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BIOCHEMISTRY III > LECTURE 6 (Lipid metabolism) > Flashcards

LECTURE 6 (Lipid metabolism) Flashcards

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1
Q

What are the properties of Ketone bodies?

A
  • Alternative fuel for some cells
  • During fasting/starvation fatty acids are sent to liver -> converted into ACETYL-COA via B-OXIDATION
  • High levels of acetyl-CoA exceeds capacity of TCA cycle -> ACETYL-COA shunted towards ketone bodies
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2
Q

What causes high levels of Acetyl-CoA?

A
  • Decreased pyruvate dehydrogenase activity
  • B-oxidation of fatty acids
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3
Q

Where does Ketogenesis occur?

A
  • Liver hepatocytes (mostly)
  • Kidney epithelia
  • Astrocytes
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4
Q

Describe the importance of Ketones in the brain

A

Brain utilises ketone bodies during fasting to reduce reliance on glucose -> Brain is entirely dependent on glucose since FATTY ACIDS cannot penetrate through BLOOD-BRAIN BARRIER -> has to use ketone bodies instead of glucose during fasting -> Ketone bodies allow use of fatty acids energy by brain

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5
Q

What is the pathway from fatty acids to the its use in the brain?

A

Fatty acids -> Liver -> Ketone bodies -> Brain -> Acetyl-CoA

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6
Q

Why are Ketone bodies used by other tissues during a state of fasting?

A

To reserve glucose for brain

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7
Q

What are the properties of Acetone?

A
  • Not used as fuel
  • Excreted by lungs
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8
Q

What happens when Fatty acid levels are high during fasting?

A

Increased synthesis of ketone bodies

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9
Q

Can the liver use ketone bodies? (YES/NO)

A

NO

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10
Q

What is Ketolysis?

A

The process by which HYDROXYBUTYRATE and ACETOACETATE are converted into ATP

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11
Q

What happens in Ketoacidosis?

A

Ketone bodies release H+ at plasma pH -> Increase ketones in blood -> Metabolic acidosis

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12
Q

What is the link between diabetes and increased Ketone bodies production?

A
  • Low insulin -> High fatty acid utilisation -> Increased acetyl-CoA levels -> Ketone bodies production
  • OAA (Oxaloacetate) îs depleted (used for glucose production) -> TCA cycle stalls -> Increased Acetyl-CoA levels increase -> Ketone bodies production
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13
Q

How does Alcoholism lead to Ketoacidosis?

A
  • Alcohol metabolism -> excess NADH -> OAA shunted to malate -> TCA cycle stops -> Increased acetyl-CoA -> Ketone production
  • OAA depleted -> not enough for gluconeogenesis -> Hypoglycaemia
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14
Q

What is the clinical correlation of Ketoacidosis caused by Alcoholism?

A

Urinary ketones

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15
Q

In which stage of Cholesterol synthesis are Statins introduced?

A

In the conversion of HMG-COA (6C) to MEVALONATE (6C)

Explanation: It inhibits HMG-CoA reductase

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16
Q

What are the different types of Lipoproteins?

A
  • Chylomicrons
  • Very low-density lipoproteins (VLDL)
  • Intermediate-density lipoproteins (IDL)
  • Low-density lipoproteins (LDL)
  • High-density lipoproteins (HDL)
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17
Q

What are Apolipoproteins?

A
  • Proteins in lipoproteins that bind lipids
  • FUNCTION: surface receptors & co-factors for enzymes
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18
Q

How are Chylomicrons formed?

A
  • Fatty acids -> converted into TRIGLYCERIDES
  • Cholesterol converted into CHOLESTERYL ESTER by ACAT (Cholesterol Acyltransferase)
  • Triglycerides and Cholesteryl esters are packaged into CHYLOMICRONS by intestinal cells -> To lymph -> To bloodstream
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19
Q

What is found in Chylomicrons?

A
  • Triglycerides
  • Cholesteryl esters
  • Vitamins A, D, E & K
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20
Q

What happens once chylomicrons begin to circulate in the bloodstream?

A

They encounter the extracellular enzyme LIPOPROTEIN LIPASE (anchored to capillary walls)

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21
Q

What are the properties of Lipoprotein lipase?

Study These Flashcards
A
  • Located mostly in adipose tissue, muscle and heart
    [not liver - liver has hepatic lipase]
  • Converts triglycerides into fatty acids & glycerol -> fatty acids are used for storage or fuel
  • Required APO C-II for activation (carried on chylomicrons)
22
Q

Describe Lipid transport

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A

1) Chylomicron enters lymphatics
2) HDL transfers APO CII and APO E and Chylomicron APO CII activated LIPOPROTEIN LIPASE
[Impaired in type I familia dyslipidemia]
3) Liver releases VLDL
[overproduction in type IV familial dyslipidemia]
4) VLDL APO CII activated LIPOPROTEIN LIPASE
5) IDL delivers TaGs and cholesterol to liver via APO E
6) Endocytosis of LDL
[impaired in type II familial dyslipidemia]

23
Q

What are Lipoproteins composed of?

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A
  • Cholesterol
  • Triglycerides
  • Phospholipids
  • LDL & HDL (carry the most cholesterol)
24
Q

What is the function of Chylomicrons?

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A
  • Delivers dietary triglycerides to peripheral tissues
  • Delivers cholesterol to liver in the form of chylomicron remnants

SYNTHESIS: Secreted by intestinal epithelial cells

25
What is the function of cholesterol?
- Maintains cell membrane integrity - Synthesises bile acids, steroid and vitamin D
26
What is the function of VLDL?
Delivers hepatic triglycerides to peripheral SYNTHESIS: secreted by liver
27
What is the function of IDL?
Delivers triglycerides and cholesterol to liver SYNTHESIS: formed from degradation of VLDL
28
What is the function of LDL?
- Delivers hepatic cholesterol to peripheral tissues - Formed by hepatic lipase modification of IDL in liver and peripheral tissue - Taken up by target cells via receptor-mediated endocytosis
29
What is the function of HDL?
- Mediates reverse cholesterol transport from peripheral tissues to liver - Acts as a repository for apolipoproteins C and E
30
What is Atherosclerosis?
A form of arteriosclerosis caused by buildup of cholesterol plaques in intima LOCATION: - abdominal aorta - coronary artery - popliteal artery - carotid artery - circle of willis RISK FACTORS: - hypertension - smoking - dyslipidemia - diabetes - age - being male - postmenopausal status - family history PROGRESSION: Endothelial cell dysfunction -> macrophage and LDL accumulation -> foam cell formation -> fatty streaks -> fibrous plaque -> calcification
31
What are the properties of Hyperlipidemia?
- Elevated total cholesterol, LDL or triglycerides - Risk factor for coronary disease and stroke - A modifiable risk factor (related to lifestyle factors)
32
What are the signs of Hyperlipidemia?
Most patients have no signs/symptoms However, those with severe hyperlipidemia have: - XANTHOMAS = plaques of lipid-laden macrophages. Appear as skin bumps or on eyelids. - TENDINOUS XANTHOMA = lipid deposits on tendons (common in Achilles) - CORNEAL ARCUS = lipid deposit in cornea
33
What are the properties of Pancreatitis?
- Occurs when triglycerides are elevated - Exact mechanism is unclear - May involve increase chylomicrons in plasma
34
What is the mechanism behind Pancreatitis?
When triglycerides are too high, they may obstruct capillaries -> ischemia -> vessel damage can expose triglycerides to pancreatic lipases -> triglycerides breakdown and release free fatty acids -> acid leads to tissue injury and pancreatitis
35
Describe Type I Familial Hypercholesterolemia Hyperchylomicronemia
Autosomal recessive CAUSES: - Lipoprotein lipase deficiency [degrades triglycerides in circulating microns] - ApoC-II deficiency [Cofactor of LPL} = increased levels of chylomicrons and triglycerides SYMPTOMS: - Recurrent pancreatitis - Hepatosplenomegaly - Eruptive/pruritic xanthomas - Creamy layer in supernatant TREATMENT: - very low-fat diet
36
Describe Type II Familial Hypercholesterolemia Familial Dyslipidemia
Autosomal dominant CAUSES: - Absent or defective LDL receptors [LDL delivers hepatic cholesterol to peripheral tissues] - Defective ApoB-100 [B-100 binds LDL receptor] = Very high LDL SYMPTOMS: - Accelerated atherosclerosis (may have MI before 20) - Tendon (Achilles) xanthomas - Corneal arcus
37
Describe Type III Familial Hypercholesterolemia Familial Dysbetalipoproteinemia
Autosomal recessive CAUSES: - Defective ApoE [Mediates remnant uptake] = accumulation of chylomicron remnants and VLDL SYMPTOMS: - Premature atherosclerosis - Tuberoeruptive and palmar xanthomas
38
What is the difference between the ApoE2 and ApoE4 allele subtype?
ApoE2 allele = decreased risk of Alzheimer's ApoE4 allele = increased risk of Alzheimer's
39
Describe Type IV Familial Hypercholesterolemia Familial Hypertriglyceridemia
Autosomal dominant CAUSES: - Hepatic overproduction of VLDL or impaired catabolism = increased VLDL and triglycerides SYMPTOMS: - Hypertriglyceridemia -> can cause acute pancreatitis - Related to insulin resistance
40
Describe Abetalipoproteinemia
Autosomal recessive CAUSES: Mutation in a gene that encodes MICROSOMAL TRANSFER PROTEIN (MTP). MTO forms/secretes lipoproteins with ApoB (chylomicrons from intestine (ApoB-48) & VLDL from liver (B-100) -> Chylomicrons, VLDL and LDL present -> Very low triglycerides and total cholesterol levels DEFICIENCY: - ApoB-48 - ApoB-100 SYMPTOMS IN INFANTS: - Severe fat malabsorption - Steatorrhea - Failure to thrive LATER SYMPTOMS: - Retinis pigmentosa (Vitamin A deficient) - Spinocerebellar degeneration due to Vitamin E deficiency - Progressive Ataxia - Acanthocytosis (Abnormal RBC membrane lipids) DIAGNOSIS: - Intestinal biopsy: lipid-laden enterocytes TREATMENT: - Restriction of long-chain fatty acids - Large doses of oral vitamin E
41
What is the difference between Apo B48, Apo C-II & Apo E?
Apo B48 - contains 48% of apo-B protein - required for secretion from enterocytes Apo C-II - cofactor for lipoprotein lipase - carried by chylomicrons, VLDL/IDL Apo E - binds to liver receptors - required for uptake of remnants after chylomicrons have done their job
42
What are the properties of Chylomicron remnants?
- Have Apo-E receptors on liver -> take up remnants via receptor-mediated endocytosis - Usually only present after meals - Give plasma milky appearance
43
Summarise the function of Chylomicrons
1) Secreted from enterocytes with Apo B48 2) Pick up Apo C-II & Apo E from HDL 3) Carry triglycerides & Cholesteryl esters 4) Deliver triglycerides to cells and LIPOPROTEIN LIPASE (w/ co-factor Apo C-II) stimulates breakdown 5) Returns to liver as Chylomicron remnants (Apo E receptor on liver)
44
What are the 2 main lipoproteins secreted by the liver to deliver cholesterol & triglycerides to tissues?
VLDL & HDL
45
What are the properties of HDL?
- Bring cholesterol from periphery to liver - High HDL -> associated with decreased risk of cardiovascular events - KEY APOLIPOPROTEINS = A-I, C-II & APO E - Carries LECITHIN-CHOLESTEROL ACYL TRANSFERASE (LCAT) which esterifies esters + packs esters densely in core (activated by A-I) - Carries CHOLESTERYL ESTER TRANSFER PROTEIN (CETP) which takes triglycerides from VLDL and gives it more densely packed esters in return
46
What are the properties of VLDL?
- Carries triglycerides & cholesterol to tissues - Secreted by liver as nascent VLDL (only B-100) -> pick up C-II & Apo E from HDL -> LPL removes triglycerides + CETP in HDL removes triglycerides from VLDL -> VLDL is now IDL
47
What are the properties of IDL?
- Formed from VLDL - HEPATIC LIPASE removes triglycerides - HDL removes C-II and Apo E -> End result: LDL with only B-100 -> Less triglyceride content & greater cholesterol
48
What are the properties of Hepatic Lipase?
- Found in liver capillaries - Release fatty acids - Very important for IDL to LDL conversion
49
What are the properties of LDL?
- Contains small amount of triglycerides & high concentration of cholesterol/cholesteryl esters - Transfers cholesterol to cells with LDL receptor -> receptor-mediated endocytosis - LDL receptors recognise B100 - High LDL -> increased risk of cardiovascular disease
50
What are Foam cells?
- Macrophages filled with cholesterol - Found in atherosclerotic plaques in patients with vascular disease - Contain LDL receptors and can consume LDL particles
51

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