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POM Exam 1 > L14: Lipid Metabolism > Flashcards

L14: Lipid Metabolism Flashcards

1
Q

fatty acid

A
  • long hydrocarbon chains ending in a carboxylic acid group
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2
Q

saturated

A
  • no double bonds
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3
Q

unsaturated

A
  • double bonds
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4
Q

cis configuration

A
  • Hs on the same side
  • causes chain to kink
  • most double bonds are bound in cis
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5
Q

trans configuration

A
  • Hs on opposite side
  • does not kink
  • resembles saturated fatty acid
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6
Q

double bonds and Tm

A
  • more double bonds - lower Tm

- cis double bond - lower Tm than trans

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7
Q

length and Tm

A
  • longer length - higher Tm
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8
Q

good for energy storage

A
  • reduced and anhydrous
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9
Q

caloric yield

A
  • oxidation provides a good bit of energy
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10
Q

lack of hydration

A
  • have no H20 so pack well
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11
Q

storage of triglycerides

A
  • stored in adipose cells
    • fat cells accumulate around skin and internal organs
    • droplets of triacylglycerides coalesce into lipid droplets
    • lipid droplets surrounded by a membrane with proteins involved in fatty acid metabolism
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12
Q

issues in lipid digestion

A
  • triacylglycerides are insoluble in water

- enzymes that degrade them are water soluble

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13
Q

solution to insolubility of triacylglycerides

A
  • digestion takes place at lipid-water interfaces
  • lipids are emulsified so lipase have access to their surface
  • emulsification occurs through chewing, intestinal churning, and bile salts
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14
Q

acid lipases

A
  • lingual

- gastric

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15
Q

alkaline lipases

A
  • pancreatic lipase
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16
Q

degradation and transport of triacylglycerides

A
  • degraded fatty acids form micelles transported to intestine
  • reassemble into triacylglycerides and are packing into chylomicrons for release into lymph and blood
  • fat cells and muscle bind particles
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17
Q

fat cells use of chylomicrons

A
  • degrade them into fatty acids and monoglycerides for storage
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18
Q

muscle use of chylomicrons

A
  • oxidize them for energy
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19
Q

fasting state hormones

A
  • glucagon (alpha cells) bind glucagon receptor
  • epinephrine (adrenal medulla) binds adrenergic receptor
  • GCPR pathway
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20
Q

fatty acid mobilization by hormone induction

A
  • glucagon and epinephrine trigger a rise in cAMP that stimulates protein kinase A
  • protein kinase A phosphorylates perilipin and hormone sensitive lipase
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21
Q

functions of perilipin

A
  • restructure fat droplets to triacylglycerides are more accessible to mobilization
  • triggers release of a coactivator of adipose triglyceride lipase
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22
Q

function of adipose triglyceride lipase

A
  • degrades triacylglycerides into diacylglycerides
    • DAG degraded to monoacylglycerol
    • monoacylglycerol degraded to fatty acids and glycerol
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23
Q

Chanarin-Dorfman Syndrome genetics

A
  • mutation in coactivator for adipose triglyceride lipase
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24
Q

Chanarin-Dorfman Syndrome result

A
  • fat accumulate throughout body since fatty acids cannot be degraded and released by adipose triglyceride lipase
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25
Q

Chanarin-Dorfman Syndrome symptoms

A
  • dry skin
  • enlarged liver
  • muscle weakness - can’t break down for energy
  • overheating
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26
Q

fatty acid and glycerol transport

A
  • bind to albumin in blood

- since they are not water soluble

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27
Q

glycerol utilization

A
  • absorbed in liver
  • converted to glyceraldehyde-3-phosphate
    • intermediate in glycolytic and gluconeogenic pathways
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28
Q

fatty acid utilization

A
  • fatty acids separate from albumin and are transported into cell
  • enter mitochondria for oxidation to acetyl CoA that enters TCA
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29
Q

activation of fatty acids

A
  • before transport into mitochondria
  • fatty acids linked to coenzyme A at outer mitochondrial membrane
    • via thioester
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30
Q

thirster linkage between fatty acid and acetyl CoA

A
  • forms acyl-CoA
  • catalyzed by fatty acid CoA synthetase
  • AMP exchanged for CoA (use of ATP)
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31
Q

conjugation for transport

A
  • conjugation to carnitine to form acylcarnitine by carnitine acyltransferases
  • loses CoA
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32
Q

acylcarnitine transport

A
  • shuttled across inner mitochondrial membrane by translocase
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33
Q

once acylcarnitine is in mitochondria

A
  • reaction is reversed
  • acyl CoA reformed
  • carnitine also reformed for transport back to the cytoplasmic side
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34
Q

carnitine deficiencies cause

A
  • defects in multiple proteins

- including acyltransferases

35
Q

carnitine deficiencies result

A
  • affects transport of long-chain fatty acids into mitochondria
  • lipid deposits accumulate
36
Q

carnitine deficiencies symptoms

A
  • weakness
  • hypoglycemic
  • hypoketoic
  • precipitated by exercise or fasting
37
Q

carnintine deficiency example

A
  • systemic primary carnitine deficiency

- defect in translocase

38
Q

beta oxidation of fatty acids occurs where

A
  • in the mitochondria
39
Q

four reactions for beta oxidation

A
  • oxidation by FAD and acyl CoA dehydrogenase
  • hydration by enol CoA hydrates
  • oxidation by NAD+ and beta hydroxyl acyl CoA dehydrogenase
  • thiolysis by CoA-beta-keto thiolase
40
Q

continual degradation of fatty acids

A
  • further degraded by acyl CoA dehydrogenase with different enzymes depending on size of fatty acid
  • long
  • medium
  • short
41
Q

medium chain acyl-CoA dehydrogenase deficiency result

A
  • accumulation of medium-chain fatty acids and derivates
42
Q

medium chain acyl-CoA dehydrogenase deficiency symptoms

A
  • lethargy
  • hypoglycemia
  • sudden death precipitated by fasting or vomiting
43
Q

key difference between odd-chain and even chain fatty acid metabolism

A
  • end product is one propionyl CoA and one acetyl CoA

- instead of two acetyl CoA

44
Q

fate of propionyl CoA

A
  • enters TCA cycle after conversion to succinyl CoA

- used to produce glucose via gluconeogenesis

45
Q

acetyl CoA gives how many ATPs?

A
  • 10
46
Q

palmitate activation takes how many ATPs

A
  • use 2 ATP to start it
47
Q

fatty acid energy yield

A
  • n cycles

- n FADH2, n NADH, n H+, n+1 acetyl CoA

48
Q

main source of ketones

A
  • the liver
  • fatty acids
  • amino acids from protein breakdown
49
Q

is acetone an energy source

A
  • no
50
Q

formation of ketones

A
  • acetyl-CoA formed during fatty acid oxidation only enters TCA cycle in presence of oxaloacetate
  • oxaloacetate is present only when an adequate supply of glucose
  • during fasting or with diabetes, oxaloacetate is used to form glucose and can’t react with acetyl-CoA
  • acetyl-CoA diverted to form ketone bodies instead
51
Q

what is one way to diagnose if someone has high levels of ketones?

A
  • acetone on the breath

- smells fruity

52
Q

ketone as fuel

A
  • acetoacetate converted to acetyl-CoA

- d-beta-hydroxybutyrate oxidized to NAD+ to yield acetoacetate

53
Q

then glucose isn’t present, what does the brain use?

A
  • uses ketone bodies for fuel during starvation
  • after about 3 days of fasting
  • glycerol converted into glucose
54
Q

how fatty acid breakdown causes ketone levels to rise

A
  • adipose cells supply fatty acids for breakdown during fasting
  • liver converts them into ketone bodies but doesn’t use them for fuel
  • supply peripheral organs with a fuel source
  • glucose saved for brain
55
Q

type I diabetes

A
  • cannot produce insulin - take up glucose or curtail fatty acid mobilization
  • liver can’t absorb glucose or provide oxaloacetate to process fatty-acid derived acetyl-CoA
  • adipose cells release fatty acids that are taken up by liver and converted to ketone bodies
  • ketone bodies are strong acids
56
Q

high levels of ketone bodies

A
  • decrease blood pH
  • impair tissue function
  • especially in CNS
57
Q

what organs can synthesize fatty acids

A
  • liver and adipose cells
58
Q

major source of carbon for fatty acid synthesis

A
  • carbohydrate, but protein can be used
59
Q

start fatty acid synthesis

A
  • start with acetyl-CoA
60
Q

transport of acetyl coA

A
  • formed in mitochondria and must be transported to cytoplasm
  • reacts with oxaloacetate to form citrate in mitochondrial matrix
  • citrate transported to cytoplasm through citrate shuttle and cleaves by ATP-citrate lyase to form acetyl-CoA
61
Q

bring oxaloacetate back to mitochondria

A
  • oxaloacetate reduced to malate by malate dehydrogenase
    • requires NADH
  • malate decarboxylated to pyruvate by malic enzymes
    • generates NADPH
  • pyruvate enters mitochondria and is carboxylated to oxaloacetate by pyruvate carboxylase
62
Q

energy requirement of fatty acid synthesis

A
  • requires NADPH
  • comes from PPP
  • or reduction of malate
63
Q

committed step of fatty acid synthesis

A
  • formation of malonyl CoA by acetyl-CoA carboxylase
64
Q

formation of malonyl CoA

A
  • glucose -> acetyl CoA

- acetyl coA -> malonyl CoA

65
Q

biotin

A
  • vitamin B7
66
Q

fatty acid intermediates attached to

A
  • acyl carrier protein linked to fatty acid synthase

- serine of ACP linked to phosphopantetheine that contains pantothenic acid

67
Q

pantothenic acid

A
  • vitamin B5
68
Q

condensation reactions

A
  • ACP transfers reduced product to ketosynthesase and is recharged with another malonyl CoA to extend the chain
  • process repeated until thioesterase releases final C16 palmitic acid
69
Q

synthesis of triacylglycerides

A
  • formed from glycerol-3-phosphate and fatty acid acyl CoA to form phosphatidic acid
  • phosphatic acid dephoshorylated to form diacylglyceride
  • fatty acyl CoA interacts with diacylglyceride to form triacylglyceride
70
Q

transport of triacylglycerides

A
  • synthesized in liver

- packages in very low density lipoproteins for transport to adipose cells or muscle

71
Q

fate of very low density lipoproteins

A
  • on capillaries adjacent to muscle and liver cells they are digested by lipoprotein lipase into fatty acids and glycerol
  • fatty acids enter cell and used for energy in muscle and stored in adipose cells and reassembled as triacylglycerides
  • glycerol shunted back to the liver for use in triacylglyceride synthesis and glujconeogeneis or glycolysis
72
Q

regulated step in fatty acid synthesis

A
  • acetyl-CoA - > malonyl CoA

- by acetyl CoA carboxylase

73
Q

activators of fatty acid synthesis

A
  • citrate

- causes enzyme to polymerize into active filaments and make more fatty acids

74
Q

inhibitors of fatty acid synthesis

A
  • palmitoyl CoA

- negative feedback

75
Q

fed state

A
  • energy levels and glucose high
  • fatty acid synthesized for storage
  • insulin inhibition mobilization and stimulates fatty acid storage
76
Q

insulin and fatty acid synthesis

A
  • stimulates phosphatase that dephosphorylates and activates acetyl CoA carboxylase
77
Q

high carb, low fat diets

A
  • increase in amounts of acetyl-CoA carboxylase and fatty acid synthase
  • increase in fatty acid synthesis
78
Q

fasting state

A
  • low energy status (AMP high)
  • stimulates AMP kinase
  • phosphorylates and inhibits acetyl-CoA carboxylase (enzyme that synthesizes fatty acids)
    • utilizes ATP
79
Q

glucagon

A
  • stimulates breakdown of triacylglycerides from fat cells
80
Q

tumor cells

A
  • use fatty acid synthesis to generate signaling molecules and membrane phospholipids
  • enzymes of fatty acid synthesis over expressed
81
Q

anti-tumor therapies

A
  • inhibit fatty acid synthesis enzymes
82
Q

inhibiting beta-ketoacyl-ACP synthase

A
  • reduces phospholipid synthesis and cell growth

- leads to apoptosis

83
Q

inhibiting acetyl-CoA carboxylase

A
  • induces apoptosis in cancer cell lines

POM Exam 1 (16 decks)

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