L13 Lipid Metabolism + Control of Blood Lipids Flashcards Preview

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Flashcards in L13 Lipid Metabolism + Control of Blood Lipids Deck (28):
1

Learning Outcomes (for general perusal)

  1. List the types of lipids and their physiological importance
  2. Outline the pathway of lipids from ingestion to utilisation in the tissues
  3. Describe the types of lipoproteins and understand the differences between them
  4. Understand the key factors in the regulation of blood lipid quantity
  5. Understand what is dyslipidemia and why it is a health risk

2

What is Triaclyglycerol

A triglyceride.

An ester formed from glycerol and 3 fatty acids

Neutral fat

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Palmitic Fatty Acid

  1. Name the family
  2. Nomenclature
  3. Main dietary source

  1. Saturated
  2. 16:0
  3. Animal Fat

4

Oleic Fatty Acid

  1. Name the family
  2. Nomenclature
  3. Main dietary source

 

  1. Monounsaturated
  2. 18:1, w-6
  3. Vegetable oils

5

α-Linolenic

  1. Name the family
  2. Nomenclature
  3. Main dietary source

  1. Polyunsaturated
  2. 18:3, w-3
  3. Oily fish, linseed

6

Explain the nomenclature

18:3, w-3

18 Carbons, 3 double bonds

3 is the position of the first double bond from the n-terminus or omega end (methyl end)

7

Name 3 membrane lipids

 

Phospholipids - glycerol has a phosphate attached

Sphingolipids - make up the myelin sheath in nerves

Cholesterol - containing steroid core made up of fatty acid portions which inserts itself between fatty acid chains, preventing crystallisation, giving membrane fluidity

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What are the sources of fatty acids?

 

 

Name two essential fatty acids

  1. Dietary fatty acids
  2. Adipose tissue
  3. Endogenously synthesized fatty acids 

 

Linoleic and Linolenic Acid (2nd messenger production and prostaglandin production)

9

10

How are free fatty acids transported to target tissues?

In a complex with albumin

(3-30 per one albumin molecule)

11

Summarize fatty acid absorption

(L2 and 3)

Fatty acids are liberated by the action of pancreatic lipase on dietary triglycerides and, in the presence of bile salts, form micelles, which diffuse through the (unstirred) mucosal layer to the muscosal surface

 

Absorbed fatty acids and monoglycerides are re-esterified to form triglyceride in the smooth endoplasmic reticulum. Apoproteins synthesized in the rough endoplasmic reticulum are coated around lipid cores, are the resulting chylomicrons are secreted from the basolateral pole of epithelial cells by exocytosis

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12

What are the tree main pathways responsible for the generation and transport of lipids within the body?

  1. exogenous pathway - dietary triG being absorbed and transported to the liver
  2. endogenous pathway- fats made in liver and brought to tissues around body
  3. reverse cholesterol transport - being made in all other cells and being brought back to the liver.

13

  1. What are lipoproteins?
  2. What is their function?
  3. How do they differ?

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  1.   Molecular complexes that consist of lipids and proteins. 
  2. They function as transport vehicles for lipids in blood plasma. Lipoproteins deliver the lipid components (cholesterol and triglyceride 

  3. ratio of protein to lipids, & in the particular apoproteins & lipids that they contain. Vary in size & density. As density increases, size decreases. (VLDL are larger in size, HDLs are smaller - no triglyceride) 

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14

Name the 6 types of prinicpal lipoproteins and their origins and sizes

 

Which are the 'good' lipoproteins?

  1. Chylomicrons INTESTINE (up to 1 microm)
  2. Chylomicron reminants CHYLOMICRONS (30-50nm)
  3. VLDL Very low density lipoproteins LIVER (40-100nm)
  4. IDL Intermediate density lipoproteins VLDL (25-35 nm)
  5. LDL Low density lipoproteins IDL (18-28nm)
  6. HDL High density lipoproteins INTESTINE, LIVER (5-10nm)

 

"good" = HDL - bringing from tissues to liver for processing

 

"bad" =  LDL - bringing cholesterol TO the tissues

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15

What are the major core lipids of

  1. Chylomicrons
  2. Chylomicron reminants
  3. VLDL
  4. IDL
  5. LDL
  6. HDL

  1. dietary triglycerides (TGs)
  2. dietary cholesteryl esters (ChEs)
  3. endogenous TGs
  4. endogenous TGs and ChEs
  5. endogenous ChEs
  6. endogenous ChEs

16

What are the major apoproteins of

  1. Chylomicrons
  2. Chylomicron reminants
  3. VLDL
  4. IDL
  5. LDL
  6. HDL

  1. B-48, E, A's, C's
  2. B-48, E
  3. B-100, E, C's
  4. B-100, E
  5. B-100
  6. A-I, A-II, E, C's

17

What is the mechanism of catabolism of 

  1. Chylomicrons
  2. Chylomicron reminants
  3. VLDL
  4. IDL
  5. LDL
  6. HDL

  1. hydrolysis by LPL in tissues
  2. receptor-mediated endocytosis in liver
  3. hydrolysis by LPL in tissues
  4. ~50% receptor-mediated endocytosis in liver;

    ~50% conversion to LDL

  5. receptor-mediated endocytosis in liver or tissues

  6. receptor-mediated endocytosis in liver

18

Exogenous Lipid Pathway (lipoprotein transport)

 

 

 give an outline

 

 

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Removal of chylomicrons from the blood - Plasma triacylglycerol and cholesterol transport

  1. Chylomicrons bind dietary triacylglycerols (TAGs) and cholesterol in the intestines
  2. In the bloodstream the chylomicrons bind to the endothelium of caps of  skeletal muscle and adipose tissue.
  3. The enzyme lipoprotein lipase hydrolyses the TAGs and free fatty acids are released into the tissues
  4. Chylomicron reminants (containing mostly cholesterol) return from the caps
  5. The liver takes up these reminants through a receptor, and dietary cholesterol is delivered. Bile acids and cholesterol are delivered from the liver to the intestines

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What makes up a chylomicron?

primarily TAG, 9% phospholipids, 3% cholesterol, 1% apoB (non-HDL)

20

Endogenous Lipid Pathway (lipoprotein transport)

 

Give an outline

VLDLs are synthesize in the liver and they deliver endogenous TAGs and cholesterol to the tissues

  1. By action of lipoprotein lipase, VLDL are delipidated to release free fatty acids which are taken up by the cells of muscle and adipose tissue
  2. The glycerol backbone is delivered to the liver and kidney cells to be converted to dihydroxyacetone phosphate
  3. Delipidated VLDL emerge from the caps as IDL (TAG lost)
  4. After degradation from IDL to LDL, about half are taken up by the liver via receptor mediated endocytosis
  5. Tissues (other than the liver) take up cholesterol from LDL via LDL receptors.

 

Cholesterol is removed from the cell surface membranes by HDL, this cholesterol is delivered to the liver by a process (still poorly understood)

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21

Outline their roles in cholestrol transport

  1. LDL
  2. HDL

 

(Need cholesterol for synthesis of certain hormones eg. vit d)

  1. Brings cholestrol TO the extrahepatic tissues
  2. brings cholestrol FROM the extrahepatic tissues for processing

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22

Outline Adipose tissue triglyceride synthesis

TAG delivered by VLDL chylomicrons 

Action of lipoprotein lipase (on cap endothelium) on TAG to give 2xFAs and monoacylglycerol

Transported into Adipocyte from Circulation

FAs are added to TAG liquid droplet in adipocyte

 

Glucose IN via GLUT4, to glycerol-3-P then into TAG lipid droplet

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23

Use of triglycerides for energy - explain what happens to 

  1. Fatty Acids
  2. Glycerol

  1. Enter the mitochondria via the carnitine cycle and undergo beta-oxidation
  2. Phosphorylated into glycerol-3-phosphate, enters the glycolytic pathway, eventually acetyl co-A is formed, into Kreb's Cycle etc.

24

Almost all cells use fatty acids for energy, but what are the exceptions?

Brain tissue and Red Blood Cells

 

(glucose sparing effect - glucose is saved for the tissues that really need it and FAs are used elsewhere)

25

  1. What happens to FAs in the carnitine cycle?
  2. What is produced?
  3. What is the ATP yield?
  4. What is the ATP yield with glucose?
  5. What does this mean?

1. Beta-oxidation

 

2. Acteyl Co-A and reduced nucleotides

Ketones (Acetoacetic acid, β-hydroxybutyric acid & acetone)

3. eg. Stearic Acid

Krebs Cycle 9ATPs, Oxidation 139 ATPs, Total = 148 ATP

4. 38

5. fats are a much more efficient energy store than glucose

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26

Regulation of Blood Lipid Levels

  1. What does the 'fat-sparing effect' mean?
  2. When to triglycerides become the principal source of energy?
  3. Which hormones act to regulate blood lipid levels?
  4. Which one has a negative effect?

  1. preferential utilisation of carbohydrates (if they are available) over fats

  2. In the absence of carbohydrates

  3. Insulin, Adrenaline and noradrenaline, Glucocorticoids, Growth hormone, Thyroid Hormone

  4. Insulin

27

Regulation of Blood Lipid Levels outline the role of

  1. Insulin
  2. Adrenaline and noradrenaline
  3. Glucocorticoids (cortisol)
  4. Growth hormone
  5. Thyroid Hormone

 

  1. promotion of fat synthesis and storage
  2. postive effect on Hormone-Sensitive Triglyceride Lipase
  3. postive effect on Hormone-Sensitive Triglyceride Lipase
  4. postive effect on Hormone-Sensitive Triglyceride Lipase
  5. accerleration of metabolic processess

 

2-5 bring about metabolism of fatty acids and depletion of fat reserves

1 stimulates promotion of fat synthesis and storage

28

Dyslipidaemias

  1. What are they?
  2. Give examples
  3. Which are most common? What are the risks?

  1. Higher or lower than normal concentration of lipoproteins in the plasma (disorders of lipoprotein metabolism)

  2. Disorders of chylomicrons & VLDL metabolism: lipoprotein lipase deficiency & apoC-II deficiency

  3. Disorders of LDL metabolism: heterozygous familial hypercholesterolaemia - defective gene coding for apoB/E receptor.

    1. Increases the risk for CV disease & atheroma

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