37°C or 98.6°F) versus shell temperature (1-6°C lower) • Heat production is proportional to metabolic rate. Several factors affect metabolic rate: exercise, some hormones (ie. thyroid hormones, GH), sympathetic nervous system, fever, ingestion of food, younger age, etc.
  • 18. Body Temperature Homeostasis • Heat can be lost through – Conduction to solid materials in contact with body – Convection is the transfer of heat by movement of a gas or liquid – Radiation is the transfer of heat in form of infrared rays – Evaporation from exhaled air and skin surface (insensible water loss) • Hypothalamic thermostat in preoptic area (anterior part of hypothalamus) – Heat-losing center and heat-promoting center
  • 19. Thermoregulation • If core temperature declines – Skin blood vessels constrict – Release of thyroid hormones, epinephrine and norepinephrine increases cellular metabolism – Shivering • If core body temperature too high – Dilation of skin blood vessels – Decrease metabolic rate – Stimulate sweat glands
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  • 21. Hypothermia • The lowering of core body temperature to 35-degree-Celcius or below • Causes: exposure to extreme coldness, metabolic diseases, drugs, burns, malnutrition • Characterized by the following as core body temp. falls: sensation of cold, shivering, confusion, vasoconstriction, muscle rigidity, bradycardia, acidosis, hypoventilation, hypotension, loss of spontaneous movement, coma and death (usually d/t cardiac arrhythmias)
  • 22. Energy homeostasis • Energy homeostasis: energy intake (depends only on the amount of food consumed) = energy expenditure • 3 components contribute to energy expenditure – BMR (60%) – Physical activity (30-35%) – Food induced thermogenesis (5-10%) – heat produced while food is digested/absorbed/stored • Major site of stored chemical energy is adipose tissue
  • 23. Regulation of food intake No sensory receptors exist to monitor our weight or size. Regulation of food depends on several factors • Neural and endocrine signals • Nutrient levels in the blood • Psychological elements • Signals from GI tract and special senses • Neural connections b/w hypothalamus and other parts of the brain – Clusters of hypothalamic neurons (arcuate and peraventricular nuclei) receive signals that indicate hunger and satiety (feeling of fullness)
  • 24. Emotional eating • Eating in response to emotional drives, such as feeling stressed, bored or tired • Very common; if done within limits, is considered part of normal behaviour • Excess can lead to physical (obesity) and emotional (low-self esteem) problems • Emotional eaters typically overconsume carbohydrate foods (sweets and starches), which may raise brain serotonin levels and lead to feelings of relaxation