Rumen Metabolism Flashcards

(41 cards)

1
Q

what is the major type of rumen microflora

A

bacteria

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2
Q

what do microbes use as substrates

A

carbon and nitrogen

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3
Q

what kind of environment do microbes need

A

acidic (pH 6.6-6.8)
anaerobic
reduced (minimal reducing agents)

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4
Q

are microbes efficient at using fat

A

no - will need to hydrogenate NEFAs/unsaturated FA before incorporating into cell membranes to prevent kinks

diets should be 3-5% fat

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5
Q

what do microbes produce

A

VFAs and protein

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6
Q

what are the main 3 VFAs produced by microbes

A

acetate > propionate > butyrate

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7
Q

how many carbons are each of the VFAs

A

acetate: 2C
propionate: 3C
butyrate: 4C

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8
Q

what component of the plant cell wall is not able to be broken down by microbes

A

lignin

becomes more abundant in plants as they get older/dried

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9
Q

what are the steps of carbohydrate fermentation

A
  1. microbes secrete enzymes that break down polysaccharides into monosaccharides (extracellular)
  2. monosaccharides enter glycolysis to form pyruvate
  3. pyruvate + ATP + reducing equivalents [H] forms VFAs + ATP + methane + CO2
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10
Q

what is the function of reducing equivalents

A

carry unionized hydrogens (NADH, NADPH, FADH, etc) that are required for substrate level phosphorylation

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11
Q

what is substrate level phosphorylation

A

anaerobic phosphorylation in the rumen

produces 2 acetates + 2 CO2 + 8 [H] + 4 ATP

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12
Q

what happens to the 8 reducing equivalents produced by substrate level phosphorylation

A

they get used by methanogens to produce methane

need to get used in order to maintain reduced environment

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13
Q

how are VFAs absorbed across the rumen

A

binding free ionized H+

it does this to act as a buffer - picking up free H+ prevents rumen acidosis

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14
Q

why does the rumen need to be kept in a reduced (low [H]) environment

A

reduced environment favors ATP and VFA production because ATP/VFA production also generates [H], so if the rumen was high in [H] then ATP/VFA production would slow

need methanogens to maintain the reduced environment so that VFAs can get produced

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15
Q

acetate production

A

hexose + ADP –> 2 acetate + 2CO2 + 8 [H] + 4 ATP

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16
Q

propionate production (from succinate)

A

most common pathway because it generates more energy

hexose + ADP + 4 [H] –> 2 propionate + 4 ATP

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17
Q

propionate production (from lactate)

A

less common pathway because it generates less energy

hexose + ADP + [H] –> 2 propionate + 2 ATP

18
Q

butyrate production

A

hexose + ADP –> butyrate + 2 CO2 + 4 [H] + 3 ATP

19
Q

can there ever be more propionate in the rumen than acetate

A

NO because propionate production requires [H]

relies on acetate and butyrate production to produce [H]

20
Q

can there ever be more propionate in the rumen than butyrate

A

yes because butyrate production is used less than acetate since it yields less ATP and [H], so the [H] produced during acetate production is enough to facilitate propionate production

21
Q

what are the gases produced by the microbes

A
  1. CO2 - majority
  2. CH4 - produced by methanogens from [H]
  3. H2 - minimal (reducing agent, gets rapidly used)
  4. H+ - released from VFAs and lactic acid; will inhibit methanogens
22
Q

can methanogens work in too acidic of an environment

A

no - get inhibited by H+

23
Q

what does the rumen produce on a forage (grazing) diet

A
  • significantly more acetate than propionate
  • high hexose
  • high methane
  • 75% VFAs
24
Q

what does the rumen produce on a grain (feedlot) diet

A
  • almost equal amounts of acetate and propionate
  • low hexose
  • low methane
  • 85% VFAs
25
what do ionophores do
stalls gram positive rumen bacteria by "poking holes" in their membranes --> requires them to devote more energy toward fixing holes than producing VFAs --> allows starch digesters (gram neg) to grow --> releases more [H] --> promotes propionate production
26
how does starch affect the diet
starch = high grain diet promotes lactic acid production which increases free H+ ions --> inhibits methanogens
27
how do unsaturated FA affect the diet
toxic to microbes - requires hydrogenation before it can be used --> uses up [H] --> methanogens unable to use [H] --> decreases methane production
28
what are the steps of protein digestion in the rumen
proteins --> AAs amino acids get catabolized into ammonia and carbon skeletons components are able to get used to reform whatever amino acids the animal needs
29
what is nitrogen recycling in the rumen
ammonia travels to the liver to get converted to urea which can get recycled during rumination (in saliva) and reused for its nitrogen
30
is the rumen well adapted for high nitrogen conditions
yes, there are many ways the rumen can use excess N
31
what hydrolyzes triglycerides in the rumen
microbial lipases
32
are cows hyper or hypoglycemic normally
hypoglycemic --> requires mechanisms to converse glucose in the body
33
what mechanisms are there to converse glucose
1. acetate is the primary energy source (not glucose) 2. propionate is used for gluconeogenesis 3. liver is dedicated primarily to gluconeogenesis (compartmentalization) 4. butyrate is oxidized by rumen wall to form ketones or used for FA synthesis
34
gluconeogenesis in ruminants
occurs in the liver substrates: propionate and glucogenic AA
35
FA synthesis in ruminants
occurs in adipose tissue (NOT liver) - produces lactate --> high lactate in liver - lipid transport is primarily HDL substrate: acetate
36
what is compartmentalization
the liver does NOT have the enzymes needed for FA synthesis (citrate lyase + malic enzyme) allows liver to be dedicated to gluconeogenesis
37
what does starvation in ruminants refer to
lack of glucose; can be caused by: 1. lack of propionate 2. lack of glucogenic AAs 3. liver dysfunction
38
what is the process of developing ketosis
starvation --> increased FA mobilization --> partial FA metabolism (lack of glucose prevents complete metabolism) --> produces ketones instead --> ketosis
39
primary vs secondary ketosis
primary: occurs due to lack of food (ex. did not get fed) secondary: occurs due to underlying primary disease that prevents the animal from being able to eat (ex. lameness)
40
diagnosing ketosis
hypoglycemia + elevated ketones
41
how to prevent ketosis
high grain/starch diet administer glucose precursors consistent feeding