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Metabolism > Fat metabolism > Flashcards

Fat metabolism Flashcards

1
Q

Do lipids provide a long term energy store or short term energy store

A

Long term energy store

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2
Q

why is triglycerides the ideal form of energy

A
  • high energy density

- has a limitless capacity for storage

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3
Q

what is the main storage tissue for triglycerides

A

fat droplets

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4
Q

what does lipolysis do

A
  • breaks down triglycerides into fatty acids and glycerol
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5
Q

what can fatty acids be used for

A
  • they can be oxidised for energy - this happens in oxidative tissues such as muscle and liver
  • or they can be converted to ketone bodies and used in non-oxidative tissues
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6
Q

what can glycerol be used for

A

glucose synthesis

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7
Q

what are the sites of lipogenesis

A

Liver
White adipose tissue
Lactating mammary gland

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8
Q

how are fatty acids stored

A
  • they are stored in adipose tissue as triglycerides
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9
Q

what are the two stages of lipogenesis

A
  1. Formation of malonyl-CoA from acetyl-CoA

2. Elongation of the chain via fatty acid synthetase

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10
Q

what is lipogenesis

A

this is the formation of lipid molecules

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11
Q

How does lipogenesis happen

A
  • Glucose enters the cell and is converted to pyruvate via glycolysis
  • the Pyruvate then enters the mitochondria and takes part in the krebs cycle.
  • The citrate produced in the krebs cycle, leaves the mitochondria, and is converted to acetylCoA in the cytoplasm.
  • This then is converted to malonylCoA
  • then to palmitate, which is acted upon by fatty acid synthetase to produce fatty acids
  • this can be used to extend fatty acid chains by 2 carbon units
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12
Q

what is palmitate

A

this is the first fatty acid produced during FA synthesis and is the precursor to longer fatty acid

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13
Q

How is lipogenesis controlled

A
  • it is controlled by Acetyl-CoA carboxylase
  • this catlayses the irreversible carboxylation of acetyl-CoA to produce Malonyl-CoA
  • Malonyl-CoA inhibits the carnitine shuttle and therefore prevents beta oxidation and fatty acid oxidation
  • Acetyl-CoA carboxylase is active when dephopshorylated
  • AMPK is the main kinase regulator of Acetyl-CoA carboxylase and is able to phosphorylate the serine residues on it therefore it deactivates it
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14
Q

what enzyme controls Acetyl-CoA carboxylase

A

AMPK

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15
Q

how does AMPK control Acetyl-CoA carboxylase

A
  • AMPK is the main kinase regulator of Acetyl-CoA carboxylase and is able to phosphorylate the serine residues on it therefore it deactivates it
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16
Q

what are the three ways in which Acetyl-CoA carboxylase (ACC) is controlled

A
  1. Polymerisation – by citrate (activation), this increases ACC activity
    - This is inihibted by palmitoyl-CoA
  2. Phosphorylation by AMP dependent kinase and PKA (inactivation)
  3. Genetic control (long term)
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17
Q

How do hormones control Acetyl-CoA carboxylaseACC

A
  • Insulin stimulates ACC and thus stimulates fatty acid synthesis by dephophosphrylating it
  • glucagon and adnrelaine dephosphorylate it thus inhibiting fatty acid synthesis
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18
Q

what is lipolysis

A
  • breakdown of lipids
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19
Q

when is lipolysis required

A

Used to mobilise energy stores during exercise or fasting

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20
Q

what stimulates lipolysis

A

Glucagon
Adrenaline and noradrenaline
Growth hormone
Cortisol

21
Q

How is lipolysis controlled

A
  • it is controlled by the enzyme hormone sensitive lipase (HSL)
  • HSL is sensitive to the levels of cAMP which are regulated via hormonal levels
  • cAMP is increased by glucagon and adrenaline
  • cAMP is decreased by insulin

it is also controlled by ATGL - enzyme adipose triglyceride lipase
- this enzyme produces the diacylglycerol for the HSL to act upon therefore the HSL converts diacylglycerol to fatty acids and glycerol

22
Q

what cells in the body metabolise fatty acids

A
  • most living cells in the Body

- except red blood cells and neurones in the CNS can metabolise fatty acdsi

23
Q

what are the 3 step process of the oxidation of fatty acids (overview)

A
  1. Once inside the cell, the fatty acid is activated by acetyl-coA
  2. This activated fatty acid is transported into the mitochondira via the carnitine shuttle
  3. Finally, ß-oxidation takes place
24
Q

how does fatty acid activation happens

A
  • this occurs in cytoplasm
  • the fatty acid is converted to fatty acyl-CoA by the enzyme acyl-Coa synthetase
  • This causes ATP to be converted to AMP
  • this produces fatty acyl-CoA
25
Q

How does the carnitine shuttle work

A
  1. the fatty acyl-CoA is converted to fatty acyl-carnitine by CPT-I enzyme which is located in the outer mitochondrial memrbane
    0 it is moved into the intermemrbane space
  2. the fatty acyl-carnitine is transferred into the mitochondrial matrix by a translocate enzyme
  3. this is then converted back to fatty acyl-CoA by CPT-II enzyme
  4. the free carnitine is shuttled back to the cytoplasm as the acyl-CoA is shuttled into the matrix of the mitochondria
26
Q

what is the carnitine shuttle used for

A

it is used for acyl-CoA to enter the mitochondria

27
Q

what is beta oxidation

A

this is the process by which the fatty acids are broken down

28
Q

where does beta oxidation happen

A
  • mitochondrial matrix
29
Q

how does beta oxidation happen

A
  • the long chains of fatty acids are broken down into 2 carbon units by acyl-CoA dehydrogenase
  • this produces acetyl-CoA, NADH and FADH2
  • the acetyl-CoA will enter the TCA cycle
  • the NADH and FADH2 are coenzymes that will be used in the ETC to produce ATP
30
Q

what are the products of beta oxidation

A
  • this produces acetyl-CoA, NADH and FADH2
31
Q

when will beta oxidation stop

A

-it will proceed until only 2 carbon units remain

32
Q

how do you control fatty acid breakdown

A
  • main point of control is transport via CPTI (once in the mitochondria there is little control)
  • this is inhibited by malonyl-CoA this is produced when glucose is in high concentration which is involved in fatty acid synthesis
  • it is stimulated by glucagon via cAMP
  • carnitine shuttle is also controlled by transcription, levels rise in extended fasting and diabetes
33
Q

where and what are ketone bodies produced from

A
  • they are produced from acetyl-CoA this is only in the liver within the mitochondria
34
Q

what are ketone bodies

A

They are soluble fuels, which can be used by tissues such as the brain, heart and muscle

35
Q

what are examples of ketone bodies

A

Acetoacetate and beta-hydroxybutyrate

36
Q

when does ketogensis take place

A
  • takes place when blood glucose levels are low after glycogen stores have been used up
  • for example in starvation
37
Q

what activates ketogensis

A

excess acetyl-CoA in the liver

38
Q

explain how excess acetyl-CoA in the liver causes the activation of ketosis

A
  • in starvation oxaloacetate is used for gluconeogensis in the liver
  • this means that there is not enough to take part in the TCA cycle
  • this leaves excess acetyl-CoA which is then converted into ketones
39
Q

how do you control ketogensis

A

HMG-CoA synthase

  • this is activated in deactivated form
  • gene expression increased by PPARa (this is a lipid regulated transcription factor)
  • it is used in the conversion of acetyl-CoA to ketone bodies
40
Q

what happens when ketone bodies reach the tissues

A

When ketones reach the tissues, they are reconverted back to acetyl-CoA, which can then enter the TCA cycle, followed by the ETC to produce ATP

  • Most tissues in the body, have alternative fuel sources if glucose concentrations are low – such as fatty acids
  • However, the brain requires glucose, so during starvation it will get a portion of its fuel requirements from ketone bodies
41
Q

what can’t ketone bodies be used as fuel by the liver

A

Ketone bodies cannot be used as fuel by the liver, because the liver lacks the enzyme β-ketoacyl-CoA transferase, also called thiophorase.

42
Q

what inhibits ketone body production

A

-insulin inhibits ketone body production

43
Q

what happens to diabetic in relation to ketones

A
  • uncontrolled diabetes means that there is a lack of insulin
  • this can lead to excess ketone production and therefore cause diabetic Ketoacidosis
44
Q

in beta oxidation what are the different forms of the enzymes

A

 Different isoforms of enzymes with differing chain length preferences

45
Q

where does beta oxidation occur

A

Occurs in most tissues that have mitochondria (except the brain) and therefore no beta oxidation occurs in red blood cells

46
Q

what is metabolic flexibility

A
  • this is the ability to switch between using glucose and lipids for energy production
47
Q

what kind range of metabolic flexibility is in active individuals compared to sedentary people

A

• In skeletal muscle there is a smaller range of switching in sedentary people that more active individuals

48
Q

how are fatty acids transported

A
  • they are transported bound to albumin

- they are not water soluble

49
Q

what are the 5 stages of glucose homeostasis

A
  • Food goes in first using glucose coming in from food
  • As this depletes start using glycogen
  • As this depletes liver gluconeogenesis happens
  • As this depletes there is an distinct drop of in gluconeogenesis
  • Glucose is now being replaced by ketone bodies

Metabolism (26 decks)

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