The Most important metabolic troubles of Peripartuient Dairy cows and their prevention (ketosis)

Question 1

Difference between ketosis, ketogenesis and ketolysis

Answer 1

Ketosis- the incr of KB’s in the blood (the body is attempting to use KB’s for energy

Ketogenesis: in the production of KB’s form AcCoA that cannot enter the krebs cycle because the animal is using the OAA for GNG

Ketolysis: the breakdown of KB’s for E

Question 2

Glucose

Answer 2

Is a key substanec for lactating

Needed for milk fat and lactose synth

De Novo synth (GNG) requires NADPH+H+ produced by the PPP

Question 3

Reasoning behind the NEB associated with lactation

Answer 3

Diet does not meet E demands, in order to maintain the milk prod the mobilizes fat to cover- the endproduct is AcCoA! There is an xs of AcCoA because it cannot enter the krebs cycle because the OAA is being used for GNG!

This AcCoA is made into KB’s instead- will see an increased amount in th eblood, urine and milk!

When ketonuria occurs- there is E loss because the animals is not utilizing these KB’s for E

Question 4

What does ketosis lead to?

Answer 4

Metab acidosis!!. and then

Decr milk production and decr fertility

Question 5

What type of BC is ketosis more frequent in and why?

Answer 5

Obese (BCS of>3-3.5) because incr leptin!

Inhib of NPY

Appetite and DMI is decreased therefore NEB

Question 6

Repercussions of NEB (look at diagram) 4 main mechanisms

Answer 6

1. Decr glucose
2. decr insulin
3. Decr IGF 1
4. Decr IGF-BP-2

Question 7

1. Decr Glucose

Answer 7

Decr GnRH– Decr LH secretion– unsuccessful ovulation of dominant follicle– delayed conception therefore decreased fertility

This decr GnRH also leads to a decr of ovarian E

Question 8

2. decr insulin

Answer 8

Also aids in the decr of ovarian E

Question 9

3. Decr IGF-1

Answer 9

Affects the LH receptors- the granulosa cell and steroid hormone synth decr in response in order to increase the sensitivity to LH stimulation

Incr GH– incr lipolysis– incr NEFA leading to fatty liver and ketosis

Furthermore the GH stops follicle development

Question 10

4. IGF-BP-2 incr

Answer 10

This has a blocking effect on IGF-1

** sidenote: there is a decr P4 from somewhere that leads to early embryonic mortality**

Question 11

Diet to prevent NEB

Answer 11

Before partuition- decr DMI (due to obesity)

After partutition- max DMI

*note this is not the case for horses-this would cause weight loss, decr milk prod and decr fertility. They require an iseal BCS at time of partuition

Question 12

NB to include in the diet to prevent NEB (6)

Answer 12

TMR: should be homogenous! non-lignin cellulose and hemicelluolse, cracked grains in corn silage

Concentrates and cereal grains

Rumen protected glucose

Sugar beet pulp/molasses

By pass fat: full fat soya or hot pressed rapeseed cake

Heaptoprotective and glucoplastic substances

Question 13

How much cracked grains should you give in the NEB diet

Answer 13

optimum 70% / 4.5mm

Question 14

How much by-pass fat shpuld you give in NEB diet and what is the function?

Answer 14

max 6% of DM

to decr NEB, for normal bact fermentation, and for normal milk fat %

Question 15

What are the hepatoprotective and glucoplastic substances and their function

Answer 15

Propylene glycol and glycerol– incr glucose and insulin, decr NEFA’s

By pass mehtionine, choline, Niacin– decr lipolysis– decr NEFA’s

Question 16

What are the methods of treating ketone bodies in the milk and urine (i.e E supplementation via drenching) (7)

Answer 16

1. Ca proprionate- decr hypocalcaemia
2. Propyelene glycol
3. Cholin: methyl donot, prevents fatty liver
4. yeast: incr DMI and DCF, decr acidosis
5. MgSO4: maintain Ca:Mg ratio
6. KCl- for electrolytes
7. Retard buffers- provide electrolytes

Overall: decr nutritional disorders and incr milk yield