Nutrition Exam 3

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107 Terms

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what happens to excess cholesterol
can be offloaded into HDL or synthesized by the liver
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what stabilizes the Pi group on ATP
Mg+
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1st reaction of betaoxidation produces how many ATP; 3rd
2;3
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how many steps in betaoxidation
4
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How many cycles does a FA go through (beta oxidation)
(n/2)-1
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how much ATP does acetyl CoA produce
12
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the brain can use
BOHB
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when does ketosis occur
when feed intake decreases prior to parturition in overconditioned animals
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what happens in ketosis
massive mobilization of fat stores dumping; large quantities of NEFAs into the blood, FA undergo betaoxidation and the acetyl coa that is produced enters the kreb’s cycle; large amounts of acetyl coa are taken up by the liver and turned into ketone bodies; ketone bodies are strong acids leading to systemic acidosis
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response to glucagon
is proportional to how much triglyceride tehre is
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why does blood pH drop
acetyl coa turning into ACAC and BOHB
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who is susceptible and why
small ruminants-don’t have the bases to counteract the acids, cows do
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ketosis treatment
give IV glucose which is difficult, give propylene glycol
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why does propylene glycol work and when and how many doses
at succinyl CoA stage of kreb’s cycle, increases OAA to work off of; 2-3 times a day for 7 days
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obese animals have reduced
milk production
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why can’t you use oral glucose
rumen bugs say nom
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pregnancy toxemia occurs in and why
small ruminants with 2-3 fetuses; fetuses press on rumen and restrict the amount of food they can eat, animals may not live to birth/much long after
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how to prevent pregnancy toxemia
high quality forage at 3rd trimester
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what is fatty liver disease
huge fat stores, low feed intake prior to birth, large amounts of fas are hydrolyzed from adipose and dumped into blood as NEFAs, fat is taken up by liver disrupts the integrity of the liver=liver failure
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obese animal to birth to
lower DMI to low blood glucose to increased glucagon to hormone sensitive lipase to NEFAs in blood to liver taking and storing triglycerides
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how fast can the liver fail
24 hours
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biological function of protein (8)

1. tissue proteins
2. keratin
3. blood proteins
4. enzymes
5. hormones and growth factors
6. immunologic function
7. special function (purine/pyrimidine synthesis, histamine system, pigments, vitamin synthesis
8. oxidative metabolism- uses as an energy source
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hormones and growth factors are
very specific, highly regulated and in limited amounts
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why don’t we use protein as oxidative metabolism
protein is very expensive and metabolically inefficient, creates a large load on the kidney and liver and can result in organ failure, excesses of some aa can affect uptake of other aa
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how is protein digested in monogastric and lower GI of ruminants

1. denaturation occurs due to acidic conditions in stomach (3 & 4 structure is lost and opens the protein to further degradation)
2. pespin indiscriminately hydrolyzes peptide bonds
3. peptides go to duodenum and are subjected to exoendopeptidases secreted by the pancreas and small intestine where they are hydrolyzed to small di and tripeptides and free aa
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aa are absorbed in
small intestine
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ammonia absorbed
across rumen wall and goes to liver
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what happens to the ammonia in the liver
is excreted as urea or turned into saliva
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pepsinogen-activator, enzyme, site of activity, substrate, end products
HCl or pepsin; pepsin; stomach; most aa; peptides
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trypsinogen-activator, enzyme, site of activity, substrate, end products
enteropeptidase or trypsin; trypsin; intestine; basic aa; smaller peptides and free aa
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chymotrypsinogen-activator, enzyme, site of activity, substrate, end products
trypsin; chymotrypsin; intestine; peptides; smaller peptides
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procaboxygepeptidases-activator, enzyme, site of activity, substrate, end products
trypsin, carboxypeptidase; intestines; A-c terminal neutral aa, free aa; B-c terminal basic aa, free aa; aminopeptides-n terminal aa, free aa
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endopeptidases
trypsin, chymotyrpsin, elastase
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exopeptidases
carboxypeptidase a and b
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trypsin inhibitors mean
no active digestive protein enzymes
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single aa transport uses
transport proteins and Na
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what does Na do
binds to transport protein, changes conformation, binds aa, aa brought into IMC, NA pumped out of IMC via sodium potassium pump; requires energy
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transport of dipeptides

1. peptides are transported into intestinal cell with H+ using PEPT1
2. the H+ are transported back into the intestinal lumen and Na is pumped into the cell
3. sodium potassium pump moves Na out of cell in exchange for K (requires energy)
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what does high blood urea nitrogen indicate
oversupply of protein or wasting disease
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lactogenesis
start of lactation, IgG moves from blood to colostrum via FcRn (transport protein) that attaches to constant region of IgG
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what is the threshold for successful passive immunity
greater than 10mg/100 ml
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NEAA can be synthesized by
metabolites of the biochem pathways and an amine group
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interconversion accomplished by
transferring an anime group from an aa to a carbon skeleton
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amine group is transferred from aa to
a ketoacid
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amine group from a ketoacid transferred to; by
aa; transaminase
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alanine and a ketoglutarate
pyruvate and glutamate
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aspartate and a ketoglutarate
oxaloacetate and glutamate
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aa through microbial/enzymatic action
a ketoacid and NH3 (toxic in high amounts)
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what happens to ammonia in transamination

1. can be used in the synthesis of NEAA
2. excess ammonia absorbed into blood and is taken up by the liver where it is converted to urea and excreted by the kidney in urine
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how are aa absorbed
active transport, carrier mediated; several mechanisms exists and are classified on the type of aa transported
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IgG1 in colostrum are
absorbed intact through the intestinal wall by endocytosis
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gut closure
occurs 24 hours post partum after which colostral ab are not absorbed because it takes about 24 hours for proteolytic enzymes to kick in
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when is growth achieved
when the rate of photosynthesis is greater than the rate of degradation
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efficiency of protein utilization
a mature, nonpregnant, not lactating, Maintenace animal=0
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what type of cow uses protein more efficently
lactating dairy cow
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macrominerals and ex
required in large amounts (%); sodium, potassium, calcium, magnesium, phosphorus, sulfur, chlorine
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micro/trace minerals and ex
required in small amounts (ppm); iron, copper, cobalt, zinc, manganese, selenium, fluorine, molybdenum, chromium, silicon, iodine
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valence states
some are needed, others aren’t
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realtive amount/ concentratio requires doesn’t equate to
the importance of the element
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minerals that are possibly required
aluminum, arsenic, cadmium, nickel, lead, vanadium, tin, boron, bromine, lithium
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toxic minerals
arsenic, lead, mercury, fluorine, molybdenum, selenium
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roles of minerals
signal transduction, secondary messenger, structural function, osmotic pressure, acid-base balance, enzyme function, muscle function
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mineral-mineral interactions
Ca-P; Ca-Mg-Zn; Se-S; Fe-Cu (problem); Cu-S-Mo
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mineral-vitamin relaitonships
Ca-P-Vit D; Se-Vit E (can replace 1/2 of the Se requirement)
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chelated mineral
a mineral bound to an organic compound, either naturally occurring or can be commercially synthesized; can enhance or reduce bioavailability of bound mineral
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ca function
structural component of bone, muscular contractile ability, nervous impulse transmission, secondary messenger function, critical role in blood coagulation cascade
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ca tissue stores
99% bones and teeth, 1% extracellular fluid (blood levels are about 10mg/100ml and half is in ionized form, rest is complexed with organic and inorganic acids)
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ca absorption
variable depending on ca status, age, and presence of chelating agents; is absorbed in duodenum by active transport initiated by the parathyroid hormone upregulating ca transport in the IMC and increased formation of vit D
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how does vit D affect calcium
decreases kidney excretion of ca and increases gut absorption of dietary ca and enhances bone resorption
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what is vit d’s precursor
25-hydroxycholecaliferol
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what is involved in Ca homeostasis
bone stores, parathyroid hormone, calcitonin, ca binding protein, vit d3, kidney, SI
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ca deficiency
involves phosphorous and vit d3 levels-deficiency in any of the 3= weak bones; osteoporosis (reduction of bone mass with tendency to fracture) is also related to a decrease in estrogen secretion
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ca is of critical importance in
adolescent and geriatric human nutrition
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laying hens and Ca
require 3.5-4% ca in diet (eggshell formation requires 30% of ca intake)(lethal to ruminants), lower levels of dietary ca result in bone fractures=cage layer fatigue
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dairy cattle and ca
milk fever or parturient paresis-problem in peri-parturient dairy cows, affecting 5-10% of dairy cows. high colostrum production with high ca concentrations represents a significant draw on ca pool; resorption of ca from bones takes a minute to kick in resulting in hypocalcemia

listless/sluggish behavior, subnormal body temperature with cool extremities, general ataxia deteriorating into sternal recumbency, coma, and death (muscle contraction stops) without tx

tx-iv calcium gluconate solution, often induces muscle spasms, expelling feces and attempts to stand within minutes
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Ca deficiency prevention

1. high ca diet in dry period 60 days before calving-made things worse
2. low ca diets in dry period 60 days before calving-made things better
3. administering vit d-never know when cow will calves too many days in a row=death
4. dietary cation/anion balance-want slight systemic acidosis just prior to parturition; want anions>cation to lower pH which increases ca and bone resorption
5. low potassium diet- lower P in dry period, reduced milk fever
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as anion salts increase
DMI decreases
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where is excess ca excreted
urine and feces
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high dietary ca is absorbed
through passive diffusion because active transport gets overwhelmed
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chronic ca toxicity leads to
osteopetrosis, excessive ca deposition in the bone and soft tissues leading to muscle and urinary calculi, interference with Zn, Mg, P, Fe, I, Mn, and Cu utlilzation
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P exists in what form and what is its source
compounds with O2; igneous rock deposits found in N and S Carolina and Florida
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p deposits contain what and what must be done to it
fluorine, be extracted prior to P use as a food supplement
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what percentage and forms is P found in the body
80%-skeleton and part of the hydroxyapatite

20%- soft tissues and as organic forms
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what must be present for bone ossification to occur
ca and po4
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prolonged deficiencies of either ca or po4 leads to
osteomalacia or rickets
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how is P absorbed
in the duodenum; is dependent on: source (plant v animal phytic acid), Ca:P ratio, intestinal pH, levels of other minerals, P status of the body (greater need= better absorption)
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what is the absorption mech
similar to Ca and is regulated by parathyroid hormone, calcitonin, and vit D
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P excretion
urine and small mounts of endogenous P excreted in the feces
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P biological role
major component of bone, essential component of organic compounds involved in almost every aspect of tissue metabolism (muscle, energy, fat, carbs, aa, nerves)
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P deficiencies and imbalance
fragile/weak bones, weakness, weight loss, emaciation, decreased feed intake, milk production, and reproductive efficiency, chewing wood, bones, and other objects (pika)
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How to assess P levels
blood plasma-normal=4.5-6mg/100m; deficient-2-3mg/100ml; values below 4.5 mg/100ml in cattle and sheep indicate deficiency, usually inversely related to plasma Ca levels
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P toxicosis
urinary calculi in the kidney or bladder resulting in a burst bladder, increase in the blood P which results in lower blood ca causing the parathyroid to increase serum Ca by resorption of the bones to increase renal P excretion-due to excess P or insufficient Ca
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Ca:P nutrition (3)

1. meet requirements
2. reach proper ratio= growing-1-2:1 or 2:1 Ca:P, dont want
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wheat mill run
midds, cheap, high P, low Ca= problem if not balanced
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where is Mg in the body
50-60% in the bones (of this 30% is associated with bone phosphorous and the rets is absorbed on the surface of the bone mineral structure) 40-50% associated with the soft tissues and concentrated in the cells; liver and skeletal muscles have the highest concentration of Mg, RBC have a significant amount too
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serum levels of Mg
183mg/100ml
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Mg absorption
mech unknown; ileum in monogastrics and reticulorumen in ruminants; mg absorption declines with increasing dietary levels and is altered by Mg status, availability of carb source (+), and presence of organic acids in feeds (-)
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Mg absorption decreases with
increasing Ca, P, and K
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Mg excretion
urine (1st) and fecesvia bile acids, pancreatic enzymes, saliva, gastric juices, intestinal secretions, and intestinal defoliation
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mg biological role
component of bone and needed for bone development, activator of enzyme systems-protein synthesis (binding of mRNA to ribosome), nucleic acid, fat, and coenzyme synthesis and neuromuscular transmission