Nutr 3210
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| show | Vitamins A, B6, B12, E, K, thiamin, riboflavin, niacin, biotin, pantothenic acid, folate
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| show | Vitamins C (for rats, in humans-essential), D (as long as there is enough light) and choline
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| show | Ca, P, Mg, Na, Cl, K
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| show | Fe, I, Zn, Se, Cu
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| show | metabolic rate drops, high levels of TSH cause goiter formation - hyperplasia due to thyroid attempt to put out more T3 and T4, goiter during pregnancy leads to birth defects - cretinism
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| show | bind to nuclear receptors, form transcription factors which bind to response elements in promoter regions of DNA - proteins responsible for increased metabolic rate and fetal development
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| What is the role of vitamin A? | show 🗑
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| What are the animal sources of vit A? | show 🗑
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| What are the plant sources of vit A? | show 🗑
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| What are the common characteristics of vit A? | show 🗑
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| What are the mechanisms of vit A digestion and absorption? | show 🗑
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| Where are carotenoids and retinoids metabolized? | show 🗑
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| Where are retinols metabolized? | show 🗑
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| What happens when retinols reach the liver? | show 🗑
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| show | retinyl palmitate can be stored in stellate or parenchymal cells. low blood [retinol] results in removal of ester and transported by RBP and TTR to the eye
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| show | transported out as VLDL and converted to LDL in the bloodstream to be stored in adipose tissue
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| show | retinol oxidized to all trans retinol in retina, isomerized to 11-cis retinal, binds with opsin to from rhodopsin
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| What happens when rhodopsin is bleached? | show 🗑
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| What is retinoic acid signaling? | show 🗑
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| show | differentiation, growth (bones), fertility (sperm), fetal development
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| What happens with retinoic acid deficiency? | show 🗑
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| show | sunshine (skin), egg, milk, salmon, liver, beef, veal, fortified foods
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| show | cholesterol converted to 7-dehydrocholesterol in sebaceous glands. UVB radiation converts to lumisterol (sloughed off from skin) and previtamin D3. Thermal isomerization produces cholecalciferol (vit D3) and UVB radiation gives off tachysterol (sloughed).
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| show | latitude, skin exposure, air pollution, skin pigment
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| show | diffuses through skin to blood, 60% bound to DBP, deposited in adipose/muscle and then goes to liver
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| show | absorbed from small intestine lumen through BBM, packaged into chylomicrons (makes up 40% of circulating D3), transported through BLM to liver
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| show | cholecalciferol is hydoxylated in liver mito. by 25-hydroxylase to calcidiol (25-OH D3) and transported to the blood via DBP. In kidney mito. hydroxylated by 1-hydroxylase to calcitriol. Carried to blood via DBP to bones, kidney and intestines.
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| What is the role of calcitriol? | show 🗑
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| show | Low Ca stimulates secretion of PTH, PTH stimulates kidneys to ^ Ca absorption & stimulates calcitriol synth. Calcitriol stimulates Ca absorption in GI. PTH and calcitriol stim. bone resorption.
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| How is calcitriol excreted? | show 🗑
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| What are the side effects of over supply of vitamin D? | show 🗑
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| show | not enough - rickets. too much - toxic
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| show | failure of bone mineralization, edema in wrists, ankles and knees, bowed legs and curved spine
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| show | lack of vit D -> poor absorption of Ca. PTH increases, promotes bone resorption -> bones demineralize but bone mass is preserved
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| show | low intake of Ca leads to decreased bone mass (density) but normal mineralization. Fractures are an issue.
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| show | Decreased sunlight exposure and synthesis in skin. Dietary intake is lower and absorption, hydroxylation and reabsorption is decreased.
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| What are the benefits of increasing vit D serum concentration? | show 🗑
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| What are the main roles of vitamin D? | show 🗑
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| show | 99% localized to teeth and bones (rest in ECF for cell signaling). hydroxyapatite in bones - support and storage. If blood and ECF Ca levels drop = death, bones always compromised first.
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| What is the role of phosphorous? | show 🗑
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| show | post translational modification (dependent on vit K) in proteins that need to bind Ca.
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| show | Forms fluorapatite, detine layer of teeth and smaller amounts of bone
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| Where is Ca located in body? | show 🗑
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| show | PTH and vitamin D increase calcium. Thyroid releases calcitonin to decrease Ca.
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| show | phytate from grains and legumes forms insoluble complex with Ca and prevents absorption of P. Oxalates in spinach, rhubarb and alfalfa chelate Ca and increase excretion in feces.
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| Why is vitamin K important? | show 🗑
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| show | Phyloquinone (K1,plants-saturated) in green leafy vegetables and oils/margarines (canola&soy). Menaquinone (K2, bacteria-unsaturated) in human colon, not suffcnt. to meet human needs. Menadione (K3, synthetic) not commonly used, liver tox. in infants
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| show | similar to vit A - absorbed in SI, brought to liver by chylomicron remnant, distributed by VLDL/LDL, little storage. status decreased by fat malabsorption
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| show | vit K dependent gamma carboxylation of proteins - occurs on glutamic acid side chain to form gamma carboxyglutamate residues
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| show | fluorapatite in tooth enamel resists bacteria-induced degredation. Tooth decay if deficient.
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| show | Mainly cosmetic. Dusty white or mottled patches on teeth
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| show | sterility in males, inability to maintain pregnancy, anemia, muscle pathology, neural defects - deficiency in selenium can also have same side effects - both involved in antioxidant defense
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| show | 2 families - tocopherols (saturated) and tocotrienols (unsaturated). 4 compounds each.
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| show | hemorrhage and heart failure. Supplements only partially active but fully contribute to UL - can take too much.
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| show | organ meats, muscle meats, cereal.
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| What are the dietary forms of selenium? | show 🗑
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| show | Ascorbic acid (reduced) and dehydroascorbic acid (oxidized)
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| show | primates, certain small mammals (guinea pigs, fruit bats), some birds, some fish (salmon)
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| What are the functions of vitamin C? | show 🗑
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| What are the oxidant defense mechanisms of vitamin C? | show 🗑
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| What are the signs of vitamin C deficiency? | show 🗑
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| Why is niacin (B3) important? | show 🗑
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| What are the sources for niacin? | show 🗑
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| show | 4 D's: dermatitis, dementia, diarrhea, death
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| show | Plays a key role on metabolism of fats, ketone bodies, carbs, proteins
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| what are the sources for riboflavin? | show 🗑
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| show | energy metabolism. Thiamin works with CoA, FAD & NAD to move sugars, AA, FA into aerobic metabolism and ATP production. Plays role in NADPH and ribose synth. and also in nervous transmission.
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| What is wet beriberi? | show 🗑
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| show | Absence of TPP in nervous tissue leads to neurological symptoms. Wasting (numbness in legs), irritability and disordered thinking. Related to older age.
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| show | occurs at 2-5 months of age. Onset is rapid and must be treated within hours. Causes cyanosis, tachycardia and convulsions.
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| What is the role of pantothenic (B5) acid? | show 🗑
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| show | Necessary in the TCA cycle, production of fatty acids and glucose. Necessary in ruminants to produce succinyl CoA to produce glucose. No RDA because bacteria in colon produce enough.
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| show | necessary for the production and maintenance of new cells. Important in pregnancy and fetal development and in infancy. Needed to synthesize DNA bases and replication.
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| What does folate (B9) deficiency lead to? | show 🗑
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| What are sources of folate? | show 🗑
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| What is the significance of vitamin B12? | show 🗑
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| show | bacteria (slightly spoiled food)
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| What are the functions of B6? | show 🗑
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| show | methylates compounds for phosphatidylcholine, epinephrine, creatine, methylates DNA, drug metabolism
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| What is the importance of dTMP? | show 🗑
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| What are the neuroactive amines that vit B6 synthesizes? | show 🗑
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| What occurs with B6 deficiency? | show 🗑
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| What are the sources for iron? | show 🗑
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| show | Varies. Heme iron is more readily absorbed than non heme and Fe3+ is not readily absorbed (vit C can reduce to Fe2+). Inhibited by chelators that form insoluble complexes (oxalate, phytate, cellulose) and enhanced by soluble (vit C, AAs and pectins)
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| What is transferrin? | show 🗑
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| show | Fe3+ is converted to Fe2+ by vit C in the SI lumen then transported into the mucosa. Heme iron is also transported in and then hydrolyzed. Form Fe pool that transports Fe out to plasma-binds to transferrin in Fe3+ form or stored bound to Ferritin.
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| show | oxygen transport in RBC - hemoglobin & myoglobin. Redox active component of cytochromes (heme) and iron sulfur centres (non heme). iron metalloenzymes (non heme).
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| show | anemia. poor capacity for physical work and impaired cognitive development related to oxygen transport and metabolism of neurotransmitters.
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| What are the mechanisms of iron transport? | show 🗑
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| How does vitamin B6 play a role in anemia? | show 🗑
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| show | It is absorbed at 50% from luminal side and reduced in lumen. Transported in plasma by albumin and AAs to liver where it is incorporated into ceruloplasmin.
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| show | In the mucosal cells. High Cu absorption is impaired by Zn. induces thionein to bind to Cu (Cu-metallothionein).
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| What are the sources for Cu? | show 🗑
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| What affects Cu absorption? | show 🗑
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| What are the functions of Cu? | show 🗑
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| show | anemia (related to Fe transport), hemorrhaging (poor elastin in arteries - aortic rupture), depigmentation of skin (tyrosinase is a Cu enzyme required to make melanin)
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| show | it is the breakdown of RBC due to a shortage of vit E, selenium or cysteine. Weak due to lack of antioxidants, attacked by free oxygen radicals.
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| show | deficiency of folate or B12 affects DNA synthesis and produces immature, enlarged RBCs. RBC count is low.
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| What is microcytic anemia? | show 🗑
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| show | contains <200 known enzymes, involved in all pathways of metabolism, oxygen radical metabolism, zinc fingers & DNA binding, induce metallothionein in mucosa cells - binds Cu
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| show | normally complexed with peptides/proteins, nucleic acids. in red meats, organ meats, whole grains, leafy vegetables.
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| What are the symptoms of zinc deficiency? | show 🗑
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| show | loops of DNA-binding AAs which are held in the right position by the binding of a zinc ion. Zn binds to histidine and cysteine side chains
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| How is dietary protein metabolized? | show 🗑
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| What are the basic AAs? | show 🗑
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| show | Asparate (asparagine) and glutamate (glutamine)
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| What are the neutral AAs - aliphatic, straight? | show 🗑
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| What are the neutral AAs - aliphatic, branched? | show 🗑
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| show | serine, threonine - tyrosine is also hydroxylated but is an aromatic
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| show | cysteine, methionine
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| What are the neutral AAs - aromatics? | show 🗑
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| What is the neutral AAs - imino? | show 🗑
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| What are the essential amino acids? | show 🗑
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| Where do complete proteins come from? | show 🗑
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| show | Legumes (SAA), vegetables, cereal, grains (lysine).
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| show | young rats fed a diet deficient in protein (10% DM) over four weeks, rats weighed at beginning and end, growth is measured (weakness). total body weight gain/test protein consumed (weighed in grams)
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| show | hydrolyze protein to free AAs and quantify by HPLC. compare to composition of whole egg. limiting AA determines score. (limiting AA/amount of same AA in whole egg)x100. weakness - doesn't account for digestibility
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| show | NB = N intake - N loss (urine, feces). growth, NB positive; adults, ~0; old age, NB negative. Marginal protein quality reduces NB.
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| show | cancer, CVD (too much animal protein), aggravates kidney disease
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| What are the causes and symptoms of Kwashiorkor? | show 🗑
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| show | Diet deficient in energy and protein (balanced diet but not enough). complete loss of body fat. infants developing marasmus can shift to Kwash. due to stress. leads to immune depression.
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| What are the mechanisms of protein digestion in the stomach? | show 🗑
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| How is the pancreas involved in protein digestion? | show 🗑
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| What happens to the zymogens released by the pancreas? | show 🗑
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| What do the endopeptidases do in protein digestion? | show 🗑
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| Where does trypsin attack on a peptide chain? | show 🗑
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| show | aromatics, methionine, asparagine, histidine
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| show | on neutral aliphatics, polypeptides to oligopeptides and tripeptides.
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| show | It is an exopeptidase and it attacks at the N terminal. Carboxypeptidases attack at C terminal- A cleaves aromatic neutrals or neutral AAs, B cleaves basic AAs
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| What does active transport require? | show 🗑
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| show | to the liver through the portal vein where free AAs synthesized into liver enzymes, liver proteins, albumin (+other transport proteins), peptide hormones. BCAA go to systemic circ. excess AA degraded, NH3 to urea cycle, alpha keto acids to energy stores.
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| show | Processed in liver. Can go to kidneys for excretion, to parotid for salivary secretion or back to the rumen
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| show | Mechanical mixing, HCl secretion (protein denaturation of hydrogen and electrostatic bonds), enzymatic digestion
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| What is the role of the small intestine? | show 🗑
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| show | peptides and H+ are transported across the BBM. H+ is pumped out and N+ is pumped in across BBM at the same time that Na+ is pumped out and K+ is pumped in at BLM, to maintain gradient.
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| Why is non protein nitrogen used? | show 🗑
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| What are the three fates of nitrogen in the ruminant nitrogen cycle? | show 🗑
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