lipids pt 2 Flashcards

1
Q

sphingomyelin

A

a sphingolipid found in nerve cells. consists of sphingosine, fatty acid and phosophocholine

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2
Q

what are eicosanoids

A

special type of COOH that acts as intracellular messenger . derived from a 20 c arachidonic acidthey are short lived, act near point of synthesis e.g prostaglandins and leukotriens

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3
Q

lipoproteins and classification

A

non covalent complex of lipids and proteins involving H bonds , job is to transport lipids around

the smaller they are in size the heavier they are

CM

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4
Q

lipoproteins and classification

A

non covalent complex of lipids and proteins involving H bonds , job is to transport lipids around

the smaller they are in size the heavier they are

CM (lowest density) -mosly TAG
VLDL - TAG and chol
LDL-cholesterol
HDL-cholesterol
VHDL- complex of albumin with free FFA
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5
Q

Stages of CM

A
  1. nascent
  2. Mature
  3. remnant- travels to the liver
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6
Q

exogenous pathway

A

involves the liver packaging chol and TAG into VLDL to take to tissues, on the way VLDL becomes LDL because muscle and adipose have recieved

the ldl gets taken up by cells via ldl recpetor mediated endocytosis

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7
Q

enzymes in LP metabolism

A

lipoprotein lipase- found in the walls of blood vessels anchored by heparan sulfate. found in the heart adipose tissue lactating mamary gland but not active in adult liver

catalyses the breakdown of TAG in CM AND VLDL becuase they both have apo C2.

needs apo c2 to be activated
apo 2 and c3 inactivators

activated by insulin , makes sense because its an anabolic process youv’e just ate

Hepatic lipase:
bound to the sinusoidal surface of liver cells, does not readily interact with CM OR VLDL but is important in CM remenant and HDL metabolism.

LCAT

made in liver
associated with HDL- activated by apo a1
helps transport chol esters to the liver thus participating in cholesterol esters

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8
Q

adipose tissue characteristics

A

adipose is an energetic store of TAG
an organ with multiple organisation, visceral - (more metabolically active) and subcutaneous (less)

adipose is considered an organ and is an active organ involved in the hometostatis, regulation of neuroendocrine and immune system

white and brown

white:
large
spherical
large lipid vacuole

brown:
many mitochondria with many cristae
integral protein thermogenin 
rich blood supply 
have innervations from the sympathetic nervous system
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9
Q

adipokines

A

cytokines secreted by adipocytes

leptin was the first to be discovered-produced mainly by white adipoctes. small amounts found in placenta, ovary and mammary gland: limits our food intake and increasing energy use. receptors are in the hypothalamus. Also associated with bone mass + blood pressure.
obese individuals have higher levels of leptin which leads to increased macrophage inflammatory response- direct correlation between leptin levels and artherosclerosis.

obese people have ligh levels but there in no effect on appetite ‘leptin resistance’

defenciy in leptin:

pathological obesity
diabetes
immune suppression

increase in l tells brain to eat less and burn more

also sexual dimorphism, higher in females

leptin is also involved in inflammatory respsonses - modulates T cell function so too much is not beneficial - abnormally strong immune response - autoimmune disease.

adiponectin - sexual dimorphism higher in females. different to leptin because high levels means obesity . low levels correlates with insulin resistance- type 2 diabetes. secreted from both white and brown unlike leptin which was just white

and resistin

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10
Q

obesity

A

BMI below 25 - normal

25-30- is overweight

30+ Obese

in adults is due to

  1. overfeeding
  2. decreased physical activity
    associated with shortness of breath,, joint pain, high bp MI
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11
Q

fatty liver

A

liver has a high amount of TAG, usally around 4%. TAG is not exported with VLDL. can cause inflammation which can damage liver and cause scarring

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12
Q

hyperlipidemia and hypercholestemi a

A

classified according to which type of fat is elevated ( TAH, CHOL, lipoprotein .

Hyperlipidemias are divided into primary and secondary subtypes. Primary hyperlipidemia is usually due to genetic causes (such as a mutation in a receptor protein), while secondary hyperlipidemia arises due to other underlying causes such as diabetes.

  • hypercholesteremia
  • hypertriglyceridemia

2 causes of hypercholesteremia

  1. problems in the receptors for chol
  2. problems with the integral proteins for recognition

homozygous- very sevre/death (3 -5 x increase)

heterozygous- not so severe, can be controlled by diet and exercise

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13
Q

different types of fatty acids

A

plasma - long chain combined with albumin (VHDL)

Blood- shorter chains , more water soluable

cells- FA are attached to a fatty acid binding protein

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14
Q

why is beta oxidation called so

A

cos its an oxidation of the 3rd carbon from the COOH group and also because reducing equivalents NAD and FAD are produced

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15
Q

why do we need the carnitine shuttle?

carnitine shuttle

A

because the inner mitochondrial membrane is impermeable to the FA, so they need to be taken up by a cartine molcule in order to pass

carntine palmitoyl transferase 1 - outer membrane, transfers a carnitine to the fatty acyl coA forming acyl carnitine

carnitine acycarnitine translocase transports it to the matrix where we now need to get the acyl co a

this is the job of the last enzyme carnitine palmitoyl transferease 2 adds co A to acyl carnitne froming acy coa and carnitine which goes back to continue

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16
Q

where does fa activation occur for b oxidation

A

cytoplasm or EPR

17
Q

regulation of b oxidation

A

carnitine palmitoyl transferase 1 is inhibited by malonyl COA- allosteric inhibitor prevents the fatty acids from joining with carntine.

the enzyme is low activity after feeding but high activity after stravation

18
Q

oxidation of odd number fatty acids

A

propinoyl COA - propinoyl coA carboxylase

D methyl malonyl COA- methylmalonyl racemase
L methy malonyl COA - methylmaolony coa mutase (B12)
Succinyl coa- TCA

19
Q

how do we calculate the cycles of oxidation

A

n/2 - 1

20
Q

vitamin b12 deficiency and vitamin B12

A

pernicious anemia

neurological problems due to a build up of methylmalonate

vitamin b12 is cobalamin- water soluble vitamin and is uniuqe because it needs its own transporter called transcobalamin

intrinsic factor is needed for the absorption of b12

b9 + b12 = erythropoiesis (mainly b9)

deficient in just b9 or both- megaloblastic anemia

21
Q

oxidation of very long chain FA

A

occurs in peroxisomes

a modified version of B oxidation occurs which leads to acetyle COA + h202 which is broken down by catatlase which is fad dependant.

oxidation happens until octanoyl COA (8) then you resume with nomaal B oxidation in mitochondria

the oxidation in peroxisomes in not coupled with phosphorylation- NO ATP PRODUCED - free oxidation

22
Q

clinical significance

A

carnitine deficinecy

found mainly in muscles
made by liver and kidney
newborns and patients undergoing hemodialysis more likely to have it

deficiency of carnitine palmitoyl transferase 1
- low blood sugar (hypoglycemic)

defiicnecy of CPT2_
muscle pain and fatigue

  • deficiency in Acyl co-a DH (one of the enzymes of B ocidation) Fad dependant
    coma + hypoglycemia
    medium chain Acyl Coa dh is the most common form of acyl DH deficinecy
23
Q

which pathways need NADPH

A

cholesterol synthesis
fatty acid synthesis
cytochromes

24
Q

explain the different routes of Acetyl Co A

A

usually it would go to krebs but if youh have plenty of ATp then its a watse and oxaloacetate would soon be a limiting factor anyway. so then acetyl coa can be used for

  • fatty acid synthesis
  • cholesterol synthesis
25
Q

deficiency of PUFA

A

quite rare

  • alopecia
  • scaly dermatitis
26
Q

sphingolipidoses

A

are a class of lipid storage disordes relating to sphingolipid metabolis. Main members of this group are
Tay Sachs- progressive destruction of nervous system. they lack an enzyme that breaks down fat so it accumalates in the brain, liver
Gaucher disease
Fabry disease
Niemann-pick disease