Disorders of Lipid Metabolism Flashcards

1
Q

How are triglycerides transported?

A

Via lipoproteins

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2
Q

What are the two major lipoproteins?

A
  • Chylomicrons (large and synthesised by enterocytes)
  • Very low density lipoproteins (second largest and rich in triglyceride, synthesised by the liver)
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3
Q

Name four major points about chylomicrons

A
  1. largest lipoprotein and the richest in triglyceride
  2. synthesised by enterocytes
  3. secreted into lymph
  4. transport lipid to tissues
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4
Q

Why cant TG’s be transported via aqueous media

A

TG’s are hydrophobic

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5
Q

What is lipolysis?

A

TG is broken down into glycerol and three NEFA’s

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6
Q

What is the name of the enzyme that transfers TG via VLDL to tissues?

A

lipoprotein lipase

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7
Q

What enzyme removes lipoprotein remnants from the liver?

A

hepatic lipase

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8
Q

Why does Insulin inhibit ketogenesis?

A

Insulin increases the uptake of fatty acids
fewer fatty acids = less ketogenesis

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9
Q

What are the four main disorders of lipid metabolism?

A
  • Hyperlipaemia
  • Hepatic lipidosis
  • Pregnancy ketosis
  • Acetonaemia
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10
Q

What is the definition of hyperlipaemia in equids?

A
  • Plasma TG is higher than 5mmol/ L
  • causes an individual to become sick (low appetite)

opaque plasma

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11
Q

What is the definition of hypertriglyceridaemia in equids?

A
  • Plasma triglyceride will be higher than normal
  • not sick or inappetent
  • minimal plasma opacity
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12
Q

What is the definition of severe hypertriglyceridaemia?

A
  • Very high plasma TG
  • subject may be sick due to another process but not hypertriglyceridaemia
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13
Q

What are the clinical signs of ketosis in cattle

A
  • Increase B-hydroxybuturate
  • occurs in high yielding dairy cows
  • occurs either in late pregannacy or early lactation
  • any cow that is overconditioned (they become insulin resistant)
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14
Q

What is type I ketosis in cattle?

A
  • Occurs at peak lactation
  • When glucose availability is low due to milk
  • low glucose oxidation
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15
Q

What is type II ketosis?

A
  • Occurs immediately post-partum
  • Cows are potentially insulin resistant
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16
Q

What are the clinical features of pregnancy ketosis in sheep and goats?

similiar to type I ketosis

A
  • Usually occurs in heavily pregnant does and ewes
  • Older ewes
  • May occur if there are multiple foetuses
  • usually triggered by feed restrcition
  • diseases in late pregnancy
17
Q

What are the characteristic features of hepatic lipidosis

A
  • common cause of liver disease in cats
  • especially affects overweight cats
18
Q

What is the structure of a lipoprotein?

A
  • Outer phospholipid shell
  • Apolipoproteins within the shell
19
Q

What pathway is inhibited by insulin?

A

Lipolysis

20
Q

What pathway is stimulated by insulin?

A

Lipogenesis

21
Q

What stimulates lipolysis?

A
  • Catecholamines
  • GH
  • Cortisol
  • TNF alpha
22
Q

What enzyme helps transfer TG to tissues?

A

Lipoprotein Lipase

stimulated by insulin and heparin

Inhibited by TNF alpha

23
Q

What are the clinical features of hyperlipaemia in equids?

A

They become insulin resistant

24
Q

What is primary hyperlipaemia?

A

Occurs without pre-existing disease

Negative energy balance?

25
Q

What is secondary hyperlipaemia?

A

occurs following a separate pre-existing disease condition

Negative energy balance

26
Q

What are the characteristic clinical features of ketosis in cattle?

A
  • B-hydroxybutyrate is above 1.2 mmol / L
  • High yielding dairy cows
  • Late pregnancy/ early lactation
  • Overconditioning- insulin resistant
27
Q

What are the characteristic features of hepatic lipidosis in cats?

A
  • Most common cause of liver disease in cats
  • especially affects overweight cats
  • hepatic TG accumulation is prevalent,, hepatic ketosis also occurs and may cause a characteristic smell
28
Q

What are the characteristic features of seasonal pasture myopathy?

A
  • Acute non-exertional rhabdomyolysis syndrome
  • Affects healthy, grazing horses, ponies, donkeys, zebra
  • Largely fatal
  • Seasonal
29
Q

What is the structure of triglycerides?

A

Glycerol + Fatty acids = esterification
* Free fatty acids = non-esterified

30
Q

TG’s have to be packaged within…?

A

Lipoproteins

31
Q

What is the basic pathway of Lipid metabolism?

A
  • TF in fat stores is then converted into NEFA and glycerol in the plasma
  • In the liver they are re-converted into TG, ATP and ketones
  • TG is then incorporated into VLDL
  • Tissues extract NEFA from the VLDL
  • remnants return to the liver
32
Q

What doesa lack of glucose promote?

A
  • NEFA enters the mitochondria
  • ketone synthesis occurs
  • ketone is then used as a peripheral energy source, sparing glucose for mammary glands and foetus
33
Q

What enzyme removes TG remnants from the plasma?

A

Hepatic lipase

inhibited by TNF alpha

34
Q

What enzyme transfers TG within VLDL to tissues?

A

Lipoprotein lipase

Inhibited by TNF alpha

35
Q

How does insulin inhibit ketogenesis?

A
  • If glucose is broken down the products of glucose oxidation block CPT1 activity and NEFA entry into the mitochondria
  • therefore no ketogenesis occurs
  • ketones are usally used as aperipheral energy source
36
Q
A
37
Q

What is the pathophysiology of seasonal pasture myopathy?

A
  • hypoglycin A from sycamore seeds and seedlings
  • essentially blocks CPT1 (entry of NEFAS)
  • blocks enzymes involved in B-oxidation
  • MADD
  • No ATP production via beta-oxidation