Metabolism and Negative Energy Balance Flashcards
What molecules are metabolised during severe negative energy balance?
Triglycerides, non-esterified fatty acids (NEFA) from adipose tissue and ketone bodies from liver
What are triglycerides converted into?
Very low density lipoproteins in liver but are only available to tissues with active lipoprotein lipase in the capillary bed
When are levels of NEFA very high in plasma?
During times of starvation, stress and high metabolic load
How are ketones metabolised?
Converted to ketone bodies - B-OH-butyrate and acetoacetate which is used to provide energy by supplying acetyl-CoA into the TCA cycle
Acetone is mostly lost in expired air but a small amount is converted to glucose
What is the cause of ketosis in dairy cows?
Hyperketonaemia resulting from severe negative energy balance and hypoglycaemia
What increases the risk of ketosis?
Parity and age of cow (multiparous cows most as risk)
BCS >6 out of 8
Proximity to parturition (7 weeks prior to calving but up to 14 weeks)
What are some of the factors that cause ketosis?
Decreased energy intake (CP, ME, height or mass of pasture is poor, poor supplementation)
Limited capacity to ingest and metabolism large amount of feed in early lactation (rumen and liver not adapted)
What are the 2 types of ketosis?
Wasting form has a gradual onset
Nervous form has a rapid onset
What occurs during wasting ketosis?
Decline in appetite over 2-5 days
Lack of interest in cereal grain-based supplement but may still eat forage
Elevated B-OH-butyrate in blood
Elevated levels in ketones in urine (ketouria)
Unsteady stance and gait with head low to the ground
Rapid reduction in milk yield
Ketone smell on breath
Disinclined to move
What level does B-OH-butyrate have to be in the blood to cause ketosis?
>1.2mM = ketotic >3mM = clinical disease
What occurs during nervous ketosis?
Incessant tongue movements and unusual licking of the skin
Aimless wandering, walking in circles and bellowing for no apparent reason
How do we treat ketosis?
Glucose replacement therapy (IV of dextrose short acting, drench with propylene glycol long acting, isolate and feed high quality roughage, treat for 2-4 days, reintroduce cereal grain-based supplements) Hormonal therapy (administer a long-acting corticosteroid with glucose replacement therapy to avoid excessive muscle catabolism) Prompt treatment will usually resolve the hypoglycaemia and hyperketonaemia but production for that lactation will be greatly reduced or lost
How do we prevent ketosis?
Keep cow in BCS of 5-5.5 at calving time
Feed cereal grain supplements in the transition period leading up to calving
Identify at risk cows and drench with propylene glycol of glycerine at calving
Offer high quality pasture after calving
Feed cereal grain-based supplements during milking
What is pregnancy toxaemia in ewes a consequence of?
Hypoglycaemia
What factors predispose ewes to pregnancy toxaemia?
Inadequate pasture quality/quantity In late pregnancy Twin or triplet ewes Undersized (maiden ewe) Poor health (teeth and parasites) too thin BCS under 2.5 or too fat BCS above 4 in late pregnancy