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FOM Quiz 4 > 10/1 Metabolism > Flashcards

10/1 Metabolism Flashcards

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1
Q

What makes ketones?

A

Kidney

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2
Q

where are ketones used?

A

just about everywhere except the liver (not in the red blood cells)

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3
Q

How is most of our energy stored?

A

It is stored as fat in most cases.

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4
Q

in what ways does fatty acid oxidation support blood glucose during fasting?

A

It provides the ATP to perform gluconeogenisis. It provides energy directly to most cells to prevent them from having to use glucose – see this building up after a few hours of fasting and then peaking around 2 days.

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5
Q

how to we make use of triacylglycerols?

A

hydrolyzed by lipases, releasing fatty acids and glycerol

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6
Q

how do we get fatty acids to the mitochondria?

A

they are activated to acyl-CoAs and transfereed to carnitine for transport to the mitochondria matrix

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7
Q

how do we get fatty acids into the blood from the white adipocytes?

A

triglyceride lipases release fatty acids and glycerol into the blood

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8
Q

Adds carnitine to acyl-Coa and takes off the Coa

A

Carnitine palmitoyl Transferase I (CPTI)

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9
Q

why do we transfer a Carnitine onto Acyl-CoA and take the CoA off?

A

In order to move the acyl molecule across the mitochondrial matrix (the membrane) and into the mitochondria

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10
Q

What happens to the Acyl Carnitine once it is moved accross the mitochondrial matrix and it is now in the mitochondria

A

It interacts with carnitine palmitoyl transferase II (CPTII) and gets the carnitine group removed and a CoA added back on.

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11
Q

What is inside the mitochondria that will remove a carnitine from Acyl carnitine and add a CoA?

A

carnitine palmitoyl Transferase II (CPTII)

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12
Q

one of the adipose triacylglycerol lipases that is sensetive to the catecholamines and insulin/glucagon

A

Hormone-sensitive lipase

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13
Q

Attached to the luminal surface of endothelial cells that line the capillaries in tissues that can oxidize or store fatty acids (muslce, adipose etc.), and aids in taking up these molecules

A

Lipoprotein lipase

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14
Q

very large molecules of fatty acids

A

Chylomicron

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15
Q

triglyceride-rich lipoprotein particle sectreted by the liver – fasting serum triglycerides

A

VLDL

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16
Q

what is the key intermediate in making de novo fat from Acetyl CoA when blood glucose is high and insulin is high

A

Malonyl Coa

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17
Q

Inhibits CTPI and prevents the transfer of Acetyl CoA accross the mitochondria for use in TCA

A

Malonyl CoA

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18
Q

when is Malonyl CoA in high levels

A

when there is lots of ATP insulin and Glucose

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19
Q

how does high levels of ATP, glucose, and Insulin inhibit the use of fatty acids in mitochondria

A

by making Mallonyl CoA from acetyl CoA and then making fatty Acyl CoA from the Malonyl CoA and Malonyl CoA inhibits transport into the mitochondria.

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20
Q

when would CPT1 be activated? and inhibited?

A

it would be inhibited when glucose and insulin is low i.e. after a carbo meal; and it would be activated when fasting or exercising!

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21
Q

what is Malonyl CoA in in the metabolic map (what is its big functional role)

A

It acts as an intermediate in fatty acid synthesis (also acts to inhibit the use of fatty acids in the mitochondria by blocking CPT1)

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22
Q

Consumption of a carbohydrate-rich meal simultaneously activates fat synthesis and inhibits fat oxidation in the liver. One known
mechanism for both outcomes is:

A

Activating the synthesis of malonyl CoA

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23
Q

what hydrolyzes and releases fatty acids and glycerol from adopocytes?

A

Lipases (this is a key reg. step)

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24
Q

what happens to fatty acids once they make it into a cell with the intent of using that fatty acid for energy?

A

they are activated to acyl-CoAs and transferred to carnitine for transport into the mitochondrial matrix

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25
Q

what is the major, but not the only pathway of fatty acid oxidation?

A

beta-oxidation of fatty acids

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26
Q

What is an important fuel sorce during starvation or low carb diet that come mainly from the acetyl CoA of fatty acid oxidation?

A

Ketone bodies

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27
Q

What happens if I have very low insulin (diabetes)

A

excessive fatty acid release from adipose and excessive ketone body production in the liver!!!

28
Q

Describe the B-oxidation of fatty acids

A
  1. make FADH2 as you oxidize the beta carbon of a fatty acid with a double carbon bond.
  2. use water to oxidize the beta carbon by adding an OH group to it
  3. produce NADH by oxidizing the beta carbon by adding a oxygen double bond.
  4. add a CoA group to make an Acetyl-CoA group come off of the chain of fatty acids.
  5. repeat to make another acetyl coA!!!
29
Q

When you have an oxidation, what type of enzyme do you expect?

A

Dehydrogenase

30
Q

what could cause a low blood glucose, with beta hydrozxybutyrate and acetoacetate very low, and C8-octanoyl carnitine elevated?

A

Medium chain Acyl CA dehydrogenase deficiency!
Explination: there is a specific dehydrogenase for medium chain fatty acids, and if this is not working then there will be a build up of medium chain fatty acids as seen above.

31
Q

how could an unused medium length fatty acid chain that was in the mitochondria end up back in the blood stream?

A

in the mitochondria the addition of carnitine and the transferance of the fatty acid witht he addition of carnitine is a reversible process!!! so if it builds up in the mitochondria it will just get tagged with carnitine and sent back out of the mitochondria.

32
Q

Why would a person who can’t fully digest fat have a low blood glucose

A

Gluconeogenisis needs lots of ATP so if you are not breaking down fats then you can’t get the energy to generate glucose form gluconeogenisis. The brain would also be using more glucose instead of ketones during fasting (as other parts of the body would) therefore glucoes supply is down, and use is up!

33
Q

what do we get from metabolizing fatty acids?

A

NOT GLUCOSE – (UNLESS ODD CHAIN FATTY ACIDS) you get ketones that can feed into the TCA cycle

34
Q

What does the brain use for energy when you are fasting?

A

Ketones!!! from fatty acid beta-oxidation. But the brain can not use the fatty acid directly! It can only use glucose or keytones.

35
Q

Explain the main metabolic pathways for maintaining glucose levels

A

lucogen, gluconeogenesis, ketosis!

36
Q

what does the liver do to provide energy to the brain during times of starvation?

A

It makes acetyl CoA from fatty acids, and then makes these into acetoacetate that converts to acetone (ketones) that are sent to the brain, and then converted back to acetyl coA and used to produce ATP (energy!)

37
Q

what are the eventual products of the beta-oxidation of fatty acids in the liver?

A

TCA cycle precursor used in the liver (to produce energy and to do Gluconeogenisis, enough to meet the needs of the liver); Ketone body synthesis (to send ketones around the body for energy use); Fatty acid and sterol synthesis (stimulated by high insulin and glucose levels!).

38
Q

Why would we need to maintain a level of insulin in the blood even when we are fasting and we have no major blood glucose presence coming in?

A

we need to maintain a level of insulin to prevent ketoacidosis that occurs when the use of ketones rises way too high (4X normal), and the blood gets acidic from overwhelming the blood buffers.

39
Q

what happens when eating carbs in pancreus?

A

up insulin and down glucagon

40
Q

what happens to the liver when eat carbs?

A 
down gluconeogenisis
down glycogenlysis
down b-oxidation
up glycogen synthesis
up glycolysis
up FA synthesis
up Protein synthesis 
release VLDL
41
Q

what happens in the muscle when eat carbs

A 
up GLUT 4 transport of glucose in 
up glycolyis
up protien synthisis
up glycogen synthesis
down proteolysis
down beta-oxidation
42
Q

what happens in adiposis tissue when eat carbs

A

UP GLUT 4 transport of glucose into the cells
Up Triacyle glyceride synthesis
up glycolysis
Down Lipase activity
Down the release of fatty acids.
Increase in LPL activity (lipo protein lipase) increase the uptake and storage of fats from the blood stream (increase the fat droplet size in the adipocytes).

43
Q

where are lipoprotien lipases located and what does it do?

A

inside the lumen of the capillaries to snag and import lipase from the blood and move it into the adipocytes.

44
Q

what happens in the pancreas in the basal state (absorbed the last meal completely)

A

Down in insuin

Up in glucagon

45
Q

what happens in the liver as we go into the basal state?

A 
up gluconeogenisis
Up Break down glycogenolysis
release glucose into the blood
Up B-oxidation
down glycolysis
down glycogen synthesis
down fatty acid synthesis (not making a lot of malenocoA so allow use of fatty acids in b-ox)
46
Q

what is the first means of sustaining blood glucose (2-4 hours)?

A

Break down of glucon in the liver to send out glucose to the blood

47
Q

what happens to adipocytes as we go into the basal state?

A

they release Fatty acids
Up in lipase activity (this leads to the release of FA)
release glycerol (that can be converted to glucose)

48
Q

why do we release glycerol from adipocytes and proteins from muscle when we don’t eat much

A

They can both lead to the production of glucose!

49
Q

what happens to muscle when we go into the Basal or post-absorptive stage after finished eating for awhile?

A 
up proteolysis
up beta-oxidation
up release amino acids.
up glycogenolysis
down GLUT 4 transport of glucose 
down glycolyis
down protien synthisis
down glycogen synthesis
50
Q

what activates and inhibits lipases in the adipocytes?

A

Activated by Catecholamine (epinephrine and norepinephrine), and some lipases activated by glucagon;
and inhibited by insulin.

51
Q

when do we release fatty acids form adipose?

A

when insulin and blood glucose are low.

52
Q

what happens after 1-2 days of no carbohydrate consumption? in the liver

A

increase beta-oxidation of fatty acids in the liver. make more acetyl coA to use in TCA for liver energy needs (and maintain a level of gluconeogenesis) and then makes lots of ketones (acetone) to send into the blood!

53
Q

What happens to fatty acids in the blood when no carbs for 1-2 days?

A

increase!

54
Q

what is the result of extreme low insulin levels?

A

excessive fatty acid release from adipose and excessive ketone body production in the liver.

55
Q

pancreas after 24 hours no food

A

low insulin and high glucagon

56
Q

liver after 24 hours no food

A 
loss of glycogen stores
gluconeogenesis continues to increase (using energy from fatty acid catabolism)
Ketogenesis spikes way up
up release of ketones
lowering release of glucose
57
Q

after 24 hours no food adipose

A

constant fatty acid lipase activity and release of fatty acids
release glycerol

58
Q

after 24 hours no food muscle

A 
up proteolysis
up beta-oxidation
up release amino acids.
down GLUT 4 transport of glucose 
down glycolyis
down protien synthisis
down glycogen synthesis
59
Q

after several days of no food

A

Gluconeogenesis drops down to a low constant level
ketogenesis and use in other tissues spikes way up
Fatty acid release and use in B-oxidation stays the same

60
Q

what is an omega-3 and omega-6 fatty acid?

A

fatty acid with double bond on the third or sixth carbon from the omega end!

61
Q

why are omega-3 and omega-6 fatty acids essential

A

humans lack enzymes that can add double bonds near the omega ends of fatty acids

62
Q

what are common dietary sources of saturated fatty acids

A

butter, and other forms of solid fat

63
Q

what are common dietary sources of unsaturated fatty acids?

A

Vegie oils and other liquid fats

64
Q

the most common dietary w3 and w6 fatty acids

A

linoleic and linolenic acids.

65
Q

hydrolizes triacylglycerols

A

lipases

FOM Quiz 4 (22 decks)

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