Transcript Ch 26 Powerpoint

SALADIN C. 26
Nutrition &
Metabolism,
Body Weight & Energy Balance
• 30 – 50% of variation in human body weight
is heredity, rest is environmental factors –
eating & exercise habits.
Appetite
• Many peptide hormones & regulatory
pathways are involved in short & long term
appetite control
• Short term regulators
– Ghrelin – from stomach – sensation of
hunger + stimulates hypothalamus to
release
– GHRH
Appetite
– Peptide YY [PYY] – from ileum & colon –
secreted with feeding – proportional to
calories consumed – stop eating signal.
– CCK – from SI – stimulates secretion of
bile & pancreatic enzymes. – Also causes
appetite suppressing effect on vagus – a
stop eating signal
Appetite
• Long term regulators
– Leptin – from adipocytes – proportional to
levels of body fat – most human obesity
related to leptin is due to receptor defect,
not hormone defect
– Insulin – from pancreas – receptors in
brain – functions like leptin - weaker
Appetite
• Brain center = arcuate nucleus of
hypothalamus – 2 groups of neurons
1 – secretes neuropeptide Y – stimulates
appetite
2 – secretes melanocortin – inhibits
eating
Gastric peristalsis also stimulates hunger
Control of Feeding & Satiety
Figure 24.23
Appetite
• Neurotransmitters influence types of food
consumed
– Norepinephrine – CBH
– Galanin – fat
– Endorphins - protein
Appetite
• Obesity – more than 20% above norm for
demographic. In US 30% are obese and an
additional
• 35% are overweight.
• Predisposition to obesity is increased by
over-feeding in infancy and early childhood.
Heat – kinetic energy
• Heat = kinetic energy
• calorie-amount of heat required to
raise one gram of H2O 1oC
Energy Yields
• Carbohydrates - 4Kcal/g
• Lipid- 9 Kcal/g
• Protein – 4 Kcal/g
Nutrients
• Nutrient – a substance that promotes
normal growth, maintenance, and repair.
• Major nutrients – carbohydrates, lipids,
and proteins.
• Other nutrients – vitamins and minerals
(and technically speaking, water).
Nutrition – [see www.mypyramid.gov for details]
Figure 24.1
CBH
Fates of CBH’s
• ATP production – aerobic respiration,
anaerobic fermentation
• Glycogen & adipose storage
• Amino Acid synthesis
• Structural component of nucleotides,
glycoproteins, glycolipids
CBH
• Excretion – spill over onto urine
• Neurons & erythrocytes depend almost
entirely on CBH
• Review Insulin/glucagon homeostasis – Ch
17; CBH in API notes
Requirements –
higher than
other nutrients
• Sources – plants
• Fiber – resist
digestion – plant
& animal
CBH
• Promotes intestinal function. Water
soluble forms reduce blood cholesterol
& LDL’s.
• Blood sugar levels – 70 -110 mg/dL =
normal
Lipids
• Fatty acids, glycerol, cholesterol
• Meet 80 – 90% of resting energy needs
• Required for absorption of fat soluble
vitamins
• Membrane & hormone structural
components.
Lipids
• Needs – no more than 30% of diet –
most should be unsaturated;
• Must get linoleic acid from diet – rest
appear to be able to be made.
Lipids
Cholesterol Metabolism
• Structural unit of bile salts, steroids,
Vitamin D and cell membranes.
– 15% of blood cholesterol is from
diet
– 85% is made by the body
Lipids
• Cholesterol & Lipoproteins - transported as spheres
• The spheres are lipoproteins – hydrophobic
triglycerides & cholesterol esters are in interior,
hydrophilic phospholipid heads, cholesterol &
proteins are on exterior
Lipids
Classes
• Chylomicrons – 2% protein, 90%
triglyceride, 3% phospholipid, 5%
cholesterol
• VLDL – 8% protein, 55% triglycerides, 17%
phospholipid, 20% cholesterol
Lipids
• LDL (bad cholesterol – gets deposited in
blood vessels) 20% protein, 6% triglyceride,
21% phospholipid, 53% cholesterol – gets
deposited in vessel walls [from adipose].
• HDL – 50% protein, 5% triglyceride, 25%
phospholipid, 20% cholesterol (good
cholesterol) cleared by liver – no vascular
buildup. [transport TO liver]
Lipids
Desirable levels
• Total cholesterol - < 200mg/dL
– LDL < 130mg/dL
– HDL > 40mg/dL [60 or higher gives some
protection against heart disease]
– Total <200mg/dL
– Ratio of total/HDL <4 desired
Lipids
• Bad
– LDL > 159 mg/dL
– Total > 239 mg/dL
Lipids
Factors regulating plasma cholesterol
• Increased dietary cholesterol decreases liver
production, BUT doesn’t stop it.
• Saturated fatty acids increase liver synthesis
and decrease excretion
• Unsaturated fatty acids increase excretion
• Hydrogenated fats increase LDL’s and
decrease HDL [worst effect of all]
Proteins
Proteins  amino acids
• 8 essential amino acids - we don't or can't
make enough
• 12 non-essential - synthesized by the
body by transamination.
• Not stored – must be present from
ingestion.
• Nitrogen balance –in = out – positive with
growth, negative with insufficiency.
Vitamins & Mnerals
• Vitamins – review table 26.3
– Fat soluble - A, D, E, K
– Water soluble - B1, B2, niacin, B6, B12, Folic
acid, C
• Minerals – review table 26.2 - Ca, P, Fe, I,
Cu, Na, K, Cl, Mg, S, Zn, F, Mn
Metabolism
• Metabolism – all chemical reactions
necessary to maintain life.
• Anabolic reactions – synthesis of larger
molecules from smaller ones.
• Catabolic reactions – hydrolysis of
complex structures into simpler ones.
CBH Metabolism
• All oxidative CBH consumption is essentially
glucose catabolism
C6H12O6 + 6O2  6H2O +6CO2 + ATP [+heat]
• Glucose catabolism – glycolysis, anaerobic
fermentation, aerobic respiration
Oxidation-Reduction (Redox) Reactions
• Oxidation removes electrons.
• Reduction adds electrons.
• Coenzymes act as hydrogen (or electron
pair) acceptors.
• Two important coenzymes are
nicotinamide adenine dinucleotide
(NAD+) and flavin adenine dinucleotide
(FAD).
Carbohydrate Metabolism
• Glucose is catabolized in three
pathways:
– Glycolysis & anaerobic fermentation
– Krebs cycle
– The electron transport chain &
oxidative phosphorylation
Carbohydrate Catabolism
Figure 24.5
Glycolysis
• A three-phase pathway in which:
– Glucose is oxidized into pyruvic acid.
– NAD+ is reduced to NADH + H+.
– ATP is synthesized by substrate-level
phosphorylation.
Glycolysis
• Glycolysis – occurs in cytoplasm – converts
glucose to pyruvate
• Immediately upon entry into the cell, glucose
is converted to glucose-6-phosphate
• 10 steps –SEE HANDOUT and Figure 26.3
• Ends [for 1 glucose] 2 pyruvates, 2 net ATP
and 2NADH + 2H+
Glycolysis
Anaerobic fermentation
• Glucose Metabolism in the Absence of O2
• Lactic acid fermentation – in muscle cells
• Starts with pyruvate and NADH
– Produces lactic acid and NAD+. Lactic acid can be
used in liver for glucose synthesis.
– Renews NAD+ in cytoplasm for continued ATP
production.
Matrix Reactions
• Starts with pyruvate, NAD+ and
Coenzyme A [CoA] --> AcetylCoA + CO2
+ NADH + H+
• Runs twice per original glucose  2
Acetyl CoA’s
Matrix Reactions
• Kreb’s Cycle – in matrix of
mitochondrion
– 8 steps – SEE Handout
– Starts with Acetyl CoA, oxaloacetic acid,
NAD+, FAD+
– Runs twice per original glucose molecule
– Ends - [with 2 pyruvates] 6CO2 + 2 ATP + 8
NADH + 8H+ + 2FADH2
Figure 24.7
Membrane Reactions
• Membrane reactions - oxidize NADH &
FADH2 to move electrons, & regenerate
NAD+ & FAD+
• Electron Transport System – on inner
mitochondrial membrane – cristae pumps H+ ions for Chemiosmosis.
Membrane Reactions
• Need electron carriers – pass electrons
from one carrier to another by paired
redox reactions.
• Carriers = Flavin Mononucleotide [FMN],
cytochromes, Fe-S centers, Cu, Coenzyme
Q.
Electronic Energy Gradient
Figure 24.9
Membrane Reactions
3 pumps present
• 1 – NADH dehydrogenase complex – FMN
& 5 Fe-S centers – start – NADH + H+ is
oxidized to NAD+ and FMN is reduced to
FMNH2. Ends with Coenzyme Q – a mobile
carrier that transports the electrons it
receives to the next pump.
Membrane Reactions
• 2 – Cytochrome b-c1 complex – electrons
passed from Q to cyt b --- to cyt c –>
passes electrons to next pump
• 3 – cytochrome oxidase complex –
receives electrons from cyt c & passes
them o Cu then to cyt a, cyt a3 & then to
O. The negative O picks up 2 H+  H2O
[only place in respiration where O is
consumed!!!]
Chemiosmosis
• Energy from step-wise release powers
pumping H+ into intermembrane space
by chemiosmosis
– The concentration of H+ outside > than that
inside – this produces an electrostatic
gradient and a net voltage.
– Since it is positive charges – it is called
proton motive force instead of
electromotive force (from electron
distribution).
Chemiosmosis
– Facilitated diffusion channels containing
enzymes for ATP formation [ATP synthase]
allow the H+ to move back across the
membrane driven by this force.
– The energy from the force is used for the
ATP production.
•
Figure 24.8
Energy Yield of Cellular Respiration
Step
Product
Glycolsis
Energy (O) Energy (no O)
2 ATP
2 NADH
Transition 2NADH
Krebs
2ATP
6NADH
2ATP
4-6ATP
6ATP
2ATP
18ATP
2FADH2
4ATP
Totals
36-38ATP
2ATP
2ATP
Glycogen Metabolism
Gluconeogenesis
• Forms glucose from non-CBH molecules.
• In the liver.
• Protects the body, especially the brain, from
the damaging effects of hypoglycemia by
ensuring ATP synthesis can continue.
• Stimulated by insulin
Glycogen Metabolism
• Glycogenolysis –
breakdown of
glycogen in
response to low
blood glucose
• Stimulated by
glucagon
Figure 24.12
Glycogen Metabolism
Glycogenesis
Glucose is converted
to Glucose – 6 – P
Glucose –6 – P is
converted to glucose
-1-P which is
converted to
glycogen
Liver Disorders
Liver disorders
• Hepatitis - inflammation - viral usually - 5
strains
– A most common - transmitted in large restricted
groups & by foods
– B & C are sexually transmitted & by blood and
fluids.
– Symptoms - Fatigue, malaise, nausea, weight loss
Hepatitis C
Lipid Metabolism
Lipid transport
• Most non-polar lipids complex with protein
to produce water soluble spheres
Lipogenesis
• Excess glycerol & fatty acids undergo
lipogenesis to form triglycerides in the liver.
• Glucose or amino acids converted into lipids
Glucose  glyceraldehyde  glyceraldehyde3-phosphate  glycerol or to acetyl CoA
which can go on to form fatty acids
• Amino acids  Acetyl CoA  fatty acids, etc.
• Stimulated by Insulin
Lipid Catabolism
Lipolysis
• Lipids are split into glycerol & fatty acids.
• Fatty acids undergo beta oxidation which
produces 2-carbon acetic acid fragments,
that can enter the Krebs cycle, or form
ketone bodies
Lipid Metabolism
Figure 24.13
Protein Metabolism
• Excess protein results in amino
acids being used to make other
proteins, glucose, triglycerides or
ATP.
• Proteins are not stored.
Protein Catabolism
Use as fuel:
• Deaminated amino acids can be
converted into pyruvic acid & into
one of the keto acid intermediates
of the Krebs cycle.
Proteins
Transamination, ammonia & urea
• Amino group  ammonia  urea
• Amino group is transferred to citric acid -> --> glutamic acid --> liver --> removal
of NH2 --> ammonia --> urea
Protein synthesis - occurs on ribosomes,
directed by DNA and RNA
• Stimulated by GH, Insulin, T3, T4,
estrogen and testosterone
Summary: Carbohydrate Metabolic Reactions
Table 24.2.1
Summary: Lipid and Protein Metabolic Reactions
Table 24.2.2
Absorptive and Postabsorptive States
• Metabolic controls balance blood
concentrations of nutrients
between two states:
– Absorptive
• The time during & shortly after
nutrient intake
Absorptive and Postabsorptive States
– Postabsorptive
• The time when the GI tract is empty.
• Energy sources are supplied by the
breakdown of body reserves.
Absorptive State
• Ingested nutrients enter blood and
lymphatic system --> hepatic portal
system to liver
• Lasts about 4 hours after completing a
meal
Absorptive State
Events:
• Glucose
– Glucose uptake by liver  converted to
triglycerides and glycogen (10%)
– Adipose tissues store fat take up blood
glucose  to triglycerides (40%)
– Muscles take up glucose and store as
glycogen (50%)
Absorptive State
Events:
• Amino Acids  liver  Kreb's cycle or
gluconeogenesis or protein synthesis
• Lipids most packaged  VLDL
lipoproteins and are carried to adipose.
• Hormones -mostly, insulin
[hypoglycemic hormone]
Absorptive State
Figure 24.18a
Principal Pathways of the Absorptive State
Figure 24.18b
Postabsorptive State
• Need to maintain normal blood glucose
level [90-100mg/100mL]
• Very important for nervous system can only use glucose for energy.
Postabsorptive State
EVENTS:
• Liver glycogen is converted to glucose
- lasts about 4 hrs.
• Muscle glycogen is converted to lactic
acid  glucose in liver
• Adipose breaks triglycerides to
glycerol  glucose
Postabsorptive State
• Muscle protein  aa  converted by
liver into glucose [gluconeogenesis]
• Hormone – glucagon; Neural Control –
ANS via epinephrine
Postabsorptive State
Figure 24.20a
Principle Pathways in the Postabsorptive State
Figure 24.20b
Metabolic Rate
• Basal metabolic rate [BMR] - rate of
metabolism measured under standard
conditions - awake, resting, fasting.
• Units = Kcal/m2/hr. Can be indirectly
measured by monitoring oxygen
consumption per unit time. [averages
~2000 kcal/day]
Factors that Influence BMR
• Surface area, age, gender, stress, &
hormones.
• Ratio of surface area to volume [if
increases, BMR increases].
• Sex. [Males have a high BMR].
Factors that Influence BMR
• Stress. [Increases BMR].
• Thyroxine increases oxygen
consumption, cellular respiration, &
BMR.
Thermoregulation
Imbalances
• Hyperthermia – elevated body temperature Heat stroke, fever
• Hypothermia - too low --> death
Thermoregulation
Body temperature
• Core temperature
=~ 37.2 - 37.6 oC
[can be higher
with high activity]
• Shell temperature
=~ 36.6 - 37.0 oC
[can be higher
with high activity]
Mechanisms of Heat Exchange
• The body uses four mechanisms of heat
exchange:
– Radiation
– Conduction
– Convection
– Evaporation
Regulation of Body Temperature
Figure 24.25
Role of the Hypothalamus
• The chief thermoregulation center is the
pre-optic region of the hypothalamus.
• Thermoregulatory areas include heat-loss
& heat-promoting centers.
Heat-Promoting Mechanisms
• Activation of heat-promoting centers of
the hypothalamus causes:
– Vasoconstriction of cutaneous blood vessels.
– Shivering.
– Increased metabolic rate.
– Enhanced thyroxine release.
Heat-Loss Mechanisms
• When core temperature rises, the
heat-loss center is activated to
cause:
– Vasodilation of cutaneous blood
vessels,
– Enhanced sweating