Download - SALADIN C. 26
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]
ProteinsProteins 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 Energy (O) Energy (no O)
Glycolsis 2 ATP 2ATP2ATP
2 NADH 4-6ATPTransition 2NADH 6ATPKrebs 2ATP 2ATP
6NADH 18ATP
2FADH2 4ATP
Totals 36-38ATP 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
GlycogenesisGlucose 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 glyceraldehyde-3-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.
ProteinsTransamination, 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