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150 Cards in this Set
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- Back
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what is a PRO (greek origin) |
protos: of prime importance -organic molec 2nd most abundant comp. of plants & animals (water is numero uno) |
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list some animal & plant based sources of PRO
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animal: meat, fish, milk, eggs plant: dried beans, peas, nuts, seeds, sm vegetables/legumes, grains |
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what are PROs assembled from?
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amino acids! amino gr (NH2) - acid gr (COOH) - H - R variable |
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how many AA are there found in ALL animals? |
20 AAs |
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how many are essential & how many are nonessential |
EAA: 9 (must be ingested) nEAA: 11 (body able to synthesize) 5 are nEAA, 6 are conditional |
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what is a conditional AA? |
of the 11 nEAA, 6 of them can be made conditionally, based on the fact that we have EAA to from them *must consume an EAA to make nEAA |
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give 2 examples of conditional EAA |
tyrosine (made from phenylalanine) cysteine (made from EAA methionine) |
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what are the 3 BCAAs? |
isoleucine - leucine - valine they make up 33% of skeletal m AAs |
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what is the primary PRO structure look like? |
single string of AAs formed by peptide bonds dipeptide - tripeptide - oligopeptide (4-10 AA) - polypeptide (>10) -most natural polypeptides are 50-200 AAs long |
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what does the secondary PRO structure look like? |
additional formation of chemical bonds w/ 2 resulting shapes alpha helix (H bonds betw amino & acid gr; often in cell membranes as provides stability) beta pleated sheet (H bonds parallel layering of polypeptide portions, symmetrical, folds) |
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tertiary PRO structure |
same secondary chain w/ more complexity, structure LOSES symmetry complex PRO folding ie nonpolar AAs inside & polar AAs outside |
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quaternary PRO structure give an ex |
final functional PRO, contains >1 polypeptide chains in their tertiary structure combined each chain independently is a "subunit" ie hemoglobin Hb, tetramer, 4 subunits, 2 alpha 2 beta structures (Hb as a whole is the PRO, indiv subunits are just polypeptides) |
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list some functions of PRO |
mechanical (structure/stability to membranes) enzymes hormones immune function fluid balance acid-base balance transport (GLUT, SNAT, LAT) E (rare, only in long term exercise and only makes up 5-15% of E) |
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what is PRO turnover? |
balance betw. synthesizing new PROs & breaking them down (+ve vs -ve) ie resistance/aerobic exercise: +ve balance, adapt to exercise by up regulating PROs/enzymes to make more ATP during exercise PRO meal: +ve balance -ve balance: not ingesting enough food and we start to break down PRO for energy |
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explain PRO digestion recall digestion as breakdown 2 main places |
begins in stomach: -HCL acid in stomach denatures PROs -pepsinogen + HCL -> pepsin to b.down large peptides (accounts for 10-20% PROs digested) in small int: AAs & dipeptides enter, -proteases catalyze large peptides to small ones -from pancreas trypsin & chymotrypsin catalyze large to small ones -peptidases from microvilli in intestinal wall catalyze tri/dipeptides to indiv. AAs |
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where does PRO absorption occur recall absorption as into CV syst |
duodenum & jejenum (small int.) |
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what are the 2 ways of PRO absorption? |
1. facilitated diffusion -membrane PROs on enterocytes form chemical bonds w/ AAs to move them in 2. active transport -mainly used for BCAAs, Na pump need ATP to bring AA in, but w/ too much of 1 AA may saturate transporters thus restriction absorption of another AA -E expenditure increases with this form (b/c using ATP) |
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where are PROs stored? |
everywhere!! once absorbed we create a PRO pool no central location because they are formed into a PRO for some functional purpose |
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list the 3 main fates of PRO? |
1. PRO turnover (synthesize new PRO) 2. use carbon skeleton of AA (3 diff ways) 3. deaminate AA, take off amino gr & add CO2 to make urea -increased filtration/loss of water in urine w/ deamination (DEHYDRATION) |
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what are the 3 ways we use the carbon skeleton of AA? |
1. form new FAs (too much AA from a high PRO diet convert to fat, not common) 2. PRO gluconeogenesis, AAs -> glucose -if carb intake not sufficient 3. Energy, AA carbon skeleton has 2 Cs, acetylCoA (2Cs) put into krebs -AAs account for only 5-15% E contribution during long duration exercise |
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list some #s for PRO RDA relatively (g/kg BM) |
RDA decreases post birth to adulthood relatively (less per kg BM but we have so much kg so really a lot still)
-increases as we age b/c we lose PRO 2.2 (0-6 months of age) 0.8 (15-18 yo female) *may need more PRO if infected/burns/illness/surgery, pregnancy/lactation (remodelling) |
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how does the RDA for PRO change in strength & endurance athletes? |
strength/power: RDA is 2X that of general pop. 1.7-1.8 g/kg BM b/c of accelerated PRO turnover resulting from m "damaging" exercise endurance: 1.2-1.3 g/kg BM, m contractile activity is at low intensities but maintained for long periods of time & thus PRO used as substrate, *we become more efficient, more enzymes - more PRO |
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what does it mean to be a high quality PRO? |
provides ALL the EAA provides enough AA to serve as nitrogen sources to synthesize nEAA (i.e. conditional EAA) easy to digest & absorb ex: animal based food & soybean/quinoa of plant based foods -soybean is low in cysteine but good in large quantities w/out risk of CHOL & sat fats (decrease CV risk) |
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what is a low quality PRO? |
"incomplete" PRO based food item lacks adequate amount of AAs (doesn't give all EAAs nor a sufficient amount) -found in plant based foods...BUT -able to combine plant based foods, "complimentary", pasta & beans both low quality but together are good |
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list the 5 methods of assessment for PRO quality |
Chemical score (preschool kids) PRO efficiency ratio (PER) net PRO utilization (NPU) biological value PDCAAS (PRO digestibility connected AA score) (preschool kids) |
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what is the chemical score? |
CS= 1st limiting EAA in food / EAA in reference -looks at AA composition in food vs reference PRO -limiting AA is AA in shortest supply during synthesis (lowest quantity) (2 largest AA requirements are leucine 66 mg/g PRO and lysine 58mg/g) |
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what is the PRO efficiency ratio? |
PER= weight gain / PRO intake of a high quality PRO
measures AA composition & accounts for digestibility (b/down) concern is weight gain only being from PRO but we also consume water & other nutrients |
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what is NPU? |
net PRO utilization= (N retained/N intake)*100 measures how much dietary PRO the body uses (incorporates AA into cells) -measure N excreted -N retained is the body's ability to maximally USE all AAs we broke down |
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what is the biological value? |
BV= (N retained/N absorbed) * 100 how much N absorbed from a particular foods PRO is retained for growth/maintenance (so must get into CV syst.) ie egg PRO BV of 100 (of all AAs absorbed from egg body retains 100% to support physiology) ie corn PRO BV is 60 (only 60% absorbed is used vs 40% may be deaminated..) |
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PRO digestibility connected AA score? |
PDCAAS= chemical score * % digestibility of PRO (CS= limiting EAA/reference EAA) -PRO quality evaluation, the gold standard to determine which food source has the highest PRO quality) -accounts for both AA composition in food & digestibility of PRO) |
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what is a limit of the PDCAAS |
assumes PRO is the only macronutrient absorbed but this is false, in a meal we eat lots of stuff |
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what elicits a -ve PRO turnover? |
exercise (more breakdown then synthesis) low PRO intake (~0.36 g/kg/day), more degradation than synthesis (recall RDA is 0.8 for +ve) |
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what does it mean to say PRO synthesis is dose dependent? |
Incr intake incr PRO loss, but despite losses our turnover is still +ve b/c using PRO for functional reasons (ingest more, will excrete more) |
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which cow produces MILK |
holstein, the high milk producing dairy cow (1500lbs) |
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What is the milk production life of a cow, what is the substance before we get fresh milk? |
milk production life is 6 years, gestation is 9 months at birth colostrum is secreted from mammary glands & w/in 72 hrs becomes fresh milk *milk from infected cows should not be used (i.e. mastitis, yeast infection in udder, cows given meds) |
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how long is the lactation period of a cow |
300 days to produce 9000kg of fresh milk (~1000kg goes to newborn) lactation peaks at 10 weeks & declines at ~9%/month |
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what animal milk has the highest PRO content? |
WHALES!! 10.9 g PRO, 42.3 g fat cows: 3.2 g PRO, 3.7 g fat, .... humans: 1.1 g PRO, 4.2 g fat |
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what country is the highest producer of milk & the largest consumer of milk? |
highest consumption: Finland Highest production: USA canada is #10 on consumption |
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what is the primary purpose of drinking milk? |
to provide nourishment & immunological protection for mammalian young b/c antibodies & bacteria >100 000 diff molecular species in fresh milk |
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what is common milk composition (%) |
87% water 3.9% milk fat 8.8% nonfat solids: 3.25 PRO (3/4 casein, 1/4 whey), 4.6 lactose, 0.65 minerals (Ca/P/citrate/Mg), rest acids/vitamins/enzymes/gas |
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define what plasma, serum, solids nonfat & total milk solids are? |
plasma= milk-fat (skim milk) serum= plasma - casein micelles (left over is whey) solids nonfat: PRO, lactose, mins/vits, acids, enzymes total milk solids: fat & solids nonfat |
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what is the purpose of milk lipids (3.9% milk fat) |
flavour & nutrients (EFA & vitamins) 98% of milk fats are TGs & rest are mono/diglycerides & phospholipids *majority of milk fats are long chain FAs (C14,16,18, saturated) *most abundant unsat. FA is oleic (C18:1) *small amount of short chain FA (11%) |
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how do milk lipids exist as? |
95% of total milk fats exist as GLOBULES -low density globules will float to the top in raw milk (float above plasma) |
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what is homogenization? |
mechanical processing of fresh milk pass milk under high pressure thru small orifice will cause fat globules to break up (decrease diameter of fat & increase density) *allows them to disperse more evenly in plasma & decreases tendency of milk to cream (more stably) |
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what % of milk PRO is whey? |
25% of all milk PRO is whey 75% casein; 6% nonPRO nitrogen |
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what are the 2 major PROs in whey? |
1. beta-lactoglobulin, 65% of all whey PRO, made of 162 residues (AA) 2. alpha-lactalbumin, 25% of whey, part of lactose synthase |
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how is cheese made? |
from casein & curds whey in milk plasma (no fat) is strained from curdled milk (PRO content in cheese is less than milk b/c whey squeezed out) |
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which PRO is more digestible, whey or casein? |
whey (b/c casein in micelles) |
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what is casein PRO |
major PRO in milk & cheese (80% in cheese) diff names: alpha1, alpha 2, beta-casein, kappa casein *the insoluble form of milk PRO, forms casein micelle (not water soluble) *stable against heat denaturation & carries CaP (but b/c stable hard to breakdown & not as digestible) |
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what are 2 reasons why whey is good? |
more digestible source of our essential BCAAs (isoleucine, leucine, valine) *recall, in skeletal m these make up 33% AA |
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what is whey PRO powder vs whey PRO [ ]? |
powder: additive in baked goods, salad dressing & infant formulas [ ]: liquid milk pushed thru, compound left behind is concentrate, some lactose & water removed; some minerals/vitamins remain *25-89% PRO content (but large range since 25 is low quality) |
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whey PRO isolate vs whey PRO hydrolysate |
isolate: most pure PRO source, up to 90% PRO (removal of fat & lactose) (expensive) hydrolysate: predigested PROs, high quality, manufacturers pre-denature PROs to make it easier to ingest & absorb |
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study on PRO hydrolysate & absorption |
PRO hydrolysate increases AA digestion & absorption (25-50% more AAs in plasma apparent 6 hours later) -no difference in fractional synthetic rate between hydrolysate & control group |
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PRO ingestion before sleep improves post-exercise overnight recovery? |
good absorption (seen thru blood [ ] of EAA) -+ve turnover, synthesis following PRO drink -YES, increased rate of m tissue specific PRO synthesis after drink/overnight *whey has a > spike in blood AAs & stimulates PRO synthesis more post-resistance exercise (AA provision contributes to synthesis of new m PRO during sleep) |
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how long does PRO intake keep PRO synthesis going for? |
intake increases PRO synthesis up to 3 hours after ingestion (both EAA & nEAA) *EAAs are the primary stimulators of synthesis (leucine is good) |
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what is mTORC1 |
mammalian target of rapamycin complex 1 -5 component PRO kinase (enzyme that adds P) -can be activated internally (to the cell, m) & externally (intro of AAs, diet, hormone as stimuli) *mTORC2 regulates cell metabolism & growth/synthesis of PRO, lipid, organelle substances |
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how is mTORC1 activated? |
growth factors E status (internal factor b/c ATP levels) AAs (leucine is an independent activator of mTORC1) exercise (dependent on intensity) |
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what are the 2 AA transporters on the m cell membrane |
SNAT2 & LAT1 (LAT1 mostly EAAs) Once in the cell, the AAs will activate mTOC1 to trigger process for PRO synthesis |
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STUDY: does EAA ingestion activate PRO synthesis pathways? |
did a control group to inhibit mTORC1 -no effect betw. groups w/ digestion/absorption the group w/ inhibited mTORC1 has lower PRO synthesis & same level of FSR at baseline (b/c mTORC1 still goes at basal rates even w/out ingestion if we are exercising) *accelerated PRO synthesis/FSR in group w/ working mTORC1 |
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STUDY: does resistance exercise make m cells more sensitive to dietary AAs? |
after 1 bout of resistance exercise there was sustained increase in AA transporter expression * PRO transport > expression in older adults (better at utilizing AAs b/c have > mRNA expression) *m cell learns to make itself more sensitive to AAs (we provide the stimulus to the body & it responds) |
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how can we get optimal results for PRO synthesis? |
combining exercises & AA ingestion (both stimulate mTORC1, esp leucine) both resistance & endurance aerobic exercise work to increase synthesis |
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STUDY: does PRO supplement source influence absorption &/or m PRO synthesis? |
PRO drink: whey, soy OR casein after resistance exercise -whey had the greatest & fastest increase in blood (fastest ABSORPTION) (b/c easily digestible) -leucine is an EAA in whey & also an independent activator of mTORC1(increase PRO synthesis) soy came second, casein last (not as bioavailable, just takes longer to breakdown) |
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also no correlation betw m volume changes (hypertrophy) and FSR, (study) |
-also, insulin (hormone) is a trigger to movement of AAs into tissues after exercising our PRO drink will also contain sm amount of carbs, replace glycogen stores, insulin triggered for glucose uptake but also helps w/ AA |
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what is the chemical name of alcohol? |
ethanol ethyl alcohol CH3CH2OH organic molec w/ 1 or more hydroxyl groups (OH) consume in liquid form; also for cooking & baking -fermentation destroyed harmful bacteria (safer than water back in the day( -used as a painkiller prior to 20th century |
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what is the definition of alcohol (what makes alcohol, alcohol) |
any class of chemical compounds w/ the formula R-OH (hydroxyl gr & alkyl group) tocopherol (vit E) - retinol (vit A) - glycerol (TG backbone) |
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what is the consumable alcohol aka |
ethyl alcohol, ethanol, EtOH used in beer, wine, spirits |
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what is the simplest alcohol? (chemically) |
methanol used in paints & solvents for woodworking, paint strippers, airplane fuel, windshield washer fluid |
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what is the over the counter word for isopropanol? |
rubbing alcohol |
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list the boiling & melting points of alcohol |
boiling: 78 degrees (less than water) *when used in cooking, alcohol evaporates leaving behind flavours melting: -114 degrees (water is 0), beer will freeze b/c low alcohol content, vodka doesn't freeze b/c higher alcohol content *more Hs in water than alcohol, H binds O better than H-C, H-O stronger bond to break |
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does alcohol have a nutritive value? |
alcohol provides E (7kcal/g) but serves NO essential function in the body most CHO are converted to alcohol during production beer has some CHO/PRO/Vits but is negligible at small doses |
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what is 1 way alcohol is made?
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fermentation: yeast cells consume sugarS for E (sugars as in CHOs); anaerobic metabolism of sugars -yeast ferments sugars end product is alcohol & CO2 |
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what % of alcohol is made via fermentation? |
16% |
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aside from fermentation how else can we make alcohol? |
distillation; also increases the alcohol component *if distillation not carried out effectively it can create methanol (volatile) and other substance (congeners, dangerous, cancer causing) |
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what is the alcohol content in beer, wine, hard liquor? |
beer: 5-6% wine: 8-15% hard liquor 35-40% (proof= x2, i.e. 80 proof is 40%) |
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how strong is pure alcohol? |
95%, clear colourless liquid w/ sm water vodka is the closest pure alcohol (min 40%) beer contains sm unfermented carbs |
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what is a congener |
biologically active compounds w/ distinctive appearance & taste, responsible for hangovers) |
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what is a standard drink? what is moderate drinking levels for M&F? |
beer: 12 oz - wine: 5 oz - hard liquor: 1.5 oz moderate drinking F: 1 drink/day M: 2 drinks/day |
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what is binge drinking? |
pattern of drinking that brings sm1s BAC to 0.08 g/dL% or above for M: >= 5 drinks F: >=4 drinks ....both in 2 hours |
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where does alcohol absorption occur
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in mouth, esophagus & stomach -enzymes in stomach oxidize alcohol -in small intestine have absorption into hepatic portal circulation to liver (site of alc. metabolism) -liver cells will take alcohol 1st over CHO/PRO/lipids/nutrients |
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how can one delay alcohol absorption |
ingestion of fat delays gastric emptying, MCDs for ex slows release into small intestine (where most of alc. absorption occurs) -delay transport to small int. delays absorption into CV cyst |
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what is the 1st stage in alcohol metabolism |
ethanol --alcohol dehydrogenase --> acetylaldehyde (toxic & hihgly reactive) -4-20% occurs in digestive tract -also have NAD+ --> NADH |
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stage 2 of alcohol metabolism? |
acetylaldehyde -- acetylaldehyde dehydrogenase --> acetate again NAD+ --> NADH |
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what is stage 3 of alcohol metabolism? |
acetate combines w/ coenzyme A to form acetylCoA small amount of acetylCoA will go to Krebs, sm to FA synthesis *this slows down krebs cycle, overwhelms it, FA accumulation in liver for a fatty liver, observable results w/ 1 bout of heavy drinking but acute) |
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what is alcohol aversion therapy & what is the drug that is used? |
those w/ alcohol dependency/alcoholics are given the drug disulfiram disulfiram: acetylaldehyde dehydrogenase inhibitor, increases in accumulation of acetylaldehyde working in -ve reinforcement b/c it causes unpleasant rxn to alcohol ingestion & get severe hangover in 30 mins |
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what is MEOS stand for? |
microsomal ethanol-oxidizing system occurs w/ chronic alcohol consumption/binge drinking w/ effect of increased tolerance to alcohol (alcohol is like a form of stress, cells adapt and up regulate enzymes to deal better w/ alcohol, doesn't change upper level of toxicity tho) |
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how does MEOS work? |
microsomes (vesicles from ER) metabolize alcohol when regular dehydrogenase pathways are overwhelmed (MEOS is overflow pathway) *liver uses this system for drugs & foreign substances (but alcohol takes priority and then unmetabolized drugs may cause more severe side effects) *when dehydrogenase pathway is maximized, MEOS makes acetylaldehyde faster |
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when does 1 drink peak in BAC? |
30-45 mins, may be faster on empty stomach liver alcohol metabolism (removing from circulation) depends on amount of metabolizing enzymes (also varies among indivs/ethnicities) |
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what is the BAC formula? |
bac= alcohol absorption - liver alcohol metabolism (absorption is alcohol going from GI to CV syst before liver) *if +ve alcohol circulates thru the body & crosses the BBB, liver can't keep up & alc. will bind to neurons & affect neurofunctioning |
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how much of alcohol/ethanol is excreted into lungs, urine, skin |
10% |
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what is the rate of alcohol removal from circulation? |
15 ml/hour it is dose dependent; the more we drink the longer it takes to reach peak levels (longer to metabolize) ie 4 drinks takes ~1hr to get to peak levels *we quickly saturate the max ability of liver cells to remove alcohol (by consuming food we can mitigate this effect) |
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define hangover list some symptoms |
a physiological condition following consumption of a lot of alcohol (relatively large, variable betw BMs) -headache, fatigue, nausea, dizziness, sensitivity to light |
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what are direct effects w/ a hangover/consuming alcohol
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-dehydration (alcohol suppresses ADH secretion, reabsorption of water) -sleep disturbances -electrolyte imbalances -sweating/increased urination, vomiting, diarrhea -hypoglycemia (inhibition of liver glycogenolysis, slows down creation of glycogen) |
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what are hangover effects of alcohol metabolism? |
large amounts cause acetylaldehyde toxicity & liver processing ability decreases |
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list some nonalcoholic factors of hangover/alcohol consumption |
-congener byproduct made from distillation is bad -drinking while on drugs is bad, alcohol takes 1st priority -delays metabolism of drugs, simulates a > dosage & effect (dosage calculated based on avg person's ability to detoxify the drug, but > dosage overwhelms body's ability to met. it & side effects occur) |
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how can one treat a hangover? |
time CHO (replace E) electrolyte |
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alcohol metabolism in Ms vs Fs |
BAC increases faster in Fs than Ms, Fs become intoxicated faster than Ms & metabolize alcohol slower |
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what are 3 reasons why Fs get drunk faster than males? |
Fs have smaller body size & smaller liver (less tissue, less enzymes to metabolize alcohol, more difficult to pr same absolute level of alcohol/# of drinks) alcohol dehydrogenase in the stomach is 40% less active in Fs (more alcohol/ethanol absorbed in CV syst) Fs more likely to suffer from alcohol related problems than men (cirrhosis of liver-liver toxicity), CV problems, suicide, accidents |
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what are some problems w/ alcohol (activities of daily living for ex) |
impaired driving (any machine) alcoholism (health & social problems) FASD |
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list brain & nervous sys. problems w/ alcohol & short term effects |
-ethanol readily diffuses into brain (fat-soluble, doesn't need PRO transporter) -mouth absorption effects occur quickly -dose dependent, > ingestion > effects -1-2 drinks gives BAC of 0.04 (criminal offence if drive > 0.08) |
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how does alcohol affect GI system? |
ethanol & acetylaldehyde damages GI cells )affects the level of metabolism in the stomach) -discourages eating, impairs nutrient absorption, leads to chronic inflammation |
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how does alcohol affect the liver? |
here we metabolize & detoxify blood -w/ heavy drinking we may have a fatty liver & acute alcohol hepatitis (liver inflammation from alcohol & acetylaldehyde irritation b/c toxic--? predisposes to cancer development) |
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what is cirrhosis & where does it occur? |
replacement of liver tissue w/ fibrotic tissue (b/c of alcoholism) -a few days of heavy drinking leads to FAT accumulation in liver (this is acute & will resolve w/ abstinence) -5-15% of ppl will develop fibrosis |
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what is the problem of presence of fat in the liver? |
leads to peroxidation, oxidative degradation of lipids by free radicals leading to inflammation (free rads are highly reactive & damaging) |
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w/ ethanol metabolism we get accumulation of NADH, what effect does increased NADH have? |
NADH produced by dehydrogenase decreases TCA (krebs), (slow) -incr. NADH gets backed up & increased pyruvate 1. pyruvate + lactate dehydrogenase -> lactate and decreased pH (low pH denatures PROs) 2. pyruvate +pyruvate dehydrogenase --> acetylCoA (2C), increases fat, thus fatty liver, fibrosis, cirrhosis |
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what else does increase in NADH do? |
decrease gluconeogenesis increase ketosis (decrease pH) decrease production of key PROs (decrease leydig cells which produce testosterone in Ms) decrease drug metabolism (again b/c alcohol is priority) |
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study: post resistance exercise ethanol ingestion on acute testosterone bioavailability |
exercise increased total testosterone (lipid soluble easy to get into cells to activate PRO synthesis) -10 min later had ethanol, testosterone remains elevated in CV syst. (from before)same as baseline |
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study: alcohol ingestion impairs maximal post exercise rates of PRO synthesis |
*athletes more likely to drink alcohol in excess than general population 3 conditions: alc-CHO, alc-PRO, PRO only -BAC was > w/ CHO trial (longer to clear ethanol from CV syst w/ carb intake) -probs b/c CHO are stored in liver, thus competing metabolism alcohol vs CHO -ethanol limited body's ability to absorb BCAAs -alcohol also RESTRICTs an increase in PRO synthesis *if FSR was elevated it was due only to CHO/PRO ingestion and not b/c of alcohol (mTORC1 activated b/c of leucine in PRO & exercise as a stimulant) |
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what is the largest category of lipids? |
TGs: glycerol & 3 FAs both plant & animal origin |
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list some functions of TGs |
Energy source (beta oxidation on mitochondrial surface) insulation/protection improves bioavailability & transport of other fat-soluble nutrients (vit. A/D/E/K) flavour, texture and odour of foods |
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how much does phospholipids account for in lipids? |
makes up ~2% all dietary lipids both plant & animal sources both fat & water soluble (phospholipid bilayer) major constituent of cell membranes involved in FA transport (forms outer shell of chylomicrons & lipoproteins) |
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give some food examples of phospholipids |
recall both plant & animal sources egg yolks, soybeans, peanuts |
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what is a sterol? |
makes up <2% of all dietary lipids most popular is CHOL (made by body too) precursor to hormones (sex/cortisol), vit D, bile acids |
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how does one notate FAs? |
hydrocarbon chain can be from 4-24 Cs, short (<6) - med (6-10) - long (>12 Cs) 18:0, # Cs: # of double bonds 4:0 (saturated, Butyric acid, butter, no double bonds) 18:0 (steric acid, saturated, chocolate, meat fats, solid at room temp) |
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compare the length of a FA to its physical composition (solid vs liquid) |
longer chain: more solid at room temp shorter chain: more liquid (oils), esp unsaturated FAs are more liquid the more saturated a FA is the more solid it will be (more H atoms, stronger) flax seed oil, omega-3 PUFA, more unsaturated, less strength in bonds, more likely liquid at room temp vs coconut oil: 90% of fat is saturated, thus more stacked appearance & solid at room temp |
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what is a single bonded FA known as? |
saturated FA, all Cs are single bonded to adjacent Cs or 2 H atoms |
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what is a monounsaturated FA? give an example |
1 double bond oleic acid 18:1, olive oil (thick at room temp but may solidify w/ refrigeration, omega-9 FA) omega-9, means 1st double bond appears at 9th C |
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what is a polyunsaturated FA? and how is it defined? |
>1 double bond; PUFAs are defined by existence of omega end (methyl gr, CH3) and then the # is the location of the 1st double bond LA (linoleic acid, 18:2, omega-6 FA, 2 double bonds, 1st one appears after 6th carbon); soybean oil ALA: linolenic acid, 18:3, omega-3 FA, flaxseed oil, very thin -break PUFAs down into alpha & beta carbons (2C) and put into krebs |
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how is geometric shape determined by in a FA? |
geometric shape is determined by presence of double bond CIS vs TRANS |
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what is the difference betw a CIS & TRANS PUFA? |
CIS: bent, most common, found in natural PUFA foods -H on SAME side of double bond (U) (Hs repel) TRANS: straight, more solid at room temp, Hs on opposite side of double bond, linear -usually results from food processing (unhealthy b/c of hydrogenation) |
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what is the process of adding more Hs to an unsaturated FA |
hydrogenation make sm type of fat solid at room temp |
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pathway liver cells metabolize omega 6 FA |
ie start w/ LA 18:2, 2 double bonds (linoleic acid) -have desaturases & elongases (add another double bond & elongate enzymes) to get... ARA, arachidonic acid (20:4), a precursor to prostaglandins, trigger pro-inflammatory response, bad b/c causes low level inflammation throughout CV system *diet high in omega-6 is risky maybe |
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pathway liver cells metabolize omega 3 FA |
ie start w/ ALA, 18:3, linolenic acid (3 double bonds), plant based, desaturate & elongate to produce... EHA (CV benefits) & DHA (brain, neuron, eye development in infants & kids) *omega-3s have more health benefits |
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define sterols, ie CHOL |
CHOL (component of cell membranes, neurons & precursor of moles) -all cells synthesize CHOL, body makes ~1000 mg /day *CHOL only from animal origin! |
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what is a plant based sterol? |
phytosterols, similar in chemical structure to CHOL but reduces CV risk -poorly absorbed but help to decrease absorption of CHOL (mixed meal); used as a CHOL-reducing food agent -compete for absorption |
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where does fat metabolism/break down occur? |
occurs mainly in duodenum & jejunum of small intestine -in small intestine break fat down into MG & FA by pancreatic lipase (lipids are fat-soluble thus don't need PRO transporters to get into intestinal cells) |
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how are fats absorbed into CV system? |
once TG broken down... -glycerol moves into CV system -MG & FA mix w/ bile to form micelles (Fat cells) and move into lacteals 1st (lymphatic system) b/c fat soluble -lipid movement into CV system thru thoacic duct (lymphatic system) to jugular vein= via chylomicrons (absorptive mechanism for dietary lipids), package of CHOL & fat soluble vitamins, |
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how are lipids transported around the CV system? what are the different forms of transport? |
TG & CHOL packaged together as lipoproteins.... chylomicrons: 1st stage of lipoprotein, high TGs, low PRO/CHOL/phospholipids VLDL: less TGs & increase in CHOL/phospholipids/PRO (low density, not tightly packaged) LDL: most CHOL here, very low TG, sm phospholipid & PRO (BAD) HDL: most PRO here, least TG< low CHOL/phospholipid (FA content decreases, good CHOL, absorb more CHOL out of CV system) |
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what is the time frame of the 1st appearance of lipids in the blood?
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1-2 hours to 1st appear (b/c absorbed into lacteals 1st before CV) 3-5 hours to get to peak levels by 10hours lipids are cleared |
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compare CHOL absoprtion to that of FA |
CHOL has lower bioavailability than FAs (b/c we make CHOL & need more FAs) CHOL increases w/ increased dietary lipids (the > TG content in food, more likely to absorb CHOL b/c packaged together in chylomicrons) -provided CHOL is of animal origin |
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what is the function of LDL |
low density lipoprotein (contains the most CHOL) -CHOL-delivery mechanism to synthesize membranes & hormones (LDL delivers CHOL to cells to make membranes) -LDL has >50% CHOL & little TGs |
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how does the liver cells regulate CHOL levels? |
liver regulates blood CHOL w/ enzymes that neutralize it -cells engulf LDL and extract CHOL -meal high in sat. FA will block CHOL receptors in liver and thus good CHOL levels increase -if # of LDL receptors in liver are low (maybe genetics) we have reduced liver uptake & LDL levels increase in blood (BAD CHOL, can be mLDL and put us at risk for atherosclerosis) |
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describe the properties of HDL |
smallest lipoprotein, most dense, has capacity for absorption extra CHOL -manufactured in liver & intestine, majority PRO, very dense (<20% CHOL) GOOD: b/c low CHOL content & capacity to absorb CHOL from blood & arterial plaque |
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what is the formation of plaque on the inner lining of BV walls called? what does this plaque consist of |
atherosclerosis (decrease CSA of BV, decr blood flow, increase BP=ischemia) -plaque on inner layer of arteries plaque; CHOL & platelet aggregation |
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how does atherosclerosis form? |
LDL invades tunica intima & made worse by free radical accumulation (mLDL) -mLDL coaggulates & forms small clots -immune syst response sends macrophages to engulf mLDL, but those form foam cells -reduces CSA of BV, foam cells cause inflammation & CHOL deposition |
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what is in a foam cell? |
contains lipid droplets (now a modified macrophage) releases CHOL crystals and contributes to plaque (observable fatty streaks & decrease BV diameter) lays down more TGs & VLDL-injures endothelial cells (decreases NO bioavailability & decreases vasoreactivity; not able to sense friction in BV and thus not able to form NO & vasodilate) |
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how is NO formed? |
nitric oxide is formed from AA l-arginine (cEAA) w/ enzyme eNOS to get NO & citrulline |
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what are the top 3 causes of death in Canada & what are the top 3 modifiable RFs? |
cancer - heart disease - stroke smoking - exercise - nutrition |
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how much ALA is consumed in a day vs how much is recommended? (sidebar: 11 g of ALA we get only 1g EPA/DHA) |
1.4 g/day consumed (alpha-linolenic, omega-3, plant based, essential FA) RDA is 2.22g ALA recall, ALA then normally 5-15% range converted to EPA & even less converted to DHA omega 6:ALA ratio is 4:1 or less (altho 6 is pro-inflamm. not shown to increase CV risk) |
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what are some plant-based sources of ALA? |
omega 3 PUFA flaxseed oil > flaxseed ground > walnuts (flaxseed whole not as bioavailable b.c not broken down) |
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what is benefit of ingesting ALA (flaxseeds)? |
associated w/ lower risk of fatal ischaemic heart disease Nurses study: significant reductions of fatal CHD Mice: anti-atherogenic effect, protective effect against developing atherosclerosis |
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what is a lignan? |
chemical compound, a phytoestrogen, -most abundant source in flaxseeds -dietary lignans contain estrogen-lk or anti-estrogenic qualities -work like a tamoxifen drug to competitively bind to estrogen receptors on breast cells so natural estrogen cannot bind -hypothesized that natural estrogen accelerates development of cancer cells |
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stats on lignan efficiency? |
34% decrease in a PRO marker of cancer cell proliferation w/ those who ingested flaxseed (probability of cancer cell growth declines b/c of anti-estrogenic factors) -in flaxseed group saw 31% increase in apoptosis (cells able to naturally die off, normally cancer cells mutate apoptosis & proliferation continues) |
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what can EPA & DHA be found (in the body) |
-omega-3 PUFAs, different structures but greater degree of elongation -incorporated into plasma & membrane lipids for > health benefits -essential FAs but hard to ingest since not plant based |
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where are EPA & DHA sources found |
-ALA (flaxseed) -mackerel, herring, salmon -functional foods (fortified foods, nutrients aded for enhancing health benefits) recall: 5-15% of ALA is converted to EPA (health benefits) and then eventually even less converted to DHA (brain/neuron/eye development) |
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what is the average EPA/DHA intake in NorthAm adults |
100 mg/day recommended anti-arthymic effect of EPA/DHA is 750mg/day DHA PUFA is a cis-structure, more bend, more H repulsion supplementing w/ EPA/DHA is common but enteric coated w/ a bunch of bad stuff in order to survive the acidic stomach environment (oil more dense than a pill, sm contain vit.E-anti-oxidant) |
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are males or females more efficient at converting ALA to EPA? |
FEMALES from ALA, F able to convert 21% to EPA & 9% to DHA men convert 8% to EPA and undetected for DHA |
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how is females efficiency of ALA to EPA related to estrogen effects? |
+vely related to estrogen levels >est in 3rd trimester of pregnancy -as an evolutionary mechanism EPA/DHA supports nervous system development of fetus -but following birth estrogen & DHA decrease |
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what are some CV benefits of EPA/DHA in our diet |
-decrease in ventricular arrhythmias (irregular HBs) due to lipid incorporation into membranes -anti-thrombosis effects, decreased tendency to form blood clots -lipid-lowering effect, ingesting EPA/DHA decreases TG & VLDL levels -inhibition of atherosclerosis & inflammation |
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how does a diet low in EPA & DHA create an exaggerated platelet response to an endothelial cell lesion? |
recall: arachidonic acid (omega-6, from LA), pro-inflammatory effect COX, cyclo-oxgenase converts AA to TxA2, thromboxine) a FA that is an aggregate to platelets & will attract and activate more platelets to the damaged site membrane of platelets activated when signalled by immune system |
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how does a diet high in EPA/DHA reduce platelet activation? |
displace portion of omega-6 arachidonic acid thus having an inhibitory effect on COX which is central to TxA2 -if TxA2 not created then we have reduced platelet activation (still immune response just not as large) |
