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FINAL EXAM CONDENSED NOTES - LIFE SCI 2N03
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Department
Life Sciences
Course
LIFESCI 2N03
Professor
Danny M.Pincivero
Semester
Fall

Description
FINAL EXAM LIFE SCI 2N03 Quicknotes December 17, 2013 Lipids  Solubility – hydrophobic(water fearinand lipophilic(fat lovi; dissolve easily in organic solvents, less in water  Classes of lipids – i) triglycerides ii) phospholipids iii) sterols Triglycerides (triacylglycerol’s)  Majority of dietary lipids  Plant and animal origin  Glycerol + 3 fatty acids  Triglyceride + 2 H O H from glycerol and OH from fatty acid form 2 O; O from glycerol binds C on fatty acid  Functions 1. Energy Source  Dependent on physical activity level, glucose availability, blood insulin levels  Infants require fat intake for development and growth of NS and cell membranes 2. Insulation/Protection – i) Visceral Fat (protects visceral organs) ii) Subcutaneous Fat (insulation barrier, reduces heat transfer; below skin)  Excess visceral fat breaks down; enters hepatic portal circulation, filtered and stored by liver  fatty liver; impairs glucose handling  Too little fat  Anorexia Nervosa – eating disorder; prolonged decrease in appetite; refusal to eat; starvation  Amenorrhea – less severe form of energy imbalance; lack of menses; exacerbated by high volume exercise (athletic induced amenorrhea)  Female Athletes Triad – amenorrhea, eating disorder, osteoporosis (skeletal problems)  Infertility problems in women 3. Improves bioavailability and transport of other fat-soluble nutrients (vitamin A, D, E, K; phytochemicals – carotenoids, lycopene) 4. Flavor, texture, odor – sensory stimulation; moistens baked food; addsenergy (calories)  Fatty Acids o Notation – #Carbons : #Double Bonds  Eg/ Butyric acid 4:0 (4 carbons, saturated 0 db; butter flavor); Palmitic acid 16:0; Stearic acid 18:0 (chocolate, meat fat, solid at room T) o Length – Hydrocarbon chain (4-24carbons) – <6C = short; 6-10 = medium; >12 = long; short= more liquid at room T (eg/oils); long = more solid o Types – Saturated (all C’s single bonded to adjacent C or 2 H); Monosaturated (1 double bond); Polyunsaturated fatty acid (PUFA; >1 db) o Shapes – cis (bent; two lone H on same side; most common); trans (straight; two H’s on opposite sides of db; produced during food preparation; more solid at room T) o Non-Essential FA’s – manufactured by body; liver elongates short-chain FA’s (add C’s); mainly structural FA’s (membranes, myelin); in breast milk  Eg/ Oleic Acid – 18:1; body desaturates stearic acid (18:0) thick at room T, may solidify with refrigeration; Omega-9  Food Sources – olive oil o Essential FA’s – Omega-3 and Omega 6 FA’s; no enzymes desaturated before omega-9 C  omega-3 and omega-6 used to make other FA’s  Omega-3 FA’s – ALA, EPA, DHA  Linolenic Acid (18:3; omega-3,-6,-9; ALA = -linolenic acid) – elongates in liver and desaturates to form: o Elcosapantaenoic Acid (EPA; 20:5) – cardiovascular benefits o Doxohexaenoic Acid (DHA; 22:6) – brain, neuron, eye development; infants, children o EPA and DHA - must be ingested (only 5% of ALA is converted)  Physiological Effects – I) promotes blood vessel dilation (relaxation of smooth muscle) ii) decreases bloodpressure iii) decreases blood clotting iv) decreases inflammation v) reduces CVD risk  Food Sources – ALA = flax seed, walnuts; DHA, EPA = fish (Atlantic cod, haddock, salmon), human milk; fish (salmon, mackerel, sardines) shrimp  Omega-6 FA’s – LA, ARA, DPA  Linoleic Acid (18:2; omega-6,-9; LA) – elongates and desaturates into: o Arachidonic Acid (20:4) – precursor of prostaglandins (invaginates into injured tissue)  Function – i) blood vessel constriction ii) promote blood clotting iii) inflammation iv) thrombosis v) platelet aggregation  Food Sources – LA = cooking oils (sunflower, soybean, safflower), egg yolks, organ meats  Omega-6 to -3 recommended ratio = 2:1; target ratio = 1:1 to 1:4; NA diet 30:1 (food processing removes omega-3 to reduce rancidity) o Eicosanoids – regulates various physiological functions (>20 C’s); manufactured in the liver from omega-3 or -6 FA’s Phospholipids  ~2% of dietary lipids  Plant and animal origin  Contains glycerol and FA’s – typically 1 Glycerol, 2 FA’s, 1 Phosphate (+ N) o Hydrophobic (FA away from aqueous) and hydrophilic (Phosphate toward aqueous)  Functions 1. Cell Membrane Structure – provides fluidity; “fluid mosaic model”; makes membrane functional 2. Lipid Transport - component of bile; assists with fat emulsion; outer shell of chylomicrons and lipoproteins Sterols  <2% of dietary lipids  Ring structure, hydrophobic, lipophilic; contains no fatty acid  Precursor to hormones, vitamin D and bile acids  Phytosterols – plant based sterols; poorly absorbed; decreases cholesterol absorption; cholesterol-reducing food ingredient  Cholesterol (C27 45) – animal based sterols o Importance – i) component of cell membranes ii) precursor of molecules (vitamin D, hormones)  Too low cholesterol – stroke, lung, liver and behavioural problems; decreased immunity; AIDS (decreasing cholesterol indicates disease worsening) o Hormones  Progestin’s – progesterone, healthypregnancy  Glucocorticoids – cortisol (forms liver glycogen; fat and protein breakdown)  Mineralocorticoids – aldosterone (Na reabsorption in kidney; blood pressure regulation)  Androgens – testosterone (male sex characteristics)  Estrogens – female sex characteristics o All cells synthesize cholesterol; 1000 mg/day; eg/ cells in eye lens (prevents cataracts; brain (synthesizescholesterol during development) o Absorption – lower bioavailability than FA; increases with dietary lipids; decreases with increased dietary plant-derived food due to fiber content o Recommended daily value <300 mg 1 FINAL EXAM LIFE SCI 2N03 o Food Items – butter (1 tbsp=31 mg), egg (1=219 mg), beef (3oz=90 mg), beef liver (3oz=330 mg), beef brain (3oz=1420 mg) Absorption  Duodenum and Jejunum 1. Small Intestine – broken down to monoglycerides and FA’s by pancreatic lipase 2. Absorption – glycerol and small lipids move into CV system; monoglycerides and FA’s move into lacteal (smallest vessel of lymphatic system)  Large lipids (monoglycerides, FA’s) combine with bile forming micelles (soluble; allows penetration and diffusion into watery solution that bathes absorptive cells)  micelle lipid content diffuses into cells  reassembled into new triglycerides  New triglycerides packed with proteins to form chylomicrons  chylomicrons released into lymphatic system 3. Thoracic Duct (lymphatic system) to jugular vein – lipids move into CV system Transport  Order of production in body: (largest) Chylomicron (small intestine)  VLDL (liver)  LDL (liver)  HDL (liver, small intstines) (smallest)  Lipids in blood – measure blood lipids taken after overnight fast o 1-2 hours – first appearance of lipids in blood o 3-5 hours – peak levels of lipids in blood o 10 hours – lipids cleared  Chylomicrons – transport in CV system; lipoprotein lipase from inner lining of blood vessels lyses chylomicrons; releases Glycerol, cholesterol remnants, and FFA’s into CV o Glycerol – water soluble; cells can use to make ATP or triglycerides o Cholesterol Remnants (cholesterol released from lipoprotein)  used to make VLDL o Free Fatty Acids – bound to albumin (major blood protein)  adipocytes, skeletal/cardiac muscle to use as energy  LDL o Consists of >50% cholesterol, littleTG o Function – cholesterol delivery mechanism to synthesize membranes and hormones o Liver – regulates blood cholesterol; cells engulf LDL and extracts cholesterol  LDL receptors in liver bind LDL to make HDL  Saturated fat consumption increase blood level of cholesterol  blocks LDL receptors in the liver  reduced LDL uptake increased LDL and cholesterol levels in blood  HDL o Mostly protein; very dense; >20% cholesterol (most has been lost) o Capacity to absorb cholesterol from blood and arteriole plaques (“good cholesterol”) o Passes to IDL; taken to liver for recycling Cardiovascular System  Atherosclerosis – formation of plaque on inner lining of blood vessel wall (arteries, not arterioles); LDL accumulates, buries inside lesion, released CHOL, causes inflammation and plaque accumulation; lumen size decreases, heart must work harder to pump blood o Plaque made from i) cholesterol ii) complex CHOs iii) platelet aggregation  Arteriolosclerosis – a number of pathological conditions; thickening, hardening and loss of elasticity of artery walls (blood vessels remain constricted)  Artery and Vessel Layers o Tunica Externa o Tunica Media – thick smooth muscle; relax and constrict to control blood flow o Tunica Interna Endothelium – innermost cells; capillaries easily transfer gasses and nutrients  Arteries must be able to accommodate increased blood flow to meet oxygen and energy substrate demands of organ tissues (skeletal and cardiac muscle (working myocytes responsible forforce production))  Vasoconstriction – increases resistance to blood flow  increases preload on heart o I) Ventricles work harder II) Pathological cardiac muscle hypertr(cardiac hypertrophy = thickening of cardiac muscles (bad); hypertrophy = increase in size of skeletal muscle (good for fitness; not the same)) o Causes arteriosclerosis and atherosclerosis  Vasodilation – decreases resistanceto blood flow  blood supply to cardiac and skeletal muscles increase  decreases preload on heart 2  Vascular Endothelium – large (~350 m ) paracrine-like organ (secreted chemical that affects nearby function) that acts as an interface between blood and tissue o Endothelial tissues sense shear loadi(friction fofrom blood flow  mechanically changes endothelial shape  activates eNOS  NO ++ synthesized from L-arginine initiates enzyme-mediated cascade preventing uptake of Ca into smooth muscle cel leads to smooth muscle cell relaxation  eNOS = endothelial derived nitric oxide synthase o Endothelial cell dysfunction – causes i) impaired coronary endothelium-dependent vasodilation ii) reduced bioavailability of NO iii) increases expression of vasoconstrictors iv) increased oxidative stress v) low shear stress Reactive Oxygen Species (ROS)  Source of oxidative damage; type of free radicals (highly reactive molecules; impair physiological functions)  Inactivates NO – lose ability to signal smooth muscle relaxation (stays contracted)  O2Reduction o Mitochondrial Response – 4 protons + 4 electrons 2=O  2 2 O + ATP o ROS Response – small amounts of ROS are generated in 2 reduction to2H O; partial reduction2of O  Superoxide Dismutase- binds superoxide anion, renders it harmless; protects cell against oxidative damage; o Amount of superoxide dismutase decreases with age  Vitamin E and C = anti-oxidants; directly neutra2ize O  Circulating LDL freely diffuses through endothelial cell barrier into intimal space  LDL is oxidatively modified from prolonged oxidant (ROS) exposure - o OxLDL increases O 2roduction and inhibits eNos ability to convert L-arginine to L-citrulline and NO  decreased NO availability  Experiment o 3 Conditions – i) Low Fat Meal ii) High Fat Meal ii) High Fat Meal with Exercise (45 minutes treadmill walkin2; 60% VO ) o Experiment – measure vasodilation; eat, exercise 2 hours, measure at 4 hours o Results – low fat meal vasodilation > high fat meal vasodilation; high fat meal vasodilation with exercise o Conclusion – exercise has a protective effect; exercise 2 hours after high fat meal increased blood vessel reactivity; heightens ability to deal with LDL Proteins  “Protos” (Greek) = of prime importance 2 FINAL EXAM LIFE SCI 2N03  2 most abundance components of plants and animals (water most abundant) Food Sources  Animal Based - meat, fish, milk, eggs  Plant Based – dried bens, peas, nuts, seeds, some vegetables, legumes, grains  Recommendations (RDA’s) Age Quantity (g/kg body mass) 0-6 months 22 6 months – 1 year 1.6 1-3 years 1.2 4-6 years 1.1 7-10 years 1.0 11-14 years 1.0 15-18 years (males) 0.9 15-18 years (females) 0.8 Structures  Assemblies of amino acids – 20 = 9essential (must be ingested; not synthesized by b+ 11 non-essential (synthesized by body) o Conditionally Essential AA – body can produce it as long as an essential amino acid is present; tyrosine requires phenylalanine; cysteine requires methionine o Amino acids are unique by side chains (dictate size, shape, composition, electric charge, pH) 200 1. Primary Structure – order of aa; protein = 50-200 aa; number of proteins = 20 o Dipeptide, tripeptide, oligopeptide (4-10 aa), polypeptide (>10 aa) o Cross linking by disulphide bridges 2. Secondary Structure – additional formation of chemical bonds a. -helix – hydrogen bonds between N-H and C=O groups; interaction between non-adjacent aa; 3.6 aa/turn; eg/ myosin molecule = coiled-coil b. -pleated sheets – hydrogen bonds; parallel layering of polypeptide portions; sequence of aa folded onto another group of aa giving that portion of aa sheet-like appearance; eg/ albumin 3. Tertiary Structure – complex protein folding; non-polar aa inside, polar aa outside; protein loses symmetry 4. Quaternary Structure – more than 1 polypeptide chain (sub-unit); eg/ Hb = 2 -subunits + 2 -subunits =  2 2tetramer Denaturation  Loss of protein shape – energy input overcomes dissociation of energy of chemical bonds; pH, heat, alcohol, oxidation, mechanical agitation  Eg/ Egg Whites – ~15% protein, no CHOL, 40 different proteins; denatured by heat and mechanical agitation (air mixes with water portion to produce foam- like structure) o Ovalbumin = 54%; 385 aa, glycoproteins; denatures at 63˚C o Ovotransferrin = 12%; denatures at 80˚C (makes egg white firm o Avidin = binds to biotin (B-vitamin); if consumed chronically can result in vitamin B deficiency Function 1. Mechanical – collagen (provides tissue structure; stiffer tissue = more collagen); biomolecular motors (myosin, kinesin, dynein, ATPases) 2. Enzymes – catalyzed chemical reactions 3. Hormones – insulin, TSH (from pituitary gland), leptin (from adipose tissue; regulates/reduces feeling) 4. Immune Function – antibodies (blood proteins, neutralizes action of antigens) 5. Fluid Balance – albumin and globulin in blood (large proteins confined in CV; attract fluid out of interstitial space by osmotic pressure); decrease in blood proteins causes fluids to accumulate in tissue – edema can result as a sign of protein energy malnutrition 6. Acid-base Balance – blood proteinsbind acidic or alkaline atoms/molecules; blood pH = 7.4; eg/ Hemoglobin binds protons and buffer a decreasing pH 7. Transport Functions – 70-80% of energy expenditure at rest; ATPases (Na+, K+, Ca+); Lipoproteins 8. Energy – oxidative deamination (remove N group; C, H, O used; glucogenic aa (make glucose)or ketogenic (make ketone bodies; later converted to Acetyl CoA by neurons; Kreb’s Cycle)excess protein converted to FA’s Digestion  Stomach – begins chemical digestion; HCl denatures proteins (pH ~0.8); Pepsin (Pepsinogen + HCl; pH = 2.5) digests 10-20% proteins  Small Intestine – aa and dipeptidesenter; proteases (trypsin and chymotrypsin from pancreas) catalyze large to small peptides; peptidase from intestinal microvilli catalyze tri- and di-peptides into amino acids Absorption  Duodenum and Jejunum 1. Facilitated Diffusion – membrane proteins 2. Active Transport – membrane proteins that use ATP; Na+ exchanger – Na+ re-entry into CV system brings in aa (leucine, isoleucine, valine) a. Problem – too much of one aa may saturate the transporter, restricting other aa absorption  Absorbed aa  aa pool o Carbohydrates – liver and skeletal muscle o Lipids (triglycerides) – adipocytes o Proteins – everywhere Synthesis  Process turned on by hormones, signaling molecules, dietary proteins, muscle contractions  Ribosomes read mRNA, take up aa to form protein o Tryptophan  serotonin (regulates slee, niacin o Tyrosine  NE, epinephrine, thyroxin o Histidine  histamine Increased Protein Needs – Infections, burns, illnesses, surgery, pregnancy, lactation, athletics – Athletes o Strength/Power – need 1.7-1.8 g/kg body mass; accelerated protein turnover resulting from muscle “damaging” exercises; exercise activates intracellular “signaling molecules” for protein synthesis o Endurance – 1.2-1.3g/kg body mass; protein used as energy substrate during long duration exercise (adequate CHO intake protects proteins) o Amino Acid Supplementation – adds extra energy; may not be necessary if diet meets energy needs with high quality protein sources  Branched-Chain AA (BCAA) – essential aa; build up of muscle protein; >1/3 of all muscle aa are BCAA; 7g BCAA per serving  Excess protein intake  Individual aa can interfere with absorption of other aa  AA Enters urea cycle in kidney; leads to dehydration 3 FINAL EXAM LIFE SCI 2N03  Conversion to fat if diet is energy sufficient Quality – High Quality Protein Criteria – food i) provides all essential aa ii) provides enough aa to serve as N sources to synthesize non-essential aa iii) easy to digest and absorb – Low Quality Protein – considered incomplete protein-based food item; lacks adequate amount of aa o Plant based food (except soy); considered complimentary protein based food (eg/ beans/lentils and rice/pasta; paste low in lysine, high in methionine and cysteine, beans are opposite)  combine grains, nuts or seeds with legumes – Food Sources – yeasts, breads, pasta (common), lentils o Soybeans – complete protein  i) No CHOL and saturated fats (reduce CVD risk) ii) rich in phytochemicals iii) isoflavinoids function as antioxidants (protect LDL from oxidation) iv) genistein inhibits growth of breast and prostate cancer cells in lab v) phytoestrogens decrease risk of CVD and osteoporosis in post-menopausal women (disputed) vi) low in cysteine  Tofu (solid curdled soy milk cake), Tempeh (flat fermented soybean cake), Meat Analogs (flavored, textured), Soymilk (liquid of
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