Metabolism 1 Flashcards Preview

DMED 511 Biochemistry > Metabolism 1 > Flashcards

Flashcards in Metabolism 1 Deck (24)
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1
Q

Metabolic syndrome: associated with?

A

risk of developing cardiovascular disease and type 2 diabetes

2
Q

2 key principles of metabolic pathways

A

all obey the same fundamental principles. not all reactions occur in every organism or every cell.

3
Q

two major purposes of metabolism

A

obtain usable chemical energy from environment. make specific molecules that cells need to live and grow

4
Q

two major types of metabolic pahtways

A

catabolic: breaking down complex molecules, make ATP. anabolic: building complex molecules from simple precursors.

5
Q

catabolic vs. anabolic: ox or red?

A

catabolic = oxidative, remove electrons from molecules. anabolism = reductive, require electrons to make bonds.

6
Q

metabolic pathway: definition

A

series of consecutive, enzyme catalyzed reactions producing a specific product from a specific starting metabolite (ex: glycolysis)

7
Q

concentrations of metabolic intermediates are maintained at ____? through which two types of reactions?

A

steady levels: irreversible, rate-limiting reactions that are tightly regulated, and regulated in concert. reversible reactions that are not regulated, direction depends on [intermediates].

8
Q

Pathways are ___, but ____ occur. What is shared? Regulation?

A

directional, aka irreversible - but opposing pathways do occur. share reversible reactions, but always have unique irreversible steps. reciprocally regulated so only one is operational at a time.

9
Q

biomolecules are broken down to ____ which feeds into ____ and is broken down to ____. what happens to the electrons?

A

acetyl co A –> CAC –> Co2. Electrons from acetyl co A are “saved” in electron carriers aka enzyme cofactors: NADH and FADH2.

10
Q

reduced electrons carriers NADH and FADH2: what happens to them? requires? produces?

A

re-oxidized via ETC; requires oxygen and produces ATP.

11
Q

fuel supplies (which 2?) in the blood stream are managed by the ___, which processes them in what 3 ways?

A

glucose and fatty acids (aas not usually used as fuel). managed by the liver - uses them, storage as glycogen, processes/stores/releases as needed.

12
Q

how is excess fuel (2) stored?

A

glucose stored as glycogen in liver and skeletal (also cardiac muscle). fatty acids stored as TAGs in adipocytes.

13
Q

2 fuel users? providers?

A

users: brain and skeletal muscle. providers: liver and adipose tissue.

14
Q

brain is a ___ fuel user: why?

A

obligatory: need lots of ATP to maintain ion concentration gradients; ALWAYS needs some glucose.

15
Q

liver as a fuel provider: maintains?

A

suitable levels of fuel molecules in blood for use of all other tissues.

16
Q

primary function of adipose tissue

A

long term storage of energy

17
Q

our nutritional status (___ or ___) is signalled by?

A

fed or fasted; signalled by hormones

18
Q

fed state: signal, response, cellular effects, mode of action?

A

increasing [glucose] in blood –> insulin release –> promotes use and storage of fuel molecules –> insulin activates phosphatases in target cells, and dephosphorylates target enzymes

19
Q

fasted state: signal, response, cellular effects, mode of action?

A

decreasing blood [glucose] –> glucagon release –> promotes mobilization of fuel stores via activation of protein kinases aka phosphorylation of target enzymes

20
Q

glucose is broken down aka ___, by? synthesized by?

A

catabolized by glycolysis. synthesized by gluconeogenesis.

21
Q

glucose stored as ___ via ____, released by ______?

A

glycogen, glycogen synthesis. released by glycogen breakdown aka glycogenolysis.

22
Q

glycolysis: starts with? ends with? occurs in ___ cells? where in the cell? aerobic?

A

glucose –> pyruvate. in all cells: cytoplasm. anaerobic.

23
Q

glycolysis: 2 rate limiting steps?

A

2 RLS regulated in parallel, catlyzed by PFK 1 and PK

24
Q

glycolysis rate determined by what two things?

A

substrate availability (glucose concentration maintained by liver, and rate of transport into cells via GLUT). alterations in activity of rate limiting enzymes (allostery and reversible covalent modifications like phosphorylation)