lipid metabolism Flashcards

1
Q

name a short term energy store

A

carbohydrates

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2
Q

name long term energy stores

A

lipids and ketone bodies

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3
Q

where is fat stored in the body?

A

white adipose tissue

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4
Q

what does lipid breakdown release and how are they used?

A

fatty acids - oxidised for energy in tissues or converted to ketone bodies in the liver
glycerol - used in glucose synthesis in the liver

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5
Q

what does hormone sensitive lipase (HSL) do?

A

breaks down triglycerides into fatty acids and glycerol

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6
Q

what hormones control HSL and what control do they have?

A

glucagon - increase activity
insulin - decreased activity
Adrenaline
Adipose triglyceride lipase

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7
Q

how are fatty acids carried around the blood and why?

A

bound to albumin bc they’re not soluble

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8
Q

what are the stages of fatty acid oxidation?

A
  1. Activation of fatty acid by acetyl-CoA
  2. Transport into the mitochondria from the cytoplasm via the carnitine shuttle
  3. Beta oxidation in the mitochondria
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9
Q

what is the carnitine shuffle?

A

various steps to move fatty acid from cytosol to mitochondrial matrix to get access to the enzymes that do beta-oxidation

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10
Q

what are the stages of the carnitine shuffle?

A
  1. Fatty acid converted to fatty acyl-CoA by acyl-CoA synthase using ATP.
  2. Fatty acyl-CoA moved through outer mitochondrial membrane to form fatty acyl-carnitine by CPT-I (Carnitine palmitoyltransferase I).
  3. Fatty acyl-carnitine is moved through inner mitochondrial membrane by translocase.
  4. Converted back to fatty acyl-CoA in mitochondrial matrix by CPT-II
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11
Q

what is beta oxidation?

A

when fatty acids are oxidized by acetyl-CoA dehydrogenases in the mitochondrial matrix

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12
Q

in what tissues does beta oxidation occur?

A

all tissues apart from the brain and RBCs

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13
Q

what are the products of beta oxidation?

A

NAD and acetyl CoA

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14
Q

how is catabolism of fatty acids controlled?

A

Malonyl-CoA inhibits transports
Glucagon stimulates transport via cAMP
Regulated transcriptionally

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15
Q

what is lipogenesis?

A

the process by which acetyl-CoA is converted to triglycerides (how fat is made)

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16
Q

where does lipogenesis occur?

A

the liver, white adipose tissue and lactating mammary glands - stimulated in response to high blood sugar

17
Q

what are the stages of lipogenesis?

A

Glucose goes through glycolysis to make pyruvate –> TCA cycle –> citrate –> cytosol –> acetyl CoA –> malonyl CoA –> fatty acid chains

Formation of malonyl CoA
Fatty acid synthetase – elongates the chain by 2 carbon units

18
Q

what is the main enzyme in lipid synthesis?

A

acetyl-CoA carboxylase

19
Q

how is acetyl-CoA carboxylase controlled?

A

Polymerization: promoted by citrate
Phosphorylation: by AMP dependent kinase and PKA.
Genetic Control (longer term).

20
Q

where are ketone bodies produced?

A

in the liver by mitochondria

21
Q

explain the stages of ketogenesis

A

Starts with 2X acetyl-CoA
Combine to form acetoacetyl-CoA (CoA group removed)

Converted to 3-hydroxy-3methylglutaryl-CoA by HMG-CoA synthase

Converted to ACETOACETATE (ketone) by HMG-CoA lyase.

Acetoacetate can be split into further ketone bodies (D-beta-hydroxybutyrate and acetone).

22
Q

in starvation, what energy stores does the brain use?

A

brain switches from 100% glucose to 50% ketone bodies

23
Q

what tissues/organs use ketone bodies?

A

heart
skeletal muscle
the brain

24
Q

what are the liver phases of glucose homeostasis?

A

Stage 1 - glucose from food
Stage 2 - liver glycogen to maintain blood glucose
Stage 3 - liver gluconeogenesis
Stage 4 - drop in the rate of gluconeogenesis bc the brain is replacing glucose with ketone bodies so less gluconeogenesis is needed.

25
which hormone inhibits ketone body production?
insulin
26
why do diabetics struggle with ketoacidosis?
without insulin, more fatty acid is transported into the mitochondria of the liver --> more acetyl CoA builds up --> more acidic ketone bodies --> ketoacidosis
27
what is metabolic flexibility?
ability to switch between using glucose and lipids
28
what effect does a sedentary lifestyle have on metabolic flexibility?
less metabolic flexibility