metabolism of ruminants Flashcards

1
Q

ruminal microbes:

A

bacteria, protozoa, fungi; change in diet results in change of microbes - change must be done gradually!

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2
Q

how does microbes settle in the rumen

A

enter via feed at young age, where they start to colonize and settle.

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3
Q

absorption in rumen

A

ruminal papillae, incr. surface area

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4
Q

VFA production from

A

from pyruvate

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5
Q

VFA’s

A

acetate, butyrate, propionate

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6
Q

VFA function

A

acidosis of rumen: 5.8-6.8pH

- absorption give energy for the host

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7
Q

what are the 4 steps of nitrogen metabolism

A
  1. protein degradation
  2. ammonia production
  3. protein synthesis
  4. ammonia synthesis
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8
Q

rumen Undigestible proteins and non-protein urea

A

improving digestion and to help lactation, reproduction, and weight gain

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9
Q

NH3 toxicosis - how to prevent

A

ammonia from non-protein N-sources

  • 0.5g/body mass max
  • if urea supplementation, step by step to avoid stress and liver disease
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10
Q

NH3 toxicosis

A

accumilation of NH3 in circulation can enter the brain as it can pass the blood brain barrier, and react with alpha keto glutarate, which disrupts the glucose metabolism of the brain (inhibit TCA, not enough AKG)

treatment: starch addition, 5% acetate to decr. the pH of rumen fluid (incr. absorption),

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11
Q

NPN consist of

A

urea + ammonium acetate

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12
Q

how is ammonia produced in rumen

A

degr. og NPN and ox. deamination of aa.

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13
Q

RUP

A

bypass proteins, valuble proteins protected by encapsulation (denat. by formic/tannic acid): animal or plant-based protein source that resists degradation in the cow’s rumen in order to pass into the lower gastrointestinal tract and provide essential amino acids to the cow.

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14
Q

ruminohepatic circulation

A

ammonium is transformed to urea in liver and tp back to rumen through ruminohepatic circulation, to produce NH3, or as NPU to salivary gland to go back to rumen.

important in N- low diets (urea is broken down and the cycle repeats)

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15
Q

v. portae damaged

A

ruminohepatic circulation: no ammonia detoxification!

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16
Q

connection btw. GNG and ketogenesis

A

high GNG-> OAC used up
LL+B-ox increases to make up for it, AcCoA is made and accumilated as it cannot enter TCA without OAC -> enter ketogenesis instead

17
Q

name the 3 ketone bodies

A

Acetoacetate, acetone, B-OH-butyrate

18
Q

how can severe ketosis be detected, proportion of ketone bodies in different bodily fluids

A

if in milk -> severe

milk 1: blood 5: urine 10

19
Q

antiketosis treatment

A

propionyl glycerol: induce glucose production and produce energy, GNG doesnt have to be intensive anymore -> OAC remains to be used in TCA

20
Q

why does ketolysis not occur in the liver

A
  • OAC is present in the liver as GNG occur, but ketolysis does not.
  • dont have CoA-transferase needed to break down Acetoacetate to acetoacetyl-CoA
21
Q

FA biohydrogenization in ru

A

unsaturated FA -> saturated FA

22
Q

biohydrogenization of linoleic acid

A

vaccenic acid and conjugated linoleic acid(antiinflamm, antiox), both make stearic acid

23
Q

vaccenic acid

A

Mammals convert it into rumenic acid, a conjugated linoleic acid, where it shows anticarcinogenic properties (lowers cholesterol etc.)

24
Q

FA synth in ru (vs. other spp.)

A

butyrate/acetate -> AcCoA -> cytoplasm -> FA synth

in other spp carbs would make AcCoA

25
Q

NADPH+H⁺ source in FA synth ru vs. other spp.

A

PPP is source in both, diff. enzymes depend on it:

  • ru: cytoplasmic isocitrate dehydrogenase
  • other: malate enzyme
26
Q

regulators of ketogenesis

A
  • ketoacidosis

+ KL, KG