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unit 6 mcp > fatty acid storage, mobilization and oxidation > Flashcards

fatty acid storage, mobilization and oxidation Flashcards

1
Q

fat storage is promoted by?

A

INSULIN promotes fat storage

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2
Q

adipocytes release __________ in response to insulin?

A

LIPOPROTEIN LIPASE is released by adipocytes in response to insulin

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3
Q

Fatty acids are unloaded from____ and _____ and taken up by adipocytes?

A

CHYLOMICRONS and VLDL

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4
Q

________ promotes glucose uptake into adipocytes?

A

INSULIN

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5
Q

What is the primary fat we store?

A

TRIGLYCERIDES

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6
Q

fat storage mainly occurs in the ________ but can also occur in the ____ or ______ through break down of triglycerides

A

fat storage mainly occurs in the _ADIPOCYTES__ but can also occur in the LIVER or _MUSCLE____ through break down of triglycerides

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7
Q

How does insulin promote glucose uptake by adipocytes?

A

by promoting translocation of GLUT4 glucose transporters to the plasma membrane

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8
Q

In the fed state insulin leads to the inhibition of what enzyme and explain what that enzyme does?

A

in the fed state insulin leads to the inhibition of HORMONE SENSITIVE LIPASE which hydrolyzes stored TG.

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9
Q

Non esterified fatty acid released through the action of lipoprotein lipase are transported into adipocytes by __________?

A

FATTY ACID TRANSPORTERS ( FATP1)

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10
Q

In addition to promoting translocation of glucose transporters to the plasma membrane insulin promotes translocation of _____ to the plasma membrane?

A

Insulin promotes translocation of FATTY ACID TRANSPORTERS to the plasma membrane.

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11
Q

Once in the adipocyte long chain FATTY ACIDS are bound to?

A

ALBP ( adipocyte lipid binding protein)

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12
Q

Once in the adipocytes fatty acids can be used as fuel or stored as triglyceride. In order to use fatty acids in either case what must happen and what enzyme catalyses the reaction?

A

In oder to store fatty acids as triglycerides or use it in the adipocyte the Non esterified fatty acid must be converted to FATTY ACYL_COA via action of THIOKINASE (I aka ( ACYL-COA SYNTHETASE)

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13
Q

what happens to glycerol in the liver and kidneys but not in adipocytes?

A

in the liver and the kidneys glycerol is converted to GLYCEROL 3 PHOSPHATE but this doesn’t happen in adipocytes.

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14
Q

what two enzymes are at work in forming esterified fatty acids : a glycerol backbone?

A

THIOKINASE ANDS ACYL TRANSFERASES

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15
Q

Fat mobilization AKA LIPOLYSIS involves?

A

de-esterification: the hydrolytic release of fatty acids from triglycerides

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16
Q

Fats are successively released from triglycerides. diacylglycerol, and monoacylglycerol by _________?

A

ESTERASES

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17
Q

the best studied esterase is?

A

HORMONE SENSITIVE LIPASE

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18
Q

Hormone sensitive lipase releases fatty acids preferentially from?

A

diacylglycerols and monoacylglycerols,

in this process hormone sensitive lipase is mainly responsible for catalyzing the second and third steps yielding Non esterified fatty acid and glycerol

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19
Q

what is Hormone Sensitive Lipase activated by?

A

HSL is activated by catecholamines and glucagon

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20
Q

Hormone Sensitive Lipase has broad specificity in that?

A

in addition to preferential release of fatty acids from diacylglycerols and monoacylglycerols, it also releases fatty acids more slowly from triglycerides, retinyl esters and cholesterlyl esters

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21
Q

Where are hormone sensitive lipases usually found?

A

they are usually found in adipocytes and in cells that produce steroid hormones

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22
Q

what are some examples of enzymes other than hormone sensitive lipases which are involved in t releasing fatty acids from triglycerides?

A

adipose tryglyceride lipase

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23
Q

what is adipose tryglyceride lipase important for?

A

adipose tryglyceride lipase catalyzes the rate limiting step in lipolysis

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24
Q

is adipose triglyceride lipase found only in adipocytes only?

A

no it’s also found in other cells where triglycerides can accumulate.

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25
Q

when insulin binds and activates phosphatase what happens to hormone sensitive lipase?

A

insulin binding to phosphatase results in the decrease in production of hormone sensitive lipase.

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26
Q

phosphorylated hormone sensitive lipase is more________

A

active

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27
Q

hormone sensitive lipase is phosphorylated by ___________ in response to _____________

A

hormone sensitive lipase is phosphorylated by _CAMP DEPENDENT PROTEIN KINASE__________ in response to ___CATECHOLAMINES__________

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28
Q

Nonesterfied fatty acids inhibit hormone sensitive lipase by product inhibition. But the physiological significance of this is unclear, since albp rapidly shuttles mobilized fatty acid to the cell surface where they are loadsed onto_____

A

serum albumin

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29
Q

what is a key regulatory event in lipolysis that is even more important than the phosphorylation of hormone sensitive lipase?

A

the phosphorylation of the protein PERILIPIN by cAMP dependent protein kinase

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30
Q

what do perilipins allow for?

A

perilipins allow access to triglyceride droplets

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31
Q

are the central or peripheral lipid storage droplets the metabolically active ones?

A

the peripheral droplets are metabolically active in lipolysis

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32
Q

w/o hormone stimulation hormone sensitive lipase and other lipases can’t access the peripheral fat croplets due to_________

A

a layer of perilipins. These perlipins are phosphorylated in response to hormones which disrupts the layer and allows lipases to get to the triglycerides in the fat droplets.

33
Q

nonesterfied fatty acids are transported in the bloodstream bound to ______ which comprises about half of the total protein in plasma.

A

ALBUMIN

34
Q

once glycerol leaves via an aquaporin and is taken up by liver and kidney what process can’t be done?

A

triglycerides can’t be synthesized once glycerol leaves the fat cell.

35
Q

fatty acids are always

A

bound to something ( even if they are “ free”

36
Q

what are the two nomenclatures for naming fatty acids?

A

delta and omega

37
Q

how does the delta nomenclature of naming fatty acids work?

A

counting from the carboxyl carbon as carbon 1: the # of carbons: # of double bond, delta sign, Carbon #s of double bonds starting with the one closest to the 1st carbon. eg. 18:2 (delta)9,12 ( see page 211

38
Q

how does the omega nomenclature work for naming fatty acids?

A

counting from the methyl carbon as carbon 1: the # of carbons: # of double bond, omega sign, Carbon #s of the 1st double bondclosest to the 1st carbon. eg. 18:2 (omega)- 6 ( see page 211). The other double bonds are left out because they are usually 3 away from the first one so it can be assumed.

39
Q

what are the four classes of fatty acids?

A

omega-7. omega-9 ( nonessential)

, omega-6, and omega-3 ( essential)

40
Q

what does essentila vs nonessenial mean for fatty acids?L

A

essential fatty acids are polyunsaturated fatty acides ( omega 3’s and 6’s ) because we can’t make double bonds so close to the omega end.must be obtained from diet because we can’t make them.

41
Q

besides beta oxidation in mitochondria what 3 pathways of fatty acid oxidation exist?

A

beta oxidation of really long chain fatty acids and polyunsaturated fatty acids in peroxisome: shortened fatty acids then go to mitochondria for further oxidation,

alpha oxidation of branched chain fatty acids in the mitochondria

omega oxidation in the ER

42
Q

how may ATPS are invested in the 1st step of beta oxidation: the activation of fatty acids catalyzed by acyl-CoA synthetase ( AKA thiokinase)?

A

2 ATP are invested in the 1st step of beta oxidation

43
Q

how many phases produce ATP from fatty acids?

A

5 ( see page 213 for the list)

44
Q

what is the overall goal of phase 2 of beta oxidation?

A

getting the fatty acid into the mitochndria

45
Q

what is phase 2a of beta oxidation?

A

transfer of a long chain fatty acid moiety from CoA to Carnitine ( the enzy used is carnitine palmitoyl transferase)

46
Q

what is phase 2b of beta oxidation?

A

acyl-carnitine is transported across the Inner mitochondria matrix and the acyl moiety is transferred back to CoA

47
Q

what is phase 3 of beta oxidation?

A

acyl -CoA enters the beta oxidation pathway

48
Q

entry of long chain fatty acids into the mitochondria is

A

a major point of control in the metabolism

49
Q

long chain fatty acids can’t get into the mitochondria when a lot of what is around?

A

when a lot of malonyl-CoA is around.

50
Q

malonyl CoA is the product of the

A

first committed step in fatty acid biosynthesis

51
Q

in beta oxidation how many ATPs do we get for each reduced flavin ( FADH2)?

A

2 ATPs

52
Q

in step 1 of beta oxidation how many distinct acetyl CoA dehydrogenases are there?

A

there are 3 distinct acetyl CoA dehydrogenases for short, medium, abnd long chain fatty acids

53
Q

for steps 2-4 how many enzymes are working?

A

1 trifunctional enzyme

54
Q

how does beta oxidation compare to glycolysis in terms of energy production/efficiency?

A

beta oxidation produces 8 ATP per carbon oxidized where as glycolysis produces only 6 so beta oxidation is more efficient.

55
Q

a highly reduced compound yields more energy than a less reduced compound when it ?

A

goes through the complete oxidation

56
Q

how many ATPs does a double bond cost

A

it takes 2 or 3 ATPS to make a double bond

57
Q

what 2 problems arise in the oxidation of unsaturated fatty acids?

A

the beta , gamma double bond, and the dela 4 double bond

58
Q

how is the beta, gamma double bond problem in unsaturated fatty acid oxidation fixed?

A

through the use of enoyl-CoA isomerase which does not cost any ATP

59
Q

how is the delta 4 double bond problem in unsaturated fatty acid oxidation fixed?

A

reduction by NADPH_ dependent reductase and then a an isomerase to change the position of the double bond

60
Q

WHen and where are ketone bodies produced in a normal person

A

Ketone bodies are normally produced in the liver during fasting a starvation.

61
Q

What are ketone bodies?

A

ketone bodies are water soluble equivalents of fatty acids produced only in the liver mitochondria.

62
Q

what are the 3 ketone bodies?

A

acetoacetate, acetone, and beta hydroxybutyrate

63
Q

what is the primary ketone body made which gets converted to the other 2?

A

acetoacetate

64
Q

how does acetoacetate convert to acetate and what happens to acetate?

A

acetoacetate spontaneously converts to acetone and acetone is lost through breath or skin

65
Q

where does ketogenesis occur?

A

in the mitochondria of liver and the ketone bodies are released into the plamsa

66
Q

what are ketobodies particular important for?

A

they are used as fuel especially by the brain during starvation

67
Q

ketones are preferred over glucose in which organs?

A

in the heart muscle and in the renal cortex

68
Q

acetyl coA formed in fatty acid metabolism will enter the TCA cycle only if?

A

if fat and carbohydrate degradation are appropriately balanced

69
Q

what do high levels of acetyl coA inhibit?

A

high levels of acetyl coA inhibit pyruvate dehydrogenase

70
Q

high levels of acetyl coA activate __________ and lead to increased ________?

A

and activate pyruvate carboxylase leading to increased levels of OAA

71
Q

if glycolysis is deficien then what will be diverted for synthesis of glycolysis?

A

oxaloaxetate

72
Q

what happens when NADH is too high?

A

high levels of NADH also promote conversion of OAA to malate and malate leaves the mitochondria and is used for gluconeogenesis

73
Q

During fasting, heavy alcohol use, high fat/ low carb diets and uncontrolled diabetes excess acetyl coA produced via beta oxidation of fatty acids will not be able to enter the citric acid cycle but instead will?

A

be diverted to make ketone bodies

74
Q

can the liver use ketone bodies as fuel?

A

no the liver can’t use ketone bodies as fuel b/c the liver doesn’t have the key enzyme for ketone body utilization: acetoacetate: succinyl- CoA transferase or 3- ketoacyl CoA transferase

75
Q

what tissues can’t make ketone bodies?

A

only the liver can make ketone bodies, all extrahepatic tissues can’t make it because their mitochondria lack the high levels of HMG-CoA synthase found in the liver mitochondria and non-liver mitochondria lack HMG-CoA lyase in general.

76
Q

ketoacidosis is really a __________ problem

A

ketoacidosis is really a FAT METABOLISM problem

77
Q

what happen is ketoacidosis?

A

there is an over production of ketone bodies, the pH drops which is life threatening

78
Q

why does ketoacidosis occur more in diabetes melitus type I?

A

ketoacidosis occurs mainly in DM type 1 and not DM type 2 because in the absence of insulin and when stress hormones are high hormone sensitive lipase and perilipins are fully active leading to runaway lipolysis.

79
Q

because insulin is present in non-diabetic type I ppl, during prolonged starvation ketoacidosis doesn’t occur but what does occur

A

in normal ppl during prolonged starvation ketosis i.e. the elevated blood levels of ketone bodies occurs but ketoacidosis doesn’t occur.

unit 6 mcp (6 decks)

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