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
Q

which hormone inhibits ketone body production?

A

insulin

26
Q

why do diabetics struggle with ketoacidosis?

A

without insulin, more fatty acid is transported into the mitochondria of the liver –> more acetyl CoA builds up –> more acidic ketone bodies –> ketoacidosis

27
Q

what is metabolic flexibility?

A

ability to switch between using glucose and lipids

28
Q

what effect does a sedentary lifestyle have on metabolic flexibility?

A

less metabolic flexibility