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SEM 1 FLC > lipid transport > Flashcards

lipid transport Flashcards

1
Q

Lipids are transported from

A

from
• The gut to the liver
• Liver to non-hepatic tissue including adipocytes Non-hepatic tissue back to the liver

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2
Q

Fat and lipids in the circulation

A
  • Triagylcerols (45%)
  • Cholesterol esters cholesterol (15%)
  • Phospholipids (35%)
  • Free Fatty acids(5%)
  • Percentage greatly depends on diet All these in circulation are insoluble in water
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3
Q

Free fatty acids

A
  • Formed from triaglycerides stored in adipose tissue
  • Circulates bound to protein as Na+ salt particularly albumin as unbound DA would act as a detergent
  • Saturated at about 2mM
  • FA enter by simple diffusion Intracellular concentration of FFA kept low
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4
Q

Lipoproteins

A

• Carried in the blood as plasma lipoproteins
• Five types:
○ Chylomicrons
○ VLDL
○ IDL
○ LDL
○ HDL
○ They are characterised by how they behave under density centrifugation
• Each lipoprotein has a different function

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5
Q

Structure of lipoproteins

A
  • Contains at least one very large protein called Apolipoprotein
  • Phospholipids and cholesterol also present
  • Content is largely the phospholipids the triglycerides and cholesterol esters Single layer of molecules on what’s considered the membrane
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6
Q

Lipoprotein composition

A

• Largely the protein and triglycerides that determine the density of the lipoproteins
○ The more triglycerides the less dense
• Different lipoproteins have different apoproteins/apolipoprotein
• Different lipoproteins can interact with each other and exchange apoproteins Apoproteins are one of the largest proteins synthesised in the body

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7
Q

Functions of apoproteins

A

• Structural-backbone of lipoproteins
• Solubilise lipids-allow lipids to be soluble in aqueous encvironment
• Act as enzymes or enzyme cofactors
○ Apo C2 activates lipoprotein lipases
○ Apo A1 for lecithin: cholesterol acyltransferase
• Tissue targeting:
○ Apo B100 and Apo E bind to the LDL receptor Apo E binds to the HDL receptor

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8
Q

Synthesis of Chylomicons

A
  • Formed by cells that line the gut
  • In the lumen, triglycerides broken down to free fatty acids and monoacylglycerols under the influence of lipases • Taken into cell and reform into triglycerides These will join with apolipoproteins to from chylomicrons
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9
Q

Secretion of chylomicrons

A
  • Chylomicrons secreted into lymphatic system
  • If secreted into veins, it’ll be metabolised in the liver
  • This ensures lipids are available to the extrahepatic tissue Once in the lymphatic system, they’re carried to the superior vena cave via thoracic duct meaning it goes directly into circulation
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10
Q

Chylomicrons

A
  • Low density due to high TG
  • Majority protein is ApoB48 when first formed
  • Forms nascent chlyomicon and interacts with HDLs when in circulation
  • They’ll be exchanged with other apoproteins primarily ApoC2 and APoE forming mature chylomicon.
  • Reflect meal composition
  • Contain fat-soluble vitamins(A and E)
  • Life time in circulation is 1 hour whereas triglycerides is 5 minutes
  • As chylomicons circulate, they will be slowly depleted of their lipid content and their density will increase as triglyceride level decrease and form chylomicons remnants Remnants removed by liver with the involvement of Apo E
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11
Q

lipoprotein lipase

A

• Km of LPL in adipocytes is greater then Km in muscle
○ Meaning more saturated at much higher concentrations of circulating lipoproteins than it will be in the muscle
○ Muscle fully saturated at low levels so the muscle will be able to use the circulating lipoproteins at low concentration
• LPL on adipocytes are stimulated by insulin

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12
Q

hyperlipidaemia

A
  • Type 1: Deficiency in LPL or ApoC2-characterised by high plasma triglyceride
  • Type 2: Characterised by high LDL- most are caused by a genetic defect in the synthesis, processing or function of the LDL receptor • Type 4: Most common form results raised VLDL concentrations often due to obesity or alcohol abuse
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13
Q

VLDL

A
  • Synthesised in liver ER and modified in golgi
  • Predominant apoprotein is B100-made from the same gene as B48- only difference is that B100 is 100% of the gene whereas B48 is only 48% of the gene
  • Acquire Apo E and C from HDL
  • Responsible for transporting endogenously synthesised lipids Metabolised by LPL as they circulate
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14
Q

VLDL (Formation enhanced by)

A

○ Dietary carbohydrate
○ Circulating FFA
○ Alcohol
○ Raised Insulin and decreased glucagon

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15
Q

VLDL (Remnant removed by the liver by apoE)

A

○ One fate is when majority of triglycerides are lost, it returns to the liver
○ Other fate is of VDL’s that they form intermediate density lipoproteins
§ Takes place om the hepatic sinusoids
○ VLDL released in nascent form where they’re predominately expressing ApoB 100 interacting with HDL and gain ApoC2(involved in activating LPL) and ApoE

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16
Q

LDL

A

• Major carrier of cholesterol
• Metabolised slowly (3 days) • Carry cholesterol to the periphery and regulate de novo synthesis
• Contain 1 ApoB100 which can bind to a specific receptor on hepatocytes
• VLDL forms IDL by lipase
○ Some removed by liver whilst some formed into LDL which are rich in cholesterol ○ 60% of LDLs removed by liver and 40% by non hepatic tissue for steroid biosynthesis ○ Cholesterol used for hormone production

17
Q

HDL

A
  • Circulating reservoir of apolipoproteins(C2 and apo e) • Apolipoproteins obtained from VLDLs and chylomicrons • Remove cholesterol from plasma
  • Contain LCAT enzyme which esterifies cholesterol
  • Transported to liver and steroid producing cells
  • HDL bind to lipoproteins and cells via apoeE this is important for cholesterol transfer Return cholesterol to liver but also transfer it to VLDLs and LDLs-cholesterol ester transfer protein
18
Q

Reverse cholesterol transport

A
  • HDL remove cholesterol present in plasma membrane
  • Endothelial cells express transporter ApoA1 in order to this
  • Transporter transfers the cholesterol from the inner surface of membrane to extracellular surface where it interacts with ApoA1 on HDL • Then transported away to cells that need it or to liver.
19
Q

Normal ratio of HDL/LDL

A

3.5

20
Q

Receptor mediated endocytosis

A
  • ApoB100 and ApoE bind to LDL receptors on surface of hepatocytes
  • There are also scavenger receptors which are not regulated meaning they bind lipoproteins only at high concentrations Expressed on endothelial cells and macrophages
21
Q

LDL interaction with receptors on liver

A

• LDL will bind to LDL receptor on hepatocyte
○ Receptors are concentrated in coated pits ○ Pits have clathrin which is important for the uptake of LDL
• Membrane pinches off to form endosome
• Endosome starts to break down receptor which are recycled
• Remaining endosome with LDL will fuse into lysosomes • Cholesterol esters converted into cholesterol and diffuse into cytoplasm where they’re immediately esterified
○ Free cholesterol in cell is not desirable
• Whole process regulated by intracellular concentration of cholesterol

22
Q

Regulation of the uptake and synthesis of cholesterol

A

• Increased cholesterol inhibits HMG-CoA reductase activity
○ HMG-CoA reductase reduces LDL receptor expression
○ HMG-CoA reductase is the rate limiting step in the synthesis of cholesterol
• Statins inhibit HMG-CoA reductase, decreasing cholesterol synthesis
○ Will increase in the synthesis of LDL receptor on the cell surface
○ LDL cholesterol uptake by cells increased and therefore lowering circulating cholesterol

23
Q

Loss of LDL receptors (FH)

A

○ Recessive disorder
○ High serum cholesterol activating scavenger receptors
○ Develop blocked arteries ○ Die young from heart attacks
○ De novo synthesis is not regulated by LDL
○ Single amino acid substitution prevents localisation of the LDL receptor to the coated pits

24
Q

Two types of receptors

A

• High affinity LDL receptors and Low affinity scavenger receptor
• Present on:
○ Endothelial cells
○ Macrophages
○ VSMC
• Low affinity scavenger receptor active when plasma LDL is high

25
Q

Regulation of Lipoproteins

A
  • Hormonal regulation: Insulin, Cortisol, Thyroid hormones
  • Nutritional status: decreased synthesis during fasting, increased by dietary fats
  • LDL expression: oestrogen
26
Q

Abnormalities of Lipid transport

A
  • Diabetes Mellitus: increased FFA mobilisation, decreased Chylomicron and VLDL utilisation
  • Gene defects: apolipoproteins, enzymes or receptors.
  • Leading to: hypercholesterolemia, atherosclerosis
  • Obesity: hypertension, NIDDM, hyperlipidaemia and hyperglycaemia

SEM 1 FLC (30 decks)

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