Macronutrients Part 2: Lipids Flashcards

1
Q
# Define macronutrients. 
They are required in?
A

Macronutrients are vitamins, minerals, amino acids, and fatty acids.
Required in large amounts.

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2
Q

Define a triglyceride.

A

A triglyceride is fatty acids linked together to a glycerol backbone.

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3
Q

List the different types of lipids.

A
  1. Fats
  2. Cholesterol
  3. Phospholipids
  4. Waxes
  5. Steroids
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4
Q

Are all fats lipids?
Are all lipids fats?

A

All fats are lipids, but not all lipids are fats.

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5
Q

What is the most concentrated source of energy?

A

Lipids

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6
Q

In what situation can lipids be helpful (nutrition)?

A

Lipids could help animals with low appetite meet their nutritional requirements.

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7
Q

Are lipids polar or non-polar? Therefore they are?

A

Non-polar and are therefore water insoluble.

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8
Q

What fatty acids are not attached to glycerol?

A

Free fatty acids or non-esterefied fatty acids (NFA)

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9
Q

What varies in fatty acids?

A

Fatty acids vary in number of carbon double bonds that are not saturated with hydrogen (C=C)

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10
Q

What does it mean when a fatty acid has high fluidity?

A

That means there is a higher number of un-saturated bonds.

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11
Q

Unsaturated fats can provide?
Give an example

A

Health benefits
E.g. omega-6 and omega-3 polyunsaturated fatty acids.

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12
Q

What are fatty acids prone to?

A

Rancidity and oxidative damage.

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13
Q

Name two animal sources of common dietary fatty acids:

A
Palmatic acid (16:0)
Stearic Acid (18:0)
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14
Q

Name two marine sources of common dietary fatty acids

A

◦ Eicosapentaenoic acid(EPA; 20:5) n-3
◦ Docosahexaenoic acid (DHA; 22:6) n-3

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15
Q

Name three plant sources of common dietary fatty acids

A

◦ Alpha linolenic acid (18:3)n-3
◦ Linoleic acid (18:2) n-6
◦ Oleic (18:1) n-9

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16
Q

What, other than the body, can synthesize essential fats?

A

Gut microbes
E.g.

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17
Q

Give an example of essential fat synthesis

A

linoleic acid can be converted to arachidonic acid
◦ Cats have a slow enzymatic pathway for this, and so require arachidonic acid

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18
Q

Define linoleic acid

A

◦ An essential omega-6 fatty acid (dogs and cats)

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19
Q

List the oils that are high in Linoleic Acid

A

Corn oil, safflower oil, walnut oil, canola oil, cottonseeed oil.

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20
Q

What is the importance of linoleic acid?

A

◦ Immune function
◦ Skin barrier function

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21
Q

Define arachadonic acid

A

◦ An essential omega-6 fatty acid in cats

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22
Q

What can be metabolized from linoleic acid?

A

Arachidonic acid

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23
Q

What foods contain high amounts of arachidonic acid?

A

Animal fats such as Chicken and eggs

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24
Q

What is the importance of arachidonic acid?

A

◦ Important for immune function and primarily for reproductive success in queens

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25
Q

What is the source of alpha linolenic acid?

A

◦ plant-based (flaxseed, chia, soybean…)

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26
Q

Describe the structure and function of Alpha linolenic acid.

A

◦ essential omega-3 polyunsaturated fatty acids
◦ Ensures adequate neuronal function

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27
Q

Alpha linolenic acid can be transformed into?
In what species does this occur in?

A

◦ May be transformed to long chain omega-3 fatty acids in some species (not much in dogs and cats)

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28
Q

What is the function of EPA and DHA?

A

◦ Neural function and development
◦ Immunomodulation

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29
Q

EPA and DHA are sourced from?

A

Marine source

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30
Q

EPA and DHA are what type of fatty acid?

A

Long-chain omega-3 fatty acid

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31
Q

List the types of fat soluble bitamins

A

A, D, E, K

32
Q

What do fat soluble vitamins require?

A

• These require dietary fat to be absorbed through the intestines

33
Q

What are fat soluble vitamins at risk for? Explain why.

A

• Since these are fat soluble and not water soluble, there is higher risk for excess

34
Q

What lipoproteins made up of?

A

• Made up of droplets of fats surrounded by a single phospholipid layer

35
Q

List the different types of lipoproteins:

A

Chylomicrons
HDL
LDL
IDL
VLDL

36
Q

What is the function of HDL?

A

delivers lipids from peripheral tissue to the liver

37
Q

What forms LDL?

A

‣ formed when triglycerides are removed from VLDL by lipoprotein lipase enzyme (LPL) and become smaller and denser.

38
Q

How is VLDL formed?

A

‣ assembled in the liver from triglycerides, cholesterol, and apolipoproteins

39
Q

What is the function of VLDL?

A

VLDL transports endogenous products to the peripheral tissues

40
Q

Lipoproteins allow the transport of?

A

hydrophobic lipid molecules in blood plasma or other extracellular fluids

41
Q

What makes a lipoprotein smaller?

A

Density

42
Q

What is density determined by?

A

• Density is determined by the relative concentrations of triacylglycerols (lighter= more TG) and proteins and by the diameters

43
Q

Describe the stages of fat digestion:

A

◦ Stage 1: fat is emulsified with bile acids
‣ bile acids have both hydrophilic and hydrophobic domains
‣ the hydrophobic portions of bile acids interact with the lipid, and the hydrophilic domains remain at the surface
◦ Stage 2: hydrolysis of triglyceride into monoglyceride and free fatty acids by pancreatic lipase
‣ PL is water soluble, therefore stage 1 is required
◦ Stage 3: reformation of triglyceride molecules in the enterocytes in the small intestines
◦ Stage 4: the triglycerides are packaged with phospholipids, cholesterol, and protein (specifically, apoprotein B) to create chylomicrons
◦ Stage 5: chylomicrons are absorbed through the lymphatic vessels in the intestines which drain into the thoracic duct
◦ Stage 6: the thoracic duct is drained into the jugular vein

44
Q

What is the function of lipoprotein lipase?

A

• Lipoprotein lipase breaks down the triglycerides and allows fat absorption in peripheral tissues

45
Q

What is transported to the liver during fat digestion and absorption?

A

The remnants of chylomicrons.

46
Q

Where are VLDL and LDL formed? What happens after their formation?

A

• VLDL and LDL are formed in the liver from triglycerides and cholesterol and are transported from the liver to peripheral tissues LDL also returns to the liver and cleared from the blood stream

47
Q

Where can medium chain triglycerides be found?

A

• MCTs can be found in palm kernel oil, and in small amounts in coconut oil

48
Q

What are the two forms of MCTs?

A

Synthetic or purified

49
Q

How are MCTs absorbed?
What about in dogs and cats?

A
  • MCTs are largely absorbed through the portal vein system unlike other fats.
  • (in dogs and cats, likely portal absorption is in addition to lymphatic absorption)
50
Q

Describe the chemical structure of MCTs

A

• These are triglycerides with a hydrocarbon tail chain of 6-12 unlike other fats carbons.

51
Q

Define chylothorax

A

◦ Chylothorax is the accumulation of lymphatic fluid (chyle) in the pleural space

52
Q

In what species is chylothorax most reported? Rare in?

A

Dogs and cats, rare in horses.

53
Q

Disturbance in chyle flow may cause:

A

heart disease, enlarged thyroid, vena caval obstruction/thrombosis, heartworm disease, diaphragmatic hernia, lung lobe torsion, and neoplasia

54
Q

How would a veterinarian diagnosis chylothorax?

A

includes physical exam findings (respiratory signs), radiographic changes and analysis of the fluid via thoracentesis

55
Q

What is the treatment for chylothorax?

A

‣ Emergency: chest tube to relieve pressure on the lungs
‣ Surgical: such as thoracic duct ligation
‣ Non-surgical: low-fat diet may reduce the lipid content of the fluid and may help it reabsorb in the pleura
‣ Nutraceutical: Rutin is a medication that may stimulate macrophages and help break down the protein in the fluid.

56
Q

What is intestinal lymphangiectasia?
What is the cause?
What species is it reported in?

A
  1. Pathologic dilation of intestinal lymph vessels
  2. May be the result or the cause of another enteropathy
  3. Reported in dogs, rare in cats and horses.
57
Q

What are the clinical signs of Intestinal Lymphangiectasia?

A

‣ Chronic diarrhea
‣ Weight loss
‣ Protein loss (Protein losing enteropathy= PLE)
• Low albumin
• Ascites/pleural effusion
‣ Low calcium and vitamin D
• Seizures/tremors/ataxia/lethargy
• Face rubbing

58
Q

How would a veterinarian diagnose Intestinal Lymphangiectasia?

A

‣ Clinical signs
‣ Lab results- low albumin, low cholesterol, low lymphocytes, hypocalcemia
‣ Endoscopy: abnormal appearance of the intestinal mucosa
‣ Intestinal biopsies (full thickness)

59
Q

How would you treat Intestinal Lymphangiectasia?

A

‣ Anti-inflammatory/immunosuppressive
‣ Diet:
• Low-fat: absorption of long-chain triglycerides is a stimulus for lymph flow
• Supplementation of fat-soluble vitamins (carefully)
• Novel protein diet (?)

60
Q

Endogenous lipid abnormalities terminology?

A
61
Q

Define hyper lipids/hyper lipoproteins/dyslipidemia

A

Increase in triglycerides and cholesterol in the blood.

62
Q

Define hypercholesterolemia

A

increased cholesterol in the blood

63
Q

Define hypertriglyceridemia

A

increased blood triglycerides.

64
Q

What is the most common reason for hyperlipidemia? Explain

A

Post prandial
- Increased chylomicrons causing hyperlipidemia

65
Q

Secondary hyperlipidemia

A
  • Renal disease
  • Diabetes
  • Cushing’s disease
  • Hypothyroidism
  • Negative energy balance in overweight animals (horses)
66
Q

Primary hyperlipidemia is?

A

Genetic/familial

67
Q

Primary hyperlipidemia in cats

A

Cats: (rare) inherited fasting hyperchylomicronaemia
‣ autosomal recessive disorder resulting from reduced LPL

68
Q

Primary hyperlipidemia in dogs:

A

Hereditary
‣ Miniature Schnauzers
‣ Briard
‣ Beagle
‣ Sheltie
‣ Doberman
‣ Rottweiler
‣ Pyrenees Mountain Dog
• Primary Hyperlipidemia in dogs:
◦ The lipoprotein accumulation differs between breeds.

69
Q

What are the clinical signs of primary hyperlipidemia in dogs?
Does your course of treatment matter depending on the type of lipoproteins.

A

◦ Clinical signs:
‣ Pancreatitis
‣ Dystrophic changes
‣ Insulin resistance
‣ Hepatobiliary disease (mucocele)
‣ Seizures.

◦ There is no difference in clinical signs or approach to therapy according to the type of lipoproteins.

70
Q

How would you diagnose primary hyperlipidemia

A

◦ Diagnosis:
‣ Elevated serum triglycerides
‣ Elevated cholesterol
‣ Moderate hypertriglyceridaemia (not hyperchoelsterolaemia) can be suspected based lactescent serum/plasma.

71
Q

What can you rule out in primary hyperlipidemia?

A

◦ Rule outs:
‣ Post prandial sample (must be fasted!)
‣ Underlying metabolic disease

72
Q

What is the treatment for primary hyperlipidemia in dogs?

A

◦ Treatment:
‣ Low fat
‣ Long-chain polyunsaturated omega-3 fatty acids (PUFA)
• EPA & DHA 200 to 300 mg/kg/day PO
‣ Fibrates
• Impact lipid metabolism.
‣ Niacin
• Vitamin B3
• Reduces triglycerides biosynthesis.
‣ Statins (HMG-CoA reductive inhibitors)
• Reversible inhibitors of HMG-CoA reductive (cholesterol biosynthesis)
• In dogs, hypertriglyceridemia is of clinical importance.
• Possible hepatotoxicity.

73
Q

What diseases are secondary to diseases that affect lipid and energy metabolism?

A

◦ Cushing’s disease
◦ Hypothyroidism
◦ Diabetes mellitus
◦ Pancreatitis
◦ Obesity
◦ Hepatic Disease
◦ Treatment: treat underlying condition.

74
Q

• Protein losing nephropathy (nephrotic syndrome)
◦ Hypercholesterolemia develops with hypoalbuminemia
◦ Metabolic pathways to synthesize cholesterol are stimulated when hepatic albumin synthesis increases.

A
75
Q

Secondary hyperlipidemia affects what equine breeds?

A

◦ Ponies
◦ Miniature horses
◦ Donkeys
◦ Less common in standard adult horses
◦ Common in overweight ponies during negative energy balance

76
Q

What are can cause secondary hyperlipidemia in horses?

A

Stress
Gestation
Disease
Overproduction of lipids in the liver —> hepatic lipidosis

77
Q

What are species can develop hyperlipidemia ?

A

Alpacas and llamas