Lipid metabolism Flashcards

1
Q

lipids
- solubility in water
- how does the length of the chain and number of double bonds impact solubility in water
- 4 examples
- what 2 lipids are important energy sources

A
  • low solubility
  • longer chain, fewer double bonds, lower solubility
  • Fatty acids
  • Triacylglycerols
  • Steroid
  • Phospholipids
  • FFAs and TAG
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2
Q

difference between a saturated and unsaturated fat

A
  • unsaturated has at least 1 double bond
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3
Q

phospholipids
- what do they do
- what makes them up and the bonds

A
  • part of cell memebrane
  • hydrophilic phosphate head attached to a glycerol unit which is attached to 2 hydrophobic fatty acids, all connected via ester bonds
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4
Q

triacylglycerols
- where are they usually found
- what do they do in the body
- what are they made of

A
  • dietary lipids
  • energy store in adipose tissue and muscle
  • 1 glycerol unit and 3 fatty acids connected by ester bonds
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5
Q

digestion and absorption of triacylglycerols

A
  1. Ingestion- Large lipid droplets reduced in size to fine lipid droplets by bile acids (made in liver & released by gallbladder)
  2. Intestinal lumen- pancreatic lipase hydrolyses the ester bonds forming 2 fatty acids and 2-monoacylglycerol (1 FA to glycerol)
  3. Enterocytes- these products freely enter the intestinal cells where TAG is reformed
  4. Bloodstream- lipids packaged into chylomicrons and exported into lymph nodes, then the blood and are distributed for energy metabolism or storage
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6
Q

chylomicrons
- structure
- function

A
  • Single layer of phospholipids with a hydrophobic core
  • transport triglycerides and deliver them to body cells
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7
Q

fat content of the human body
- where are lipids stored in the body
- what is visceral fat and subcutaneous fat
- impact of lipolysis during exercise

A
  • adipose tissue, and muscle
  • sub is fat under skin, vis is fat around our internal organs
  • breakdown triacylglycerol for energy to field muscles during exercise
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8
Q

breakdown and synthesis of triacylglycerols
- where do they both occur
- 3 key enzymes that allow lipolysis
- what happens to glycerol after breakdown
- what happens to glycerol during synthesis

A
  • the cytosol of adipose tissue and muscle
    1. Adipose TAG Lipase (AGTL)
    2. Hormone-sensitive lipase (HSL)
    3. Monoacylglycerol acyltransferase (MGL)
  • to the liver to form glucose or can be used to re-synthesise triacylglycerol
  • Three fatty acids are added to glycerol in 2 steps via the enzyme glycerol phosphate acyltransferase
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9
Q

exercise and lypolysis
- 3 influencers of the rate of lipolysis
- low-moderate intensity exercise
- high intensity exercise

A

1.Epinephrine: increases lipolysis (β-adrenergic pathway)
2.Epinephrine also decreases lipolysis (α-adrenergic pathway)
3.Insulin reduces lipolysis
↑ [epinephrine] and ↓ [insulin] drive the cAMP pathway favourably to activate AGTL, HSL & MGL
↑ [epinephrine] and stable or ↑ [insulin] suppress the cAMP pathway to inhibit AGTL, HSL & MGL, carb fuel source used more due to this

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10
Q

what happens to lipolytic products during exercise of muscle and liver

A
  • Muscle – FFA are primarily used for β-oxidation and ATP provision
  • Liver – glycerol is used for gluconeogenesis and some FFA may enter for Triacylglycerol synthesis
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11
Q

fatty acid degradation in the muscle
- what is the process called
- where does it happen
- one challenge for fatty acids
- how does it overcome this challenge
- what does a single cycle of beta-oxidation produce
- what happens after 1 cycle and when does it finish

A
  • β-oxidation in the mitochondria where it must cross 2 membranes
    1. FFA’s react with Coenzyme A forming Acyl-CoA which can pass to the inter-membrane space
    2. the AA Carnitine binds to and takes the Acyl group (forming Acylcarnitine), allowing transport into the mitochondrial matrix
    3. Acyl-CoA is then reformed inside the mitochondrial matrix
    4. Acyl-coA enters the β-oxidation pathway (cleavage of the 3rd carbon = beta) in the mitochondrial matrix
  • A single cycle of β-oxidation (4 reactions that degrade acyl-coA) produces: x1 acetyl-coA, x1 FADH2, x1 NADH, and Acyl-coA (Minus 2 carbons)
  • Acyl-coA then begins another cycle until you are left with 2 carbon acetyl coA which enters the TCA cycle (fully oxidised)
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12
Q

what does acyl mean

A

Acyl denotes any fatty acid chain and therefore some fatty acids undergo more cycles of β-oxidation, e.g. palmitate (16 carbons) undergoes 7 cycles (last cycle yields 2 acetyl coA)

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13
Q

energy yield of beta oxidation

A
  • produces no ATP
  • but produces acetyl co a, NADH and FADH2 that enter the TCA cycle and ETC to the produce huge amounts of ATP
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14
Q

beta-oxidation removes 2 carbons at a time, what happens when there’s an odd number of carbons in fatty acids

A
  • once a 5 carbon acylCoA molecule is reached we get 2C AcetylCoA as normal and a 3-carbon Propionyl CoA molecule
  • This then undergoes 3 reactions, forming SuccinylCoA which enters at reaction 5 of the TCA cycle
  • then oxidised but misses reactions 4 and 5 producing NADH so less energy efficient
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15
Q

4 ways exercise speeds up fatty acid oxidation

A
  1. Stimulating lipolysis in adipose tissue and muscle
  2. Increasing blood flow to the working muscle, increasing FFA delivery
  3. fatty acid binding protein (FABP-PM) moved to a better place on plasma membrane for greater FFA uptake into muscle
  4. Increasing activity of AMP-activated protein kinase (AMPK), which deactivates acetyl coA carboxylase, reducing synthesis of longer fatty acid and triacylglycerols
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16
Q

Blood plasma fatty acid profile during low, moderate and heavy intensity exercise

A
  • Low-intensity Exercise (25% VO2 max)- Slight initial increase Maintained throughout, Small post-exercise increase, then Return to baseline
  • Moderate intensity Exercise (65% VO2 max)- Slight initial decrease, then Gradual increase throughout, Large post-exercise increase, then Return to baseline
  • High-intensity Exercise (85% VO2 max)- Large initial decrease and Sustained low throughout (mainly use CHO and anaerobic ATP resynthesis), Large post-exercise increase to baseline, then Post-exercise suppression
17
Q

ATP resynthesis rates and times they’re used
- PCr, anaerobic CHO, aerobic CHO, aerobic fat in muscle, and adipose tissue

A
  • PCr system: 2.6 mmol . kg . sec -1 (0-7 seconds)
  • Anaerobic CHO oxidation: 1.5 mmol . kg . sec -1 (5-60 seconds)
  • Aerobic CHO oxidation: 0.5 mmol . kg . sec -1 (> 60 seconds)
  • Aerobic fat oxidation in muscle: 0.3 mmol . kg . sec -1 (> 5 minutes)
  • Aerobic fat oxidation from adipose tissue TAG: 0.2 mmol . kg . sec -1 (> 5 minutes)
18
Q

why it is good to yield ATP from triacylglycerol but why it cant always happen

A
  • large quantity of high energy stores that yield high ATP
  • slow process so not always available
  • there is a max vo2 we can oxidise fats at so glycogen meets demand after that intensity
19
Q

plasma lipoproteins
- what do they do
- what are apolipoproteins
- what determines their properties and function
- 4 types of lipoprotein

A
  • carry triacylglycerol & cholesterol esters, coated by phospholipids and cholesterol to be broken down
  • recognition (signal) sites in the membranes.
  • The ratio of lipid to apolipoprotein mass
  • Chylomicrons: 0.92-0.94 g.mL-1
  • Very low density lipoproteins (VLDL): 0.96-1.00 g.mL-1
  • Low density lipoproteins (LDL): 1.02-1.06 g.mL-1
  • High density lipoproteins (HDL): 1.06-1.21 g.mL-1
20
Q

lipoprotein transport of fats
- chylomicrons
- VLDL
- LDL
- HDL
- what does the ratio of LDL:HDL mean

A
  • TAG
  • TAG
  • cholesterol
  • remove cholestrol and take it back to the liver to be processed and broken down
  • more LDL bad as it’s a key indicator of CV health
21
Q

cycle of chylomicrons to LDL

A
  • From the small intestine, chylomicrons enter the blood and are broken down into TAG by Lipases for energy provision in muscle & adipose
  • Chylomicron fragments are transported to the liver and converted to VLDL, recirculated back via the blood to the liver to then form LDL, whilst offloading more TAG (contributes to visceral fat)
22
Q

apolipoproteins in Alzheimer’s disease
- what is APOE
- what are the 3 isoforms
- what combo reduces risk of Alzheimers, but what is the drawback of one of them
- which isoform has the highest risk
- which is the most commonly carried and average risk
- how may exercise impact risk

A
  • apolipoprotein E is a membrane protein on lipoproteins
  • APOE2, APOE3, APOE4 and each person contains 2 alleles
  • 2xE2 or E2+E3 reduces risk, but increases risk of CV disease
  • E4
  • E3
  • exercise may be stronger at protecting than the APOE 4 carriers
23
Q

obesity
- what is the pathogenesis
- what are the causes

A
  • Poor energy balance leads to adipose tissue dysfunction decreasing adiponectin, which alters the lipid blood profile and increases the inflammatory profile.
    ○ adipose tissue and systemic inflammation
    ○ Blockages in blood vessels
    ○ Increased disease risk
24
Q

impact of acute exercise on the Blood lipid profile

A

can improve with a single bout

25
Q

effect of chronic exercise on overweight people

A
  • improve lipid profile
  • increase adiponectin levels - can increase lipid oxidation, improve insulin sensitivity and is linked to lower inflammation
  • so can be used to combat low levels of adiponectin in obesity
26
Q

3 reasons why people are likely to become obese and why these are the case

A
  1. Food intake – due to lack of knowledge, hunger, emotion/stress eating, snacking, lack of sleep, medication, socio-cultural background
  2. Low metabolism and energy expenditure – due to ageing, sex, genetics and epigenetics, neuroendocrine factors, prandial thermogenesis, brown fat, sarcopenia, microbiota, medications
  3. Physical inactivity – due to socio-cultural background, physical challenges, chronic fatigue, pain, low fitness, emotional barriers, work, medications, injury