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GI > FA Metabolism > Flashcards

FA Metabolism Flashcards

1
Q

Pamitate synthesis:
where does it happen?
from what?
elongated where?

A

in cytosol from acetyl CoA,

elongated in ER

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2
Q

Where does fatty acid oxidation occur?
Oxygen required?
Oxidized to what?

A

in mitochondria, oxygen required (aerobic);

oxidized to acetyl-CoA

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3
Q

Where does fatty acid synthesis occur?
Oxygen required?
Oxidized to what?

A

in cytosol:

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4
Q

What happens to fatty acids during starvation and DM?

A

fatty acid oxidation –> ketone bodies produced by liver (not good long term – fatal)

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5
Q

Gluconeogenesis is dependent on fatty acid _________.

A

oxidation

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6
Q

Describe the ways in the which the structure of the FAs differ

A

chain length and #/shape of double bonds

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7
Q

What is the difference btwn sat and unsat fats?

cis/trans bond

A

of double bonds

almost always of cis config

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8
Q

What is the role of essential FAs in prostaglandin synthesis?

A

x

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9
Q

What is the role of dietary omega-3 FAs?

A

anti-inflammatory effect

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10
Q

What is the role of dietary omega-6 FAs?

A

form the backbone of Pro inflammatory prostaglandin precursors

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11
Q

What is the role of acetyl-CoA carboxylase in FA synthesis?

A

site of regulation: first enzyme of pathway

ABC carboxylase: combining one CO2 with one acetyl CoA

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12
Q

What is the role of FATTY ACID SYNTHASE in FA synthesis?

A

catalyzes remaining several rxns in FA synthesis:

Acetyl-CoA + malonyl-CoA –> 4 C fatty acid

  • requires 2 molecules of NADPH, repeats until chain reaches 16C = palmitic acid
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13
Q

How are long chain FAs synthesized?

A

repeated condensation of two carbon units

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14
Q

What is the favored formation ___ in most tissues?

A

16-carbon palmitate: saturated FA

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15
Q

What are the co-factors required for FA synthesis?

A

x

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16
Q

What are the sources of reducing equivalents (NADPH) for FA synthesis?

A

x

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17
Q

How are FA chains elongated? Where?

A

mitochondira or ER

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18
Q

What co-factors are required for FA chain elongation?

A

acetyl-CoA Carboxylase requires Biotin, vit B7 as cofactor

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19
Q

What chemical alterations are made to the molecule after FA chain elongation?

A

x

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20
Q

How are FA chains desaturated? Where?

A

ER

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21
Q

What co-factors are required for FA chain desatuation?

A

acetyl-CoA Carboxylase requires Biotin, vit B7 as cofactor

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22
Q

What chemical alterations are made to the molecule after FA chain desaturation?

A

x

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23
Q

What are the short term regulators of FA synthesis?

A

Citrate;

Palmitoyl CoA = long chain Fatty acyl-CoA

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24
Q

What is the mechanism by which citrate regulates FA synthesis?

A

allosterically ACTIVATES acetyl CoA carboxylase by promoting formation of large (active) polymers
short term

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25
Q

What is the mechanism by which palmitoyl CoA regulates FA synthesis?

A

INHIBIT enzyme by breaking down polymers (short term reg)

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26
Q

What are the long-term regulators of FA synthesis?

A

insulin; glucagon

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27
Q

What is the mechanism by which insulin regulates FA synthesis?

A

STIMULATES acetyl CoA carboxylase by dephosphorylation (vis protein phosphatase)

(high-carb diet or fat-free diet stimulate FA synth through increased synth of acetyl CoA carboxylase)

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28
Q

What is the mechanism by which glucagon(/epi) regulates FA synthesis?

A

INHIBITS acetyl CoA carboxylase through cAMP-mediated phosphorylation (via AMPK)

(think high-fat diet or fasting causes high glucagon)

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29
Q

How does FA and TAG biosynthesis integrate into mainstream carb metabolism?

A

x

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30
Q

How is the integration of FA and TAG biosynthesis regulated?

A

x

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31
Q

What are the sources of acetyl-CoA for FA synthesis?

A

x

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32
Q

What are the glycolytic intermediates used in TAG synthesis?

A

x

eg: DHAP

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33
Q

What is the effect of insulin deficiency/insufficency on acetyl-CoA levels?

A

x

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34
Q

How are TAGs synthesized?

A

x

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35
Q

What are the starting products of TAG synthesis?

A

x

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36
Q

What are the intermediates of TAG synthesis?

A

x

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37
Q

What are the final products of TAG synthesis?

A

x

38
Q

How are TGs synthesized in liver different from TGs synthesized in adiopose?

A

x

39
Q

How are TAGs catabolized to FFAs + Glycerol?

A

x

40
Q

What is the rate of the metabolites of TAGs catabolized to FFAs + Glycerol?

A

x

41
Q

How are FFAs transported in the blood?

A

x

42
Q

How are FFAs activated and transported into the matrix of the mito for breakdown to obtain energy?

A

x

43
Q

What is the role of the carnitine shuttle for LCFA (long chain fatty acids)?
(why is a shuttle necessary to cross the mito membrane?)

A

get long chain fatty acids into the mito for beta oxidation

44
Q

What is the role of lipoprotein lipase in TG breakdown?

A

x

45
Q

What is the role of CAT-1? (CPT I)

A

CYTO (outer leaflet of mito) converts Fatty acyl CoA to acyl carnitine

(Acyl carnitine is the transported into the mitochondrial matrix via CAT)

46
Q

What is the role of CAT-2? (CPT II)

A

MITO (inner leaflet) cleaves carnitine and makes fatty acyl CoA for beta oxidation within mitochondrial matrix

47
Q

What does CAT do and where does it live?

A

Lives between the mitochondira membrane

  • shuttles acyl carnitine from cyto to mito matrix
  • shuttles carnitine from in mito matrix to cyto
48
Q

What is the regulatory role of malonyl-CoA?

A

x

49
Q

What is the fate of carnitine?

A

x

50
Q

What is the sequence of events of FA oxidation in mito?

A

x

51
Q

Explain: General features of oxidation pathway of unsat odd-chained FAs

A

x

52
Q

Explain: General features of oxidation pathway of branched-chain FAs

A

x

53
Q

What are the 3 compounds termed “ketone bodies”?

A

x

54
Q

How is #1 formed in liver mito?

A

x

55
Q

How is #2 formed in liver mito?

A

x

56
Q

How is #3 formed in liver mito?

A

x

57
Q

What is the mechanism of formation of ketone bodies?

A

x

58
Q

What are the physiological roles for ketone bodies?

A

x

59
Q

What are the pathological roles of ketone bodies?

A

x

60
Q

How does overproduction of ketone bodies lead to ketosis? ketoacidosis?

A

x

61
Q

What are the pathological conditions of ketosis? ketoacidosis?

A

x

62
Q

What is the mechanism by which hormonal activation of lipolysis in adipose tissue is coordinated with activation of gluconeogenesis in liver during fasting?

A

x

63
Q

Compare and contrast FA synthesis vs degradation at the level of:
-organ involvement

A

x

64
Q

Compare and contrast FA synthesis vs degradation at the level of:
-physiological regulation?

A

x

65
Q

What occurs with deficiencies in FA metbolism?

A

x

66
Q

MCAD deficiency

A

x

67
Q

CPT-I deficiency

A

relatively rare, affect liver primarily;
lead to FA oxidation and ketogenesis

Sx: hypoketotic hypoglycemia; elevation in blood levels of carnitine; hepatomegaly; muscle weakness

68
Q

CPT-II deficiency - 3 main forms

A

1) adult myopathic form (muscle pain; fatigue, myoglobinurina following exercise)
2) severe infantile multisystem form (manifest in first 6-24 months) - hypoketotic hypoglycemia; progress to severe hepatomegaly and cardiomyopathy
3) neonatal (lethal; rare) - sx in hours/days after birth; respiratory failure; hepatomegaly; seizures; hypoglycemia; cardiomegaly –> fatal arrhythmias

69
Q

name characteristics of:

impaired oxidation of medium-chain FAs

A

ACCUMULATION OF DICARBOXYLIC ACID

AR; hypoketotic hypoglycemia;
presents in infancy;

high concentration of: Medium-chain carboxylic acids, acyl carnitines; and dicarboxylic acids (due to omega oxidation) in plasma and urine

  • hyperammonemia (result of liver damage)
  • hypoglycemia (inability to metabolize fats during fasting: limits gluconeogenesis)

NB: deficiencies in short and long-chain FA DH have similar clinical features

70
Q

How is MCAD treated?

A

frequent feeding, avoidance of fasting, carnitine supplementation

71
Q

What are the causes and effects of accumulation of methylmalonyl-CoA?

A

CAUSES:

  • Vit B12 def
  • defect in Intrinsic Factor
  • Defect in mutase enzyme (methylmalonyl CoA mutase)

EFFECTS:
methylmalonyl acidurea
maybe: peripheral neuropathy

  • can be used to differentiate btwn folate and B12 def
72
Q

What intermediate in the oxidation of odd-chain FAs is likely to appear in the urine in vit B12 deficiency?

A

methylmalonic acid

73
Q

What is the most likely underlying cause for pt rhabdomylosis?

A

carnitine palmitoyltransferase II deficiency (CPT II)

74
Q

Why can’t liver use ketone bodies?

A

it lacks CoA transferase

75
Q

How do we use ketone bodies as alternate fuel?

A

acetoacetate–> Acetylacetyl CoA –> 2 acetyl CoA –> TCA cycle (oxaloacetate)

76
Q

How is ketone body synthesis regulated?

A

NAD+ is reversing the TCA cycle:
converting oxaloacetate to malate which can be used for gluconeogenesis

–so need build up of acetyl coA and slowing down of TCA to get formation of ketone bodies

77
Q

What does the heat muscle prefer to use as an energy source?

A

acetoacetate

78
Q

When do we use ketone bodies as an alternate fuel?

A

fasting or diabetes or

-high in lipids with low in carbs lntake

79
Q

What does the brain prefer to use as an energy source? What can it use?

A

prefers glucose;

can use acetoacetate during starvation/diabetes

80
Q

What can lead to hypoketotic hypoglycemia?

A

Defects in:

  • carnitine transporter (can’t get long chain FAs into cell from plasma to cyto as long chain Fatty acyl CoA )
  • CPT I
  • CAT
  • CPT II
  • Fatty acyl CoA DH
  • Acetyl CoA (mitochondria type; not cytosolic bc cytosolic is for cholesterol)
81
Q

Describe ketone body formation process

A

long chain FAs from adiopose tissue, broken down after Hormone sensitive lipase action —-> get into cyto via CARNITINE TRANSPORTER –> get into mito (via CPT I, CAT, CPT II) –> reduced to acetyl CoA via fatty acyl CoA DH –> ketone bodies

82
Q

What ketone bodies are increased in diabetics?

A

acetoacetate, D-beta-hydro

83
Q

Why do chronic alcoholics get fatty liver disease?

A

Alcohol inibits expore of VLDL from liver to blood.

84
Q

What is the effect of insulin with respect to glycolysis in liver and Lipoprotein lipase in Blood/adipose?

A

stimulates:
LIVER: glucose -(via glycolosis)-> DHAP –> Glycerol 3-P –> TAG –> VLDL)

insulin also stimulates LPL allow more update of 3 FA CoA in adipose to convert to –> TAG

85
Q

What is the pathway for activating Hormon-sensitive lipase?

A

ADIPOSE Glucagon (epi) –> activate adenlyl cyclase –> cAMP –> PKA –> HSL activated to get into lipid droplet to hydrolyse TAG to monoacylglycerol

–> MGL / FA –> adipocyte –> circulation –> myocyte –> beta oxidation/TCA/respiratory chain –> ATP + CO2 + Serum albumin

86
Q

Acyl-CoA DH

A

can have specificity for different FAs

-uses FAD (to FADH2) to oxidize the beta

87
Q

beta ox

A

1:16

88
Q

Which will yield more ATP:

an 18C FA with unsat (double bond) at position 9 or position 6?

A

Unsat at Position 9 (bc unsat at even posiiton results in loss of 3 ATP)

89
Q

What enzyme is required to absorb biotin in diet?

A

biotinase (remove covalently bound biotin from proteins in diet)

90
Q

How does Biotin deficincy slow FA production?

A

The formation of malonyl-CoA via acetyl-CoA carboxylase requires biotin as a cofactor

NB: citrate lyase, malic enzyme, FA synthase do not require biotin for their activity

GI (17 decks)

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