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Transcript
Chapter 24 Metabolism and Nutrition
Metabolism
•
•
= all chemical reactions of the body
anabolism
build molecules
store energy
endergonic
release energy
exergonic
• protein synthesis
• DNA synthesis
• glycogen, lipids
• ATP synthesis
•
catabolism
•
living things obtain energy from the environment, stored in chemical bonds of its nutrients
•
living things obtain building blocks from the environment
break molecules
• cell respiration
• glycogen, lipids, proteins
• food digestion
–
–
all from the sun
all from CO2 and H2O
building blocks
•
•
•
CHO
–
monosaccharides
–
glycogen
glucose
fructose
galactose
lipids
–
–
glycerol
fatty acids
proteins
–
amino acids
other players
•
•
ATP energy transfer molecule
electron carriers:
–
–
NADH
FADH2
nicotinamide adenine dinucleotide
flavin adenine dinucleotide
CHO metabolism
•
•
•
•
•
digestion
CHO

glucose
glycolysis
glucose

pyruvic acid
glycogenesis
glucose

glycogen
glycogenloysis
glycogen

glucose
gluconeogenesis
glycerol
amino acids
lactic acid



glucose
glucose
glucose
glucose’s destiny
•
•
•
•
to glycogen
glycogenesis
to pyruvic acid
glycolysis
(storage)
ATP
after glycolysis
–
–
to lactic acid
anaerobic respiration
to CO2 + H2O
aerobic respiration
ATP
lipogenesis
(storage)
to FA
Glycogen path
•
•
•
•
storage
more efficient vs glucose
glucose  gluc-6- P
traps glucose in cell
glycogenesis
gluc-6-P to
glycogen
glycogen synthetase
–
–
skeletal muscle
liver
glycogenolysis
–
–
(osmosis)
glycogen
to
gluc-6-P
glycogen phosphatase
muscle
avail for aerobic resp.
liver
avail for aerobic resp.
to glucose
 blood glucose
glucose-6-phosphatase (SGPT)
glycolysis path
•
•
•
•
Glucose

2 pyruvic acid + 2ATP + 2NADH
after glycolysis:
anaerobic respiration
–
pyruvic acid
w/o O2

• electron acceptor =
• no more ATP made
lactic acid
lactic acid
aerobic respiration
–
pyruvic acid
w/ O2

• electron acceptor
• a lot more ATP made
CO2 + H2O
= oxygen
glycolysis details
•
•
glucose enters cell
–

(use 2 ATP)
glucose-6-phosphate
–

(use 2 ATP)
•
fructose-1,6,biphosphate
•
–
2 glyceraldehyde-3-phosphate
–

(makes 4 ATP)
(2 NAD+  2 NADH + H+)
•
2 pyruvic acid
•
result: 2 pyruvic acid + 2 ATP + 2 NADH
lactic acid pathway
•
•
•
•
•
•
= anaerobic respiration
2 pyruvic acid 
=
fermentation
2 lactic acid
– NADH  NAD+ + H+
– NAD+ recycles to glycolysis
– no ATP made
RBC
only use anaerobic respiration
skeletal muscle
as O2 used up
liver lactic acid
pyruvic acid


pyruvic acid
glucose
increase lactic acid

acidosis
(LDH
)
Glycolysis and evolution
•
•
common to all living things
before Oxygen avail
–
life ~ 1 bill yrs before Oxygen
•
cytoplasm – before organelles evolved
•
•
C6H12O6 + 6O2  30ATP + 6CO2 + 6H2O + heat
aerobic respiration
•
•
Kreb’s cycle
–

acetyl CoA
CO2 + H2O + ATP + NADH
electron transport chain
–
energy transfer from NADH  ATP
produces :
energy (30ATP)
metabolic water
heat
(body temperature)
CO2
(waste)
introductory step
•
•
•
•
•
•
•
pyruvic acid enters mitochondria

acetyl CoA
pyruvic acid  Acetyl CoA + CO2 + NADH
Kreb’s cycle
citric acid cycle
keto acids
8 molecules of cycle
acetyl CoA + oxaloacetic acid 
citric acid
note:

oxaloacetic
citric acid
+ CO + ATP + NADH
C of glucose completely oxidized as CO2
NADH and FADH hold the E now
electron transport chain
•
•
•
•
•
•
several molecules in mitochondria
NADH + H+
-
e +

NAD+ + e- +
H+
H + ADP + O  ATP + H2O
+
oxidative phosphorylation
–
–
uses E from oxidation to phosphorylate ADP
ADP + P  ATP
energy
from NADH
O2
from air
(from glucose)
ETC
•
•
•
•
electrons pass to lower E molecules
electrons in O2 have lowest E
O2
=
final electron acceptor
e- and H+ to H2O
Chemiosmosis
•
•
•
•
•
E from ETC used to pump H across membrane
concentration gradient = potential E
movt of H releases E
ADP + P + E  ATP
ATP synthase
the main anabolic reaction
net results per glucose molecule
•
•
•
•
glycolysis
2 ATP
Kreb’s cycle
2 ATP
oxidative phosphorylation
26+ ATP
total
30+ ATP
energy sources so far
•
•
•
glucose
glycogen
 glucose-6-phosphate
lactic acid
 pyruvic acid
other metabolites
•
•
•
•
•
these can complete aerobic respiration
~ 16-18 ATP per unit ???
lipids
–
–
glycerol

glyceraldehyde-3-P
FA

acetyl CoA
AA

acetyl CoA ,keto acids, pyruvic acid
ketones

acetyl CoA
proteins
–
Acetyl CoA
•
•
•
•
•
•
•
acetyl coenzyme A
center of metabolic pathways

Kreb’s cycle
ATP

fatty acids
lipogenesis

cholesterol
steroids , bile, cell membrane

ketones
acetylcholine
other metabolic processes
•
•
•
•
•
•
lipogenesis
glucose 
lipolysis
trigs
ß- oxidation
fatty acids

acetylCoA
transamination
AA

other AA
deamination
AA

urea
ketogenesis
acetylCoA

ketones

triglycerides
glycerol, fatty acid
glucose metabolism
•
•
•
•
GI

liver
• used for ATP
• stored as glycogen
glycogenesis
low blood glucose
• muscle
• liver
glycogen  glucose
for own use
glycogen  glucose
to blood
high blood glucose
•
•
glycogen
glycogenesis
acetylCoA 
FA lipogenesis
low O2
• muscle
• liver
pyruvate  lactic acid
lactic acid  glucose  blood
Lipids
•
triglycerides(Trigs)
•
cholesterol
cell membrane
steroid hormones
bile
•
phospholipids
cell membrane ; myelin
lipolysis
Trigs  FA + glycerol
•
•
energy storage
• > 80% of body’s E stored as fats
lipogenesis
FA + glycerol  Trigs
lipogenesis
FA + glycerol  Trigs
lipogenesis
•
•
–
–
–
hi glucose  Acetyl CoA  FA
hi glucose  G3P  glycerol
esp. adipose cells ~ insulin
acetyl CoA 
–
–
glycerol
trigs
FA
trigs
phospholipids
–
cholesterol
steroid hormones
bile
–
ketones
lipolysis
•
•
•
•
Trigs  FA + glycerol
use in cell respiration
–
–
glycerol
 pyruvic acid
 Kreb’s
fatty acids  acetyl CoA
glycerol
ß oxidation
 Kreb’s
 glyceraldehyde-3-P
• glycolysis
• glucose
–
–
(~ 13 ATP / unit)
most cells use for E
gluconeogenesis in liver
FA  Acetyl CoA
Kreb’s cycle
most tissues
prefered E source of liver, resting muscle
Protein metabolism
•
•
•
AA absorbed from GI
to liver , tissues
AA from protein catabolism
muscle
liver
–
–
–
•
transamination
AA 
AA 
AA
(non-essential)
acetyl CoA , keto acids
deamination
AA 
urea
gluconeogenesis
AA  pyruvic acid  glucose
AA  acetylCoA  ATP
other tissues
protein synthesis
Protein anabolism
•
•
protein synthesis
–
AA  proteins
DNA  mRNA  tRNA
relatively little each day
liver
plasma proteins
transport proteins
clotting factors
•
•
•
cellular enzymes
antibodies
AA not stored -
converted to fats or used for energy
metabolic homeostasis
•
•
•
•
•
keep blood concentrations of energy sources constant
we can break metabolic events into 3 groups:
absorptive state
–
–
energy from nutrients in diet
goal: lower blood glucose (storage)
post-absorptive state
–
–
after eating
fasting (betw meals)
energy from body reserves
goal: increase blood glucose and other E sources
emergency , stress
–
–
energy from body reserves
goal: increase glucose regardless of blood levels
absorptive state
•
•
•
•
•
•
•
anabolism > catabolism
glucose is main E source
excesses stored as glycogen, trigs
insulin is main hormone
stim:
promotes anabolism
increased blood glucose , AA ; P-ANS
increases glucose usage:
increase glucose into cells
increase cell respiration
increase glycogenesis
increase lipognesis
decreases sources of glucose:
glycogenolysis
lipolysis
increases protein synthesis
post-absorptive state
•
•
•
•
•
•
•
•
catabolism
to increase/maintain blood glucose
80 – 100 mg / 100ml
FA main E source
beta- oxidation
glucagon is main hormone
affects liver , adipose
glucose sparing
only brain uses blood glucose
glycogenolysis
mostly liver
skeletal muscle
lipolysis
increase glycerol and FA
gluconeogenesis
glycerol to glucose
AA to glucose
(not FA)
emergency
•
•
•
epinephrine ; S-ANS
immediate need for glucose
cortisol
long term stress
increase glucose regardless of blood glucose levels
other hormones
•
•
•
•
•
•
 blood glucose for muscles
epinephrine; S-ANS
–
–
same effects as glucagon
stim: danger, stress
 blood glucose
corticosteroids
–
–
–
gluconeogenesis ; protein catabolism
no glycogenolysis
stim stress, injury, inflammation ACTH
P-ANS
stim insulin
GI hormones
stim insulin
thyroxine
protein synthesis
increase cell respiration
–
for brain
stim
heat
TSH
Growth hormone
–
–
stim
GHRH ; fasting
effects
increase glucose lipolysis
gluconeogenesis
CHO metabolism
•
•
•
•
aerobic respiration
thyroxine
glycogenesis
insulin
glycogenolysis
glucagon, epinephrine
gluconeogenesis
glucagon, epinephrine,
cortisol, GH
energy sources
•
•
•
•
•
•
glucose
diet, liver
glycogen
liver, skeletal muscle
fatty acids
adipose
glycerol
adipose
amino acids
lactic acid
skeletal muscle, liver
skeletal muscle
Vitamins – water soluble
•
•
•
•
•
•
•
•
B1
Thiamine
cell respiration
DNA synthesis
B2
Riboflavin
cell respiration
(FAD)
B3 Niacin
cell respiration
(NAD)
B5
Pantothenic acid
cell respiration (acetyl CoA)
B6
Pyridoxine
DNA synthesis
protein synthesis
B12 Cyanocobalamin
DNA synthesis
Folic Acid
DNA synthesis
Vit C (ascorbic acid)
collagen synthesis
antioxidant
Vitamins – fat soluble
•
•
•
•
Vit A (retinol)
vision (rhodopsin)
Vit D (calciferol)
calcium absorption
Vit E (α tocopherol)
cell membrane
antioxidant
Vit K (menaquinone)
clot factors
minerals
•
•
•
•
•
•
•
•
•
•
calcium
bone, teeth, nerve, muscle, enzymes, hemostasis
phosphorus
bone, teeth, DNA, RNA, ATP
magnesium
bone, ATP
iron
hemoglobin, myoglobin
copper
hemoglobin, melanin, cell respiration
iodine
thyroxine
cobalt
Vit B12
zinc
carbonic anhydrase, wound healing
chlorine
HCl
sulfur
AA, protein structure
Energy
•
•
•
•
•
•
•
Calorie
nutritional
kcal heat to raise kg H2O by 10 C.
1 gm CHO
- 4 kcal
1 gm protein - 4 kcal
1 gm fats
- 9 kcal
energy intake ~ energy output
if not :
gain / lose weight
regulation of food intake
•
•
•
•
•
neural
–
hypothalamus
hunger center
peptides that influence behavior
–
vagus n.
sensory presence of foods
nutrient levels
stim/inhibit hunger centers
hormones
insulin, CCK depress hunger
body temperature
increase temp decreases hunger
psychological
behavior can override hunger center
hormonal regulation of food intake
•
•
•
hypothalamus
neuropeptide Y
decrease appetite
inhibit neuropeptide Y
–
–
–
increase hunger
CCK
short term
PYY
12 hours sm intest
Leptin
long term
adipose
• maintains (defends) amt of fat storage
• obesity us not a leptin problem
stimulate hunger
Ghrelin (Ghr)
stomach
metabolic rate
•
•
•
•
•
•
•
•
•
•
metabolism
=
metabolic rate =
sum of all chemical reactions
amt. reactions / day =
work / day
kcal / day = HEAT
metabolism
synthesis of molecules
breakdown of molecules
all produce heat
BMR=
basal metabolic rate
~ 1.0 kcal / hour / kg weight
2.2 lb / kg
120 lb ÷ 2.2 = 54.5 kg
x 24 hr
= 1309 kcal / day
170 lb ÷ 2.2 = 77.3 kg
x 24 hr
= 1855 kcal / day
TMR =
–
–
–
total metabolic rate
sedentary
BMR + 40%
moderate activity
BMR + 70%
strenuous activity
BMR + 90%
affects on metabolic rate
–
–
–
–
–
–
–
–
–
–
exercise
digestion
stress
temperature (cold)
T4
thin body
stocky
body
sleep
age – children
age – senior
body temperature
•
•
•
•
•
•
96.5o - 99.5o F.
=
36o - 38o C.
homeostasis
ideal temp for enzyme activity
10 C. - increases metabolic rate 10%
core vs. shell temperatures
blood moves heat from the core organs
heat control
•
hypothalamus
–
–
–
thermostat
central thermoreceptors
blood temp
peripheral temperature receptors
skin temp
•
behavior
•
most heat from liver, brain, heart, muscles
heat production
•
•
•
•
•
thyroxine
increased metabolic rate
“
epinephrine
shivering
muscles’ cell respiration
peripheral vasoconstriction
prevents heat loss
behavior
clothing
hot fluids
change room temperature
heat loss
•
•
•
•
•
•
skin , respiratory , urine , feces
sweating
peripheral vasodilation
respiratory rate
behavior
note: heat loss depends on temperature of environment !
sweat and vapor loss depends on humidity !
Fever
•
•
pyrogens
–
–
substances that produce fever
endogenous
WBC
bacterial toxins
raise thermostat in hypothalamus
• body temp < thermostat
• Hypothalamus stim heat production :
shivering
vasoconstrict
 sweat
T4
•
•
•
•
effects :
• increase WBC activity
• kill bacteria
 pathogen 
 pyrogen

 thermostat
body temp > thermostat
 heat loss :
vasodilate + sweating  “crisis”