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biochem - lipid metabolism Flashcards

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1
Q

functions of lipids

A
  • energy source
  • components of cell membrane (phospholipids)
  • communication molecules (steroid hormones)
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2
Q

why do FAs have even number of carbons

A
  • when synthesized, 2 Cs are added at once by organisms
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3
Q

essential fatty acids in the body

A
  • omega-3 FA (double bond is on 3rd C atom, where C1 is the non-carboxylic end of FA)
  • omega-6 FA
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4
Q

problem with trans fatty acids

A
  • increase LDL, decreases HDL→ atherosclerosis
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5
Q

dietary lipids composition

A

10%
- cholesterol, cholesterol esters, phospholipids, fatty acids

90%
- TAG (triacylglycerol, aka TG triglyceride)

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6
Q

enzymes for digestion of different lipid forms

A

TAG
- digested by lipase (mouth, stomach, pancreas)
- TAG→ diacylglycerol→ 2-monoacylglycerol + 2FA

cholesterol ester
- digested by cholesterol esterase (pancreatic)
- cholesterol ester→ cholesterol + FA

phospholipid
- digested by phospholipase A2 (pancreatic)
- phospholipid→ lysophospholipid/lysolecithin + FA

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7
Q

lipid digestion based on location

A

Stomach
- lingual lipase (mouth) and gastric lipase (stomach): digest triglycerides in the stomach
- lingual lipase is more active in the stomach as it requires low pH

Small intestine
- major site of lipid digestion
- secretion of bile salts and pancreatic lipase/colipase
- emulsification of fats by bile salts to form micelles
- digestion of fats mediated by enzymes (e.g pancreatic lipase, cholesterol esterase and phospholipase A2)
- absorption into enterocytes

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8
Q

function of colipase

A
  • bind to pancreatic lipase & anchors it to micelle
  • remove inhibitory effect of bile salts on pancreatic lipase
  • essentially increases activity of pancreatic lipase
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9
Q

hormones released by small intestine for lipid digestion (2)

A

cholecystokinin (CCK)
- released by intestinal cells (when stomach content enters intestine)
- stimulate bile salt + pancreatic lipase/colipase secretion

secretin
- released by intestinal cells
- stimulate HCO3- release from pancreas→ neutralise acidic chyme from stomach→ provides optimal pH for pancreatic digestive enzymes to work

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10
Q

orlistat function & points to note when consuming

A
  • inhibit release of gastric & pancreatic lipase -> decrease fat absorption
  • take daily supplement of vit A,D,E,K (fat soluble, impaired absorption when lipids are not absorbed into body)
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11
Q

reasons for steatorrhea (excessive fat in feces) & complications

A

impaired lipid digestion
- bile salt deficiency
- pancreatic insufficiency
- disease in small intestine -> affect lipid absorption

complications:
- impaired absorption of vit A,D,E,K

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12
Q

what happens to lipids after absorption into small intestine (3)

A
  1. reforming of initial lipids
    - monoacylglycerol + 2FAs→ TAG
    - cholesterol + FA → CHOLESTEROL ESTER
    - lysophospholipid + FA→ PHOSPHOLIPID
  2. formation of nascent chylomicron
    - TAG, cholesterol esters, phospholipid + fat soluble vitamins→ form nascent chylomicron
    - ApoB-48 (produced by ENTEROCYTES) required for proper assembly of chylomicron
  3. export into lymphatic system
    - chylomicron transport out of enterocyte to lymphatics via EXOCYTOSIS
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13
Q

what is the structure of lipoproteins eg chylomicrons?

A

outer layer
- single layer phospholipid: phosphate group face out; hydrophobic FA chains face inward
- embedded apolipoproteins: essential in structure, metabolism & function of lipoprotein particles

core (lipids)
- TAG, cholesterol esters

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14
Q

where and how do nascent chylomicrons get converted to mature chylomicrons

A
  • movement from lymph nodes (nascent) into blood (mature)
  • HDLs in blood transfer apolipoproteins ApoE and ApoCII to nascent chylomicrons→ mature
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15
Q

what are the apoproteins on mature vs nascent chylomicrons?

A

nascent: ApoB48
mature: ApoCII, ApoE, ApoB48

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16
Q

why do nascent chylomicrons enter lymphatics (and not directly into blood)

A
  • too large to fit through blood vessel (lymphatics have larger gaps between endothelial cells)
  • moves to blood circulation at subclavian vein (not impt)
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17
Q

function of mature chylomicrons

A

converted to energy stores (adipose tissue) or metabolised (muscle):
- ApoCII (LPL co-factor) on mature CM→ activate LIPOPROTEINLIPASE (LPL) on capillary endothelium NEAR MUSCLE tissue/ ADIPOSE tissue→ breakdown of chylomicron core
- LPL converts TAG→ FAs + glycerol
- FA is used to generate ATP in muscle + converted to TG for storage in adipose tissue

uptake by liver for lipogenesis
- glycerol from breakdown of TAG by LPL taken up by liver
- chylomicron remnants contains ApoE -> interact with liver receptor -> uptake via ENDOCYTOSIS -> lysosome in liver fuse with endocytic chylomicron vessels -> degrade chylomicron remnants to from FA, aa, cholesterol, glycerol -> nutrients are taken up by hepatocytes

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18
Q

what are chylomicron remnants

A
  • mature chylomicrons are broken down by LPL -> process cause loss of ApoCII & change in conformation
  • chylomicron remnants no longer have ApoCII, but still contain B48 and ApoE apolipoproteins
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19
Q

hyperchylomicronemia pathogenesis

A
  • genetic, deficiency in LPL/ ApoCII -> impair hydrolysis of TAG in mature chylomicrons
  • severe hypertriglyceridemia
  • xanthoma (lipid buildup under skin) on arms, buttocks, knees due to formation of foam cells in skin (macrophage engulfing lipids)

*patients advised to maintain low fat diet

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20
Q

de novo lipogenesis

A
  • endogenous synthesis of fatty acid from non lipid precursor (usually glucose)
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21
Q

rate limiting step in de novo lipogenesis

A
  • conversion of acetyl CoA to malonyl CoA (catalysed by acetyl CoA carboxylase)
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22
Q

allosteric regulation of ACC (acetyl CoA carboxylase)

A
  • upregulated by citrate
  • inhibited by long chain fatty acyl CoA (-ve feedback)
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23
Q

hormonal regulation of ACC

A
  • upregulated by insulin
  • inactivated by glucagon and epinephrine
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24
Q

where is fatty acid synthase found

A
  • cytoplasm, converts malonyl CoA & acetyl CoA to fatty acid
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25
what is fatty acid synthase expression induced by
- insulin (signals presence of glucose for fat synthesis)
26
how is TAG (components: FA, glycerol) synthesized in liver
FAs - de novo lipogenesis from glucose glycerol - direct glycerol uptake (from chylomicron remnants) - derive from DHAP (from glucose)
27
how is TAG synthesized in adipose tissue
FAs - uptake (dietary and hepatic) glycerol - derive from DHAP
28
formation of VLDL process
- lipoprotein synthesized in liver -> secreted from liver as NASCENT VLDL (containing ApoB100) - in blood, nascent VLDL acquire ApoE, ApoCII (from HDL) -> forms MATURE VLDL contents of VLDL - contains TAG -> FAs are predominantly sythesized by DE NOVO LIPOGENESIS
29
function of VLDL
- deliver hepatic TAG to other tissue (similar MOA as chylomicrons -> VLDL taken up by muscles & adipose tissue through LPL interaction with ApoCII -> remaining glycerol is taken up by liver)
30
what happens to VLDL after losing TAG at LPL
- VLDL loses TAG -> becomes smaller sized (intermediate density lipoprotein, IDL) - IDL reuptake by liver can occur through interaction with ApoE receptor on IDL - IDL can also stay in blood circulation for longer -> lose more TAG -> becomes LDL
31
steatosis (fatty liver) types (2)
accumulation of TAG in vacuoles of hepatocytes - excessive alcohol intake -> alcoholic fatty liver disease (AFLD) - metabolic syndrome (eg obesity, diabetes, htn) -> non alcoholic fatty liver disease (NAFLD)
32
pathogenesis of steatosis in hepatocytes
- increase in FA synthesis by hepatocytes -> cause increase in TAG synthesis - rate of TAG synthesis > VLDL synthesis -> accumulation of TAG in liver - impaired VLDL secretion
33
where does fatty acid B-oxidation occur
- mitochondria
34
what does beta oxidation do
- cleaves a long chain fatty acid into many molecules of acetyl-CoA - acetyl-CoA enters TCA to produce energy - produce FADH2, NADH -> can be used for OXPHOS
35
how is FA transported into mitochondria for beta oxidation
- FA converted to fatty acyl CoA (FACoA) by acyl CoA synthetase -> transported into intermembrane - FACoA converted to fatty acylcarnitine by CPT1 -> transported into mitochondrial matrix - fatty acylcarnitine converted back to FACoA by CPT2 in mitochondrial matrix -> beta oxidation occurs *rate limiting step -> carnitine mediated entry (FA-carnitine entry into mitochondrial matrix)
36
regulation of CPT1 in beta oxidation (ie what happens in fed state)
- CPT1 is allosterically inhibited by malonyl CoA - high blood glucose (fed state) -> 1) increase insulin release + 2) more glucose converted into citrate -> activate ACC -> increase synthesis of malonyl CoA -> suppress CPT1 -> less FA-carnitine is produced - less FA-carnitine in mitochondrial intermembrane -> decrease rate limiting step of carnitine mediated entry -> decrease beta oxidation *more glucose available -> less beta oxidation to produce glucose
37
what are ketone bodies
- acetoacetate, B-hydroxybutyrate, acetone - produced by liver under fasting conditions (ketogenesis)
38
where does ketogenesis occur
- mitochondria of hepatocytes
39
how are ketone bodies produced (under fasting conditions; insulin low glucagon high)
adipose tissues: - glucagon activates HSL (hormone sensitive lipase) -> increase lipolysis -> release FAs liver - low insulin high glucagon -> inhibition of ACC (acetyl CoA carboxylase) -> increase beta oxidation (also stimulated by high FA concentration from adipocyte) - beta oxidation produce acetyl CoA -> converted to ketone bodies in mitochondria
40
HSL vs LPL
- LPL (lipoprotein lipase) cleaves FA from circulating lipoproteins; found on cell membrane of adipocyte - HSL (hormone sensitive lipase) cleaves FA from intracellular TAG; found inside adipocyte
41
function of ketone bodies
- exported for use by extrahepatic tissue as fuel (muscles) -> converted back to acetyl CoA in muscle mitochondria -> generate ATP (ketolysis) - PROLONG starvation -> used by brain to produce ATP **conversion of ketone body to acetyl coA requires 3-ketoacyl-coA transferase -> NOT PRESENT in liver -> thus liver DOES not carry out ketolysis
42
how is acetone (lowest amount of ketone body produced) detected
- sweet smell in breath as acetone is volatile
43
how does type 1 DM cause ketoacidosis
type 1 DM -> destruction of insulin producing cells in pancreas -> low insulin, high glucagon levels - high glucagon increase ketogenesis -> rate of ketogenesis > rate of ketolysis -> build up of ketone bodies -> acidosis *ketonuria present (ketone bodies are soluble in water and excreted in urine)
44
functions of cholesterol
- regulate cell membrane fluidity - precursor for synthesis of bile acids, vit D, steroid hormones
45
sources of hepatic cholesterol pool (cholesterol store in liver) (3)
- dietary cholesterol (chylomicron remnants) - de novo synthesis in liver - cholesterol from extrahepatic tissue (reverse cholesterol transport by HDL
46
how can hepatic cholesterol pool be depleted (3)
- excretion in VLDL (amongst TAG) - conversion to bile acid/ salt -> secrete into intestinal lumen - small amount of free cholesterol secreted in bile
47
how is hepatic cholesterol store filled by remnant chylomicrons
- mature chylomicrons contain cholesterol & cholesterol esters (cholesterol embedded on outer membrane, cholesterol esters are in core of lipoprotein) - after conversion to chylomicron remnants (high cholesterol content as most TAG are lost to LPL) -> ApoE allow remnant chylomicron uptake into liver -> released as cholesterol in liver
48
where does de novo cholesterol synthesis occur
- hepatocytes - in cytoplasm and endoplasmic reticulum
49
4 stages of de novo (only need to know stage 1)
1) synthesis of mevalonate 2) mevalonate -> activated isoprenes 3) isoprene -> squalene 4) squalene -> steroid
50
what is the rate limiting step in cholesterol synthesis
- conversion of HMG-CoA -> mevalonate (by HMG-CoA reductase)
51
how is HMG-CoA reductase regulated
high energy levels - insulin activate phosphatase -> dephosphorylate & ACTIVATE HMG-CoA reductase low energy levels - glucagon, AMP -> activate AMP activated protein kinase -> phosphorylate & INACTIVATE HMG-CoA reductase -> inhibit cholesterol synthesis
52
how is bile acid synthesis (from cholesterol) regulated
- 7a-hydroxylase -> negative feedback inhibition by primary bile acids
53
how are primary bile salts formed from primary bile acids
- conjugation of primary bile acids with TAURINE or GLYCINE
54
why are conjugated bile acids (bile salts) better emulsifiers
- conjugation -> lower pKa -> more molecules have deprotonoted (conjugate base, ie salt) form -> higher solubility -> better emulsifier of lipid
55
bile salt vs bile acid
- non conjugated bile acids -> higher pKa -> majority in HA form -> BILE ACID - conjugated bile acid -> lower pKa -> majority in A- (salt) form -> bile salt
56
function of bile salt
- amphipathic molecules -> interact with large lipid droplet -> hydrophobic side faces lipid core, hydrophilic face outside -> breaks down lipid droplet and surround them to form micelles
57
how are secondary bile acids formed
- intestinal bacteria convert primary bile salt to secondary bile acids (deconjugation + dehydroxylation)
58
where are bile salts reabsorbed
- primary bile salts -> reabsorbed at ILEUM via ACTIVE TRANSPORT - secondary bile acids -> reabsorbed at COLON via PASSIVE DIFFUSION (less efficient than pri BS reabsorption) *both pri and sec bile salts are transported to liver via hepatic portal vein
59
how is vitamin D3 obtained by the body
- food - endogenous synthesis
60
describe the process of endogenous active Vit D (calcitriol) synthesis in the body
- 7-dehydrocholesterol (immediate precursor of cholesterol) -> converted to Vit D3 (under UV) -> liver converts to 25-(OH)D3 -> transported to kidney - at kidney: 25-(OH)D3 binds to Vit D receptor in cytoplasm -> move to nucleus -> complex induce expression of genes -> code proteins to activate 25-(OH)D3 -> form calcitriol (active Vit D3)
61
major lipoproteins
- chylomicrons - HDL - IDL - LDL - VLDL
62
how is VLDL converted to IDL
- losing ApoCII and TGs at LPL enzyme -> increase density -> IDL
63
how is IDL converted to LDL
- IDL loses TG to HTGL (hepatic triglyceride lipase) - IDL also interacts with HDL to return ApoE receptor overall LDL has lesser TG + no ApoE (only have ApoB100)
64
fate of LDL in blood
- reabsorbed back into liver via ApoB100 receptor - deliver cholesterol/ cholesterol esters to peripheral cells by using its ApoB100 to bind to LDL receptors expressed on peripheral cells
65
what happens to LDL that is neither reabsorbed by liver nor reabsorbed by extra hepatic tissue (due to lack of LDL receptors expressed) during atherosclerosis
- damage to inner wall of artery -> LDL become trapped at damaged side and is OXIDISED -> endothelial cells secrete cytokines when exposed to oxidised LDL -> monocyte accumulation - macrophage internalize oxidised LDL -> become foam cells
66
function of HDL
- reverse cholesterol transport (transport cholesterol from extrahepatic tissue to liver)
67
direct reverse cholesterol transport
- HDL synthesized by liver, small intestine -> take cholesterol from extrahepatic tissue cell membranes (converts C to CE and stores it) - lipid rich HDL (HDL2) binds to SR-B1 receptor on liver and release C/ CE, TG removed by HTGL - lipid poor HDL (HDL3) is released -> continue to pick up more cholesterol from extrahepatic tissue
68
indirect reverse cholesterol transport
- HDL -> exchange CE for TG with VLDL (give VLDL cholesterol), via CETP (cholesterol ester transfer protein) - VLDL eventually converted to IDL/ LDL and absorbed (along with cholesterol from HDL)
69
difference between transfer of cholesterol from HDL to liver vs LDL/ IDL to liver
- direct HDL transfer DOES NOT require endocytosis of whole lipoprotein - indirect IDL/ LDL transfer require endocytosis of whole lipoprotein
70
familial hypercholesterolemia pathogenesis
- mutation in LDL receptor gene -> ApoB100 cannot induce receptor mediated endocytosis of LDL -> cause ELEVATED LDL particles + elevated LDL-cholesterol in blood - homozygous (more severe)/ heterozygous manifestations - premature coronary heart disease, AMI, atherosclerosis - xanthomas present on achilles tendons & hands of pts - common within family/ relatives if they also have defective gene thus "familial"
71
types of phospholipids (2)
- glycerophospholipid - sphingolipid
72
functions of phospholipids
- structural (present on cell membrane, mitochondria membrane, lipoproteins) - cellular signaling
73
function of sphingomyelin (specialized form of sphingolipid)
- major structural lipid components of cellular membranes - a component of the myelin of neurons -> greatly increase the speed of electrical impulses in neurons
74
how are phospholipids broken down
- phospholipases -> cleave phospholipid into its constituents (FA, glycerol, polar head)
75
examples of eicosanoids
- prostaglandins, thromboxanes, leukotrienes *ALL are derived from arachidonic acid
76
how is AA production regulated
- by regulation of phospholipase A2 - phospholipase A2 is activated by diverse stimuli (eg inflammation) -> activation & translocation from cytosol to cell membrane
77
how is arachidonic acid obtained to produce eicosanoids
- present on cell phospholipid bilayer (but exists as a phospholipid) - phospholipase A2 cleaves the phosphate head to release arachidonic acid
78
how is arachidonic acid initially synthesized (before attachment to glycerol to form phospholipid and embedded in cell membrane)
- linoleic acid (a type of essential fatty acid)
79
what are essential fatty acids
- omega-3 fatty acid (a-linoleic acid) - omega-6 fatty acid (linoleic acid) **CANNOT be synthesized by body -> must be taken up through diet
80
important products of a-linoleic (ALA) and linoleic (LA) acid
- a-linoleic acid -> synthesize docosahexanoid acid (DHA) - linoleic acid -> synthesize arachidonic acid (AA) *both DHA and AA belong to PUFA (polyunsaturated fatty acids)

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