Exam 3 (Lectures 24-26) Flashcards

(35 cards)

1
Q

NAD+ is mainly used for…

A

oxidation that powers ATP synthesis

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2
Q

NADPH is used for…

A

reduction

able to reduce reactive oxygen species to remove them

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3
Q

NAD+ in the mitochondrial matrix

A

oxidizes substrates to produce reducing equivalents: NADH

happens in: TCA cycle and Fatty Acid Oxidation

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4
Q

NADH in the mitochondrial matrix

A

reduces electron carriers to power ATP synthesis

happens in: Electron Transport Chain

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5
Q

NADPH in the cytoplasm

A

reduces substrates in reductive synthetic reactions:

Fatty Acid Synthesis

Cholesterol Synthesis

Nucleotide Synthesis

Neurotransmitter Synthesis

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6
Q

Pentose Phosphate Pathway (Oxidative)

Reaction 1 Regulation

A

High NADPH/NADP+ inhibits G6PD

Low NADPH/NADP+ activates G6PD

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7
Q

High need Ribose 5-P

Low need NADPH

A

products from glycolysis Fructose 5-P and GAP to make Ribose 5-P

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8
Q

If equal amounts of NADPH and Ribose 5-P is needed both at the same time…

A

Only oxidative PPP is used to make NADPH and Ribose 5-P

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9
Q

High need of NADPH

Low need Ribose 5-P

A

use both OPPP and non-OPPP then send products to gluconeogenesis to make more G6P for PPP

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10
Q

High need in NADPH and ATP

A

OPPP and non-OPPP are used and sent to glycolysis to make pyruvate + ATP then TCA cycle to make more ATP

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11
Q

Deficiency of Glucose 6-P Dehydrogenase

A

caused by x-linked genetic mutation

increase susceptibility to oxidative injury => Hemolytic Anemia (lysis of RBC)

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12
Q

Oxidative Challenges

A

Oxidative Drugs: antibiotics, antimalarials, fever reducers

Favism: hemolytic anemia precipitated by fava bean ingestion

Infection: peroxides are made in macrophages mobilized in reponse to infection

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13
Q

Favism

A

from fava beans that contain active oxidants (vicine & convicine)

may afford some protection from death from malarial infection

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14
Q

What is Triacylglycerol (fats)

A

high energy fuel preferred by Liver and Heart

fuel by skeletal muscles

yields greater than ATP per Glycogen

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15
Q

Where does the catabolism of dietary fats begin?

A

in the small intestine where bile salts are released after a meal

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16
Q

Where are Bile Salts synthesized, stored, and released?

A

Synthesized in the liver using cholesterol

stored in the gall bladder

released in to the small intestine

17
Q

How many cycles are needed to break n-C Saturated Fatty Acid down completely to Acetyl CoA?

How many Acetyl CoA produced?

How many NADH and FADH2 produced?

A

N/2 - 1

N/2

N/2 - 1

18
Q

Fatty Acid Synthesis Reaction 1 Regulation

A

positively regulated by citrate

negatively regulated by AMP

19
Q

We can use Acetyl CoA to make…

A

fatty acids, ketone bodies, cholesterol, CO2, H2O, ATP

20
Q

Ketone bodies are preffered fuel for…

A

heart and renal cortex

can also be with brain under starvation condition

21
Q

Ketone Bodies Synthesis

A

in the fasting state, the liver used Acetyl CoA to make ketone bodies

22
Q

What are the ketone bodies?

A

acetoacetate, D-3-hydroxybutyrate can be used to make acetyl CoA for TCA or other cells

acetone - excreted by breathing out or urine

23
Q

What are the two sources of Cholesterol?

A

Dietary and indogenous produced by the liver

24
Q

Rank the lipoproteins in increasing density

A

Chylomicron > VLDL > IDL > LDL > HDL

25
Physiological Role: Chylomicron
dietary fat transport
26
Physiological Role: VLDL
endogenous fat transport
27
Physiological Role: IDL
LDL precursor
28
Physiological Role: LDL
cholesterol transport
29
Physiological Role: HDL
reverse cholesterol transport
30
Hypercholesterolemia
Long-term ingestion of dietary cholesterol far exceeds requirement high cholesterol =\> decrease in LDL receptor synthesis
31
Familial Hypercholesterolemia (FH)
FH/FH mutation: serum cholesterol is 3 to 5 times normal levels in childhood FH/+ mutation: serum cholesterol is about twice normal levels by mid age
32
Atherosclerosis
Hardening of the arteries an inflammatory desease caused by LDL seeping past the endothelium and becoming inflammatory
33
What are HDL's protective effects?
reverse transport of cholesterol from circulating lipoprotein particles reverse transport of cholesterol from foam cells degredation of oxidized lipoprotein particle constituents trough an HDL-associated serum esterase
34
ATP III: Metabolic Syndrome
\>= 3 risk factors are present: Abdominal obesity high triacylglycerals Low HDL-C high BP high fasting glucose
35