metabolism of ruminants Flashcards
ruminal microbes:
bacteria, protozoa, fungi; change in diet results in change of microbes - change must be done gradually!
how does microbes settle in the rumen
enter via feed at young age, where they start to colonize and settle.
absorption in rumen
ruminal papillae, incr. surface area
VFA production from
from pyruvate
VFA’s
acetate, butyrate, propionate
VFA function
acidosis of rumen: 5.8-6.8pH
- absorption give energy for the host
what are the 4 steps of nitrogen metabolism
- protein degradation
- ammonia production
- protein synthesis
- ammonia synthesis
rumen Undigestible proteins and non-protein urea
improving digestion and to help lactation, reproduction, and weight gain
NH3 toxicosis - how to prevent
ammonia from non-protein N-sources
- 0.5g/body mass max
- if urea supplementation, step by step to avoid stress and liver disease
NH3 toxicosis
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),
NPN consist of
urea + ammonium acetate
how is ammonia produced in rumen
degr. og NPN and ox. deamination of aa.
RUP
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.
ruminohepatic circulation
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)
v. portae damaged
ruminohepatic circulation: no ammonia detoxification!
connection btw. GNG and ketogenesis
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
name the 3 ketone bodies
Acetoacetate, acetone, B-OH-butyrate
how can severe ketosis be detected, proportion of ketone bodies in different bodily fluids
if in milk -> severe
milk 1: blood 5: urine 10
antiketosis treatment
propionyl glycerol: induce glucose production and produce energy, GNG doesnt have to be intensive anymore -> OAC remains to be used in TCA
why does ketolysis not occur in the liver
- 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
FA biohydrogenization in ru
unsaturated FA -> saturated FA
biohydrogenization of linoleic acid
vaccenic acid and conjugated linoleic acid(antiinflamm, antiox), both make stearic acid
vaccenic acid
Mammals convert it into rumenic acid, a conjugated linoleic acid, where it shows anticarcinogenic properties (lowers cholesterol etc.)
FA synth in ru (vs. other spp.)
butyrate/acetate -> AcCoA -> cytoplasm -> FA synth
in other spp carbs would make AcCoA
NADPH+H⁺ source in FA synth ru vs. other spp.
PPP is source in both, diff. enzymes depend on it:
- ru: cytoplasmic isocitrate dehydrogenase
- other: malate enzyme
regulators of ketogenesis
- ketoacidosis
+ KL, KG
