Metabolism Flashcards

1
Q

What is normal blood pH?

A

7.35-7.45

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2
Q

What are the most common causes of ketoacidosis?

A

diabetes mellitus (typically type 1) and acute alcohol intoxication.

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3
Q

How do the symptoms of ketoacidosis manifest?

A

High circulating ketone bodies are accompanied by excretion of anions in the urine causing the loss of sodium ions and excess water, leading to dehydration. Other symptoms include excessive thirst, freq urination, N/V, abdominal pain, fruity breath odor, SOB and confusion.

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4
Q

Why do humans need to obtain n-6 and n-3 PUFAs in the diet?

A

Because humans do not express any delta-12 or delta-15 desaturates, double bonds cannot be inserted beyond the delta-9 position/carbons from the carboxyl end of the fatty acid.

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5
Q

What type of PUFA is linoleum acid?

A

18:2n-6

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6
Q

What type of PUFA is alpha-linolenic acid?

A

18:3n-3

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7
Q

What PUFAS must be obtained in the diet?

A

Linoleic Acid (18:2n-6) and alpha-linolenic acid (18:3n-3). or longer chain members of the n-6 and n-3 classes.

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8
Q

What longer chain PUFAs does Linoleic acid metabolize to?

A
Linoleic Acid (18:2n-6) > 
gamma-Linolenic Acid (18:3n-6) > > 
Arachadonic Acid (20:4n-6) >
Adrenic Acid (22:4n-6) >
Tetracosatetraenoic Acid (24:4n-6) >
Tetracosapentaenoic Acid (24:5n-6) >
Docosapentaenoic Acid (22:5n-6)
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9
Q

What longer chain PUFAs does alpha-linolenic acid metabolize to?

A
Alpha-Linoleic acid (18:3n-3) >
Stearidonic Acid (18:4n-3) >
Eicosatetraenoic Acid (18:4n-3) >
Eicosapentaenoic Acid (20:5n-3) >
Docosapentaenoic Acid (22:5n-3) >
Tetracosapentaenoic Acid (24:5n-3) >
Tetracosahexaenoic Acid (24:6n-3) >
Docosahexaenoic Acid (22:6n-3)
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10
Q

What type of fatty acids do VLDL transport?

A

De novo synthesis
dietary FAs returned to the liver via remnants (IDLs)
FAs released by action of HTGL
FAs spilled over from lipolysis by LPL

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11
Q

What type of fatty acids do chylomicrons transport?

A

mainly dietary FAs

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12
Q

How is fat metabolized in the fed state?

A

FAs from the diet or from de novo synthesis in the liver are incorporated into lipoproteins and preferentially stored directed to the adipose tissue for storage.

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13
Q

How is fat metabolized in the fasting state?

A

FAs are released from adipose TAG stores and made available as FAs, TAGs in VLDLs, and ketone bodies for tissues to use as fuel.

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14
Q

What is the carnitine shuttle?

A

the way in which nonesterified LCFAs are transported across the inner mitochondrial membrane for oxidation.

FA’s shorter than C12 do not require the carnitine shuttle for mitochondrial entry.

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15
Q

What is the function of mitochondrial fatty acid oxidation?

A

primarily to supply energy, both by direct oxidation of fatty acids to acetyl-CoA and by provision of substrate for ketone body synthesis.

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16
Q

What does adrenergic mean?

A

relating to or denoting nerve cells in which epinephrine (adrenaline), norepinephrine (noradrenaline), or a similar substance acts as a neurotransmitter.

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17
Q

What does cholinergic mean?

A

relating to or denoting nerve cells in which acetylcholine acts as a neurotransmitter.

18
Q

What are the conditions favorable for lipogenesis?

A

circulating glucose and insulin levels are high, cytosolic citrate is high, and lipolysis is inhibited.

19
Q

Why are HDLs good for us?

A

take up excess cholesterol from tissues for reverse cholesterol transport and excretion.

20
Q

What are the four major classes of lipoproteins found in plasma?

A

Chylomicrons, LDLs, VLDLs, HDLs.

21
Q

Cholesterol precursors and metabolites are important for synthesis of what?

A

isoprenoid compounds, steroid hormones, and bile acids.

22
Q

What is the apolipoprotein in nascent VLDL and where is it synthesized?

A

ApoB-100, each VLDL particle contains 1 single molecule. ApoB-100 is synthesized only in the liver.

23
Q

What is the apolipoprotein in nascent chylomicrons and where is it synthesized?

A

ApoB-48, each chylomicron contains 1 single molecule. It ApoB-48 is only synthesized in the intestine.

24
Q

What is the benefit of chylomicrons being secreted into the lymphatics rather than directly into the portal vein?

A

directs absorbed lipid to extrahepatic tissues without a first pass through the liver and facilitates removal of lipophilic toxins associated with absorbed fat by lymphatic leukocytes before the chylomicrons enter the blood.

25
Q

What apolipoproteins do nascent chylomicrons and VLDLs pick up to become mature?

A

Nascent chylomicrons carry some ApoA-I and ApoA-II out of the enterocytes.
Nascent VLDLs carry some ApoC-I and ApoE out of the hepatocytes.
Once in circulation, they pick up other apolipoproteins especially ApoC-II and ApoE from circulating HDLs to become mature chylomicrons and VLDLs.

26
Q

What does the conversion from IDL and LDL involve the loss of?

A

80-90% of the TAGs in IDLs, as well as some phospholipids, any remaining ApoC proteins, and all of the remaining ApoE.

27
Q

Plasma contains more of which ApoB and why?

A

More ApoB-100 than Apo-48 because LDLs are cleared slowly from the circulation and have a relatively long circulation time (~2 days) compared to chylomicrons and IDLs.

28
Q

What is the lipoprotein in HDLs?

A

ApoA-I

29
Q

what are the functions of cholesterol metabolism?

A

Esterified and stored in lipid droplets or secreted in lipoproteins.
Used for synthesis of steroid hormones.
Used for synthesis of oxysterols as signaling molecules.
Used for synthesis of bile.

30
Q

What is the biologically active hormone form of vitamin D?

A

1,25-dihydroxyvitamin D

31
Q

The increase in serum TAGs observed in individuals who switch to low-fat (higher CHO) diets is attributed to what?

A

a decrease in the postprandial clearance of VLDLs as opposed to an increase in de novo fatty acid synthesis (which is current popular belief).

32
Q

What are the 9 essential AA’s?

A

Phenylalanine, tryptophan, lysine, histidine, methionine, threonine, leucine, isoleucine, and valine

33
Q

What are the 2 semi-essential AA’s and what are their precursor AA’s?

A

Cysteine and it’s precursor is methionine.

Tyrosine and it’s precursor is phenylalanine.

34
Q

What are the 10 nonessential AA’s?

A

Alanine, serine, glycine, aspartate, asparagine, glutamate, glutamine, proline, selenocysteine and arginine.

35
Q

How many g of glycogen/glucose is synthesized from AA carbon in a fed human per g of protein partially oxidized?

A

0.6 g of glucose per g of protein partially oxidized (would be 60 g of glucose per day for an adult consuming 100 G protein per day).

36
Q

What organ is the major site of AA partial oxidation and glucose/glycogen synthesis?

A

liver

37
Q

What are the major end products of AA catabolism?

A

Urea and ammonium

38
Q

How are the major end products of AA catabolism excreted?

A

urine.

39
Q

How many grams of protein ingested after exercise is ceiling of benefit in regards to anabolism.

A

Studies testing more than 30 g of high quality PRO do not show additional benefit.

40
Q

What is homocysteine?

A

○ a troublesome compound created during certain metabolic processes
○ Pyridoxine, folate, and vitamin B12 convert homocysteine to two AA’s (cysteine and methionine) that the body can use in building protein.
○ With shortages of these three B vitamins, homocysteine levels rise, arterial walls can be damaged, and blood clots form, increasing heart disease risk.