Hormones and energy metabolism Flashcards

1
Q

How do hormones respond to a negative energy balance?

A
  • They aim to lower the metabolic rate so the resources last longer
  • Insulin decreases, thyroxine decreases, glucagon increase, GH increases, cortisol increases, catecholamines increase
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2
Q

List some diseases that involve an energy metabolism disorder

A
  • Hepatic lipidosis
  • Secondary ketosis
  • Feline hepatic lipidosis
  • Equine hyperlipidaemia
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3
Q

Discuss the 3 VFAs produced by fermentation in ruminants

A

1) Acetate= Ketogenic
2) Propionate= Glucogenic
3) Butyrate = Ketogenic

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4
Q

How is propionate used to make glucose?

A

Proprionic acid is converted to oxaloacetate

Oxaloacetate is converted into glucose via gluconeogenesis

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5
Q

What happens to acetate and butyrate?

A

They cannot be converted into glucose

instead they are converted to acetyl CoA and fed into the kerbs cycle to produce ATP

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6
Q

What is the role of HSL?

A

Mobilses fatty acids and glycerol from TGs

These fatty acids are used to produce ATP via beta oxidation within mitochondria

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7
Q

What inhibits HSL?

A

Insulin

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8
Q

What stimulates HSL?

A

A state of negative energy

  • Low insulin/ high glucagon
  • Stress (catecholamines)
  • GH
  • Cortisol
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9
Q

Discuss hepatic lipidosis in dairy cattle

A
Presents in periparturient dairy cows
-Lower milk production
-Loss of appetite
-Mild depression
Physical exam should show: Decreased rumen activity and ketosis
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10
Q

What factors increase the risk of dairy cattle developing fatty liver?

A
  • Obesity: animals with a higher BCS have more fat to mobilise hence more fat goes to the liver.
  • Older cows
  • Insulin resistance
  • Poor nutrition: lack of calories at start of lactation
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11
Q

Why is insulin resistance a problem in dairy cows with fatty liver?

A
  • Obesity induced

- Pregnancy/ parturition increases stress (high cortisol)

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12
Q

What are the periparturient events that can contribute to fatty liver in dairy cows?

A
  • Neg energy balance in late pregnancy: fetus increases energy demand and the cow doesn’t eat as much at parturition
  • Shift in blood hormones at parturition: insulin, IGF-1 and thyroid hormones decrease. GH, prolactin and cortisol increase
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13
Q

What is the main driving force behind hepatic lipidosis?

A

-Excessive mobilisation of fatty acids: overwhelms capacity of the liver to use fatty acids for energy production-> build up of TGs in liver-> lippid vacuoles build up in cytoplasm of hepatocytes and disrupt normal function

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14
Q

What must Acetyl CoA bind with to enter TCA cycle?

A

Oxaloacetate

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15
Q

What impact does silage conditions have on fermentation?

A

-The wetter the conditions the more likely butyric acid will be formed

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16
Q

What is the link between oxaloacetate and anorexia?

A

When the cow isn’t eating as much propionate decreases in concentration. As propionate can convert to oxaloacetate there is also reduced oxaloacetate. This makes a bottle neck in the cycle as acetate and butyrate convert to Acetyl CoA. BUT acetyl CoA cannot enter TCA cycle without oxaloacetate.

17
Q

Discuss the different problems that occur due to anorexia

A
  • Lowered propionate so lowered oxaloacetate
  • Bottle neck leading to excess acetyl CoA which forms ketone bodies
  • Excess fatty acids which re stored as TGs in liver. Lipid vacuoles in cytoplasm of liver cells affect function.
18
Q

What are the clinical affects of ketosis?

A
  • Fruity smell to breath
  • Ketoacidosis
  • Lowers blood pH and affects enzyme reactions
  • CNS depression
  • Lowers appetite= vicious cycle
19
Q

What is the TG overflow system?

A

TG’s are aloe to exit the liver as VLDLs

-Cows aren’t good at it but horses are

20
Q

What is the main risk in cats of developing hepatic lipidosis

A

Obesity and negative energy balance

-You need to get nutrition into them to try and stop the cycle

21
Q

Describe hyperlipidaemia in horses

A
  • Often follows on from choke or laminitis-> go off their feed due to pain
  • Very good at repackaging TGs into VLDLs.
  • Results in organ dysfunction due to systemic hyperlipidaemia