Lipid Synthesis & Degradation Flashcards

1
Q

what is the role of fats in the body?

A
  • membrane formatin
  • uptake of lipid soluble vitamins
  • precursors of steroid hormones
  • energy store
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2
Q

what is the energy content of fat in comparison to proteins and carbohydrates?

A

energy content is 2x/g compared to proteins and carbohydrates

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3
Q

when is the synthesis of fat triggered and what is the main source of it?

A
  • when caloric intake > consumption
  • cardiac muscle use fats as preferred energy source
  • dietary carbohydrate is the most common source bu aa can also be used
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4
Q

what is the structure of fatty acids (FA)?

A
  • chains of methyl groups with a terminal carboxyl group at one end
  • id double bonds present, in cis formation
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5
Q

why do humans need to obtain FA in diet?

A
  • humans unable to make double bodes at positions below position 9
  • bc they cannot be made in body
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6
Q

where does FA synthesis occur and what does it require?

A
  • in cytosol

- requires acetyl CoA, ATP, NADPH

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7
Q

how does the citrate-malate antipode system work and why do we need it?

A
  • pyruvate is transported from cytosol to inside of mito
  • converted to oxaloacetate where acetyl CoA is added to make citrate
  • citrate is removed form mito and back into cytosol so acetyl CoA can be released, forming oxaloacetate again
  • NADP is added to oxaloacetate to from malate which forms pyruvate when NADPH is removed
  • this is done as acetyl CoA cannot pass membrane of mito
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8
Q

what is the first step of FA synthesis?

A
  • acetyl CoA + ATP + HCO3- —-> malonyl CoA + ADP +Pi
  • acetyl CoA (C2) has C molecule added by HCO3- with ATP to form malonyl CoA (C3)
  • important, irreversible regulatory step activated by citrate and inhibited by palmitic acid
  • requires vit B7
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9
Q

what is the structure and function of cholesterol?

A
  • rigid hydrophobic molecule that is insoluble in H20
  • important membranen component and precursor of sterols, steroids and bile salts
  • transported in circulation as cholesteryl esters
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10
Q

what health issues can cholesterol imbalance lead to?

A

gallstones and atherosclerosis

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11
Q

describe cholesterol synthesis

A

-synthesised in ER (w over 30 steps involved)

  • starts w activation of acetate in acetyl CoA
  • major regulatory step is conversion of 3-hydroxyl-3-methyl-glutaryl CoA (HMG-CoA) to mevalonate
  • cholesterol inhibits HMG-CoA reductase
  • difficults to remove cholesterol by diet alone
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12
Q

what are the 3 steps of FA degradation?

A
  • mobilisation (in adipocyte)
  • activation (in liver cytosol)
  • degradation (in liver mito)
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13
Q

what happens in FA mobilisation?

A
  • GPCR activates adenylate cyclase to increase [cAMP] made from ATP, which activates protein kinase
  • protein kinase activates triglyceraol lipase
  • triglycerol lipase converts triacylglyceril to diacylglyceril
  • diacylglycerol is broken down to glycerol and FA
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14
Q

what happens to glycerol formed in FA mobilisation?

A
  • absorbed by liver
    1) glycerol phosphorylated to glycerol-3-phosphate
    2) glycerol-3-phosphate is oxidised by dihydroxyacetone phosphate
    3) dihydroxyacetone phosphate is isomerism to gform glyceraldehyde-3-phosphate (GAP)
  • most GAP is used in cluconeogenesis and some goes towards glycolysis
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15
Q

what is FA activation?

A
  • FA transported to liver and activated by acyl-CoA synthase in cytoplasm to form fatty acyl-CoA
  • fatty acyl-CoA reacts with alcohol carnitine to form fatty acyl-carnitine
  • fatty acyl-carnitine is transported across inner mito membrane by translocate
  • the fatty acyl-carnitine is broken down and releases acyl to combine with CoA, remaking acyl-CoA
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16
Q

what is FA oxidation/degradation and where does this occur?

A
  • β-oxidation
  • mito of liver
  • acyl-CoA degraded by sub sequential removal of 2C unit
17
Q

what does FA oxidation produce?

A

-FADH2, NADH, Acetyl CoA

  • FADH2 & NADH will form ATP
  • Acetyl CoA will enter citric acid cycle but only in presence of glycolysis
18
Q

why does FA oxidation occur in liver?

A
  • main production of FA oxidation is to produce acetyl-CoA which can be fed into citric acid cycle for energy
  • acetyl CoA can be converted to ketone bodies
19
Q

in non-hepatic cells, the oxidation of palmite produces how many ATP molecules?

A

106 ATP molecules

20
Q

what is ketogenesis

A

the production of ketone bodies in the metabolism of fats

21
Q

describe the stages of ketogenesis

A
  • acetyl CoA from the break down of FA is converted to acetoacetyl CoA
  • acetoacetyl-CoA is converted to HMG-CoA
  • HMG-CoA is converted to acetoacetate
  • acetoacetate can either be reduced to 3–hydroxybutyrate or acetone
22
Q

what is the fate of ketone bodies?

A
  • acetoacetate is converted in the non-hepatic tissues back to acetyl CoA = for ATP
  • major energy source for cardia muscle and renal cortex
  • during starvation ro diabetes, 75% of the brain’s energy derived from acetoacetate
  • [ketone] increases as [food intake] decreases
23
Q

how does insulin regulate fat metabolism?

A
  • increases glycolysis in liver
  • increases FA synthesis in liver
  • decreases β-oxidation
  • increases triglycerides in adipose tissue
24
Q

how do glucagon and adrenaline regulate fat metabolism?

A

increase triglyceride mobilisation

25
Q

what is formed in the breakdown of triglycerides?

A

glycerol

26
Q

what is the use of triglyceride degradation?

A
  • in liver: for synthesis of glucose in gluconeogenesis

- in muscle: used for ATP production in OXPHOS and glycolysis

27
Q

why are free FA transported into inner mito matrix?

A

enzymes required for degradation of FA are in inner mito matrix

28
Q

what is the importance of carnitine?

A
  • deficiency causes muscle weakness and even death

- required as FA degradation cannot happen without it