Nutrition Exam 3

what happens to excess cholesterol

can be offloaded into HDL or synthesized by the liver

what stabilizes the Pi group on ATP

Mg+

1st reaction of betaoxidation produces how many ATP; 3rd

2;3

how many steps in betaoxidation

4

How many cycles does a FA go through (beta oxidation)

(n/2)-1

how much ATP does acetyl CoA produce

12

the brain can use

BOHB

when does ketosis occur

when feed intake decreases prior to parturition in overconditioned animals

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

response to glucagon

is proportional to how much triglyceride tehre is

why does blood pH drop

acetyl coa turning into ACAC and BOHB

who is susceptible and why

small ruminants-don’t have the bases to counteract the acids, cows do

ketosis treatment

give IV glucose which is difficult, give propylene glycol

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

obese animals have reduced

milk production

why can’t you use oral glucose

rumen bugs say nom

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

how to prevent pregnancy toxemia

high quality forage at 3rd trimester

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

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

how fast can the liver fail

24 hours

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

hormones and growth factors are

very specific, highly regulated and in limited amounts

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

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

aa are absorbed in

small intestine

ammonia absorbed

across rumen wall and goes to liver

what happens to the ammonia in the liver

is excreted as urea or turned into saliva

pepsinogen-activator, enzyme, site of activity, substrate, end products

HCl or pepsin; pepsin; stomach; most aa; peptides

trypsinogen-activator, enzyme, site of activity, substrate, end products

enteropeptidase or trypsin; trypsin; intestine; basic aa; smaller peptides and free aa

chymotrypsinogen-activator, enzyme, site of activity, substrate, end products

trypsin; chymotrypsin; intestine; peptides; smaller peptides

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

endopeptidases

trypsin, chymotyrpsin, elastase

exopeptidases

carboxypeptidase a and b

trypsin inhibitors mean

no active digestive protein enzymes

single aa transport uses

transport proteins and Na

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

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)

what does high blood urea nitrogen indicate

oversupply of protein or wasting disease

lactogenesis

start of lactation, IgG moves from blood to colostrum via FcRn (transport protein) that attaches to constant region of IgG

what is the threshold for successful passive immunity

greater than 10mg/100 ml

NEAA can be synthesized by

metabolites of the biochem pathways and an amine group

interconversion accomplished by

transferring an anime group from an aa to a carbon skeleton

amine group is transferred from aa to

a ketoacid

amine group from a ketoacid transferred to; by

aa; transaminase

alanine and a ketoglutarate

pyruvate and glutamate

aspartate and a ketoglutarate

oxaloacetate and glutamate

aa through microbial/enzymatic action

a ketoacid and NH3 (toxic in high amounts)

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

how are aa absorbed

active transport, carrier mediated; several mechanisms exists and are classified on the type of aa transported

IgG1 in colostrum are

absorbed intact through the intestinal wall by endocytosis

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

when is growth achieved

when the rate of photosynthesis is greater than the rate of degradation

efficiency of protein utilization

a mature, nonpregnant, not lactating, Maintenace animal=0

what type of cow uses protein more efficently

lactating dairy cow

macrominerals and ex

required in large amounts (%); sodium, potassium, calcium, magnesium, phosphorus, sulfur, chlorine

micro/trace minerals and ex

required in small amounts (ppm); iron, copper, cobalt, zinc, manganese, selenium, fluorine, molybdenum, chromium, silicon, iodine

valence states

some are needed, others aren’t

realtive amount/ concentratio requires doesn’t equate to

the importance of the element

minerals that are possibly required

aluminum, arsenic, cadmium, nickel, lead, vanadium, tin, boron, bromine, lithium

toxic minerals

arsenic, lead, mercury, fluorine, molybdenum, selenium

roles of minerals

signal transduction, secondary messenger, structural function, osmotic pressure, acid-base balance, enzyme function, muscle function

mineral-mineral interactions

Ca-P; Ca-Mg-Zn; Se-S; Fe-Cu (problem); Cu-S-Mo

mineral-vitamin relaitonships

Ca-P-Vit D; Se-Vit E (can replace 1/2 of the Se requirement)

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

ca function

structural component of bone, muscular contractile ability, nervous impulse transmission, secondary messenger function, critical role in blood coagulation cascade

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)

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

how does vit D affect calcium

decreases kidney excretion of ca and increases gut absorption of dietary ca and enhances bone resorption

what is vit d’s precursor

25-hydroxycholecaliferol

what is involved in Ca homeostasis

bone stores, parathyroid hormone, calcitonin, ca binding protein, vit d3, kidney, SI

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

ca is of critical importance in

adolescent and geriatric human nutrition

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

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

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

as anion salts increase

DMI decreases

where is excess ca excreted

urine and feces

high dietary ca is absorbed

through passive diffusion because active transport gets overwhelmed

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

P exists in what form and what is its source

compounds with O2; igneous rock deposits found in N and S Carolina and Florida

p deposits contain what and what must be done to it

fluorine, be extracted prior to P use as a food supplement

what percentage and forms is P found in the body

80%-skeleton and part of the hydroxyapatite

20%- soft tissues and as organic forms

what must be present for bone ossification to occur

ca and po4

prolonged deficiencies of either ca or po4 leads to

osteomalacia or rickets

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)

what is the absorption mech

similar to Ca and is regulated by parathyroid hormone, calcitonin, and vit D

P excretion

urine and small mounts of endogenous P excreted in the feces

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)

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)

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

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

Ca:P nutrition (3)

1. meet requirements
2. reach proper ratio= growing-1-2:1 or 2:1 Ca:P, dont want

wheat mill run

midds, cheap, high P, low Ca= problem if not balanced

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

serum levels of Mg

183mg/100ml

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 (-)

Mg absorption decreases with

increasing Ca, P, and K

Mg excretion

urine (1st) and fecesvia bile acids, pancreatic enzymes, saliva, gastric juices, intestinal secretions, and intestinal defoliation

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