Physiology Ii - Metabolism Part2

Front 1

Can any ATP be generated in absense of O2?

Back 1

Yes, use lactic acid pathway to generate 2 ATP and NAD+

Front 2

How is lactate reabsorbed?

What does it form back into?

Back 2

taken by cells that have oxygen

H+ removed to form pyruvate -> enters TCA

Front 3

What enzyme responsible for converting lactate to pyruvate?

Is rxn reversible?

Back 3

LDH

Yes, whichever is higher concentration determining direction

Front 4

Gluconeogenic precursors

Back 4

* many gluconeogenic amino acids (w/amine gp. removed)
* lactate
* propionate out of
* fermentation
* glycerol (from triglyceride breakdown)

Front 5

Two classes of lipoproteins:

Back 5

1. CHYLOMICRONS
2. VLDLs (Very Low Density Lipoprotein), e.g. after
production of new lipids

Front 6

how do cells take up VLDLs?

Back 6

cells have receptor which binds apoprotein in VLDLs

after BINDING subunit of receptor which enzyme known as LPL (lipoprotein lipase)

Front 7

what does LDL do?

Back 7

enters VLDL, going thru hydrophilic surface, and hydolyzes triglycerides inside

Front 8

What happens to components of VLDL after LDL has finished?

Back 8

FFA and glycerol components diffuse down concentration gradient into cell

if fat, components join again into triglyceride

Front 9

hydrolyzes stored triglycerides -> free fatty acids (FFAs) and glycerol diffuse back into circulation

Back 9

Hormone-Sensitive Lipase (HSL)

Front 10

chylomicrons are? what do they contain?

Back 10

are lipoproteins, have apoproteins

dietary fats after absorbed by enterocyte and go into blood stream

Front 11

FFAs can originate from

Back 11

1. NEFAs
2. VLDLs
3.Chylomicrons

Front 12

FFAs that bind to plasma Albumin for transport.......are known as ?

Back 12

Non-Esterified Fatty Acids = NEFAs, which deliver FFAs to active tissues for energy gain

Front 13

What happens to acetyl CoA after β-OXIDATION ?

Back 13

Acetyl CoAs enter KREBS cycle for complete oxidation and ATP generation in the ETC

Front 14

During LIPOLYTIC phases, what organ takes up NEFAs (FFA) and makes them available to other tissues as (1) VLDLs and (2) Ketone Bodies

Back 14

Liver

Front 15

What occurs during lipogenesis?

Back 15

* new fat made from excess glucose
* glucose enter TCA and leaves as citrate, which goes to F.A. production

Front 16

Which tissue has LPL that is stimulated by insulin?

Back 16

only LPL found in fat cells is insulin dependent

Front 17

What happens if FFA accumulates in hepatocytes (in lipolysis)?
Where does it go?

Back 17

* packaged into TriG and then into VLDLs
* if in lipolytic stage (insulin absent), VLDLs still being generated, take up by muscle cells!

Front 18

How are muscle cells able to take up VLDL?

Back 18

taken up by tissues (e.g. muscle) via their endothelial LPLs

Front 19

Once VLDLs taken up by muscle, what happens to them?

Back 19

used for energy gain via beta oxidation.

Front 20

Advantage of transporting as VLDLs over FFA?

Back 20

- Advantage: albumin binding capacity for FFA is limited -> liver increases lipid transport capacity via VLDLs

Front 21

When would you expect to see rise in fat in fat plasma?

Back 21

lipolytic phase:
*more fat sucked into liver and leaves as VLDLs to be available to other tissues
* packages fat in very condensed form Very Low Density Lipoproteins (ironic huh) to be available to other tissues for B-oxidation

Front 22

How does B-oxidation

Back 22

* after cell entry, FFAs enter mitochondria and undergo progressive release of C2 segments (Acetyl CoA)

Front 23

Why would Acetyl CoA accumulate too much? What is bottle neck here?

Back 23

- as Liver ATP stores fill up, the Krebs cycle activity declines
- Oxaloacetate/Malate are WITHDRAWN from Krebs cycle for gluconeogenesis (remember Acetyl CoA cannot continue in TCA until combines w/OAA to form citrate)

Front 24

Are nothing but 2 acetyl groups condensed:

Back 24

ketone bodies (C-4 w/minor alterations)

Front 25

Where does gluconeogenesis occur?

Back 25

liver

Front 26

What happens if Aceytl CoA accumulates?
What are 3 types of products can be formed?

Back 26

accumulating Acetyl groups condense into Acetoacetic Acid, Acetone and B-Hydroxybutyrate = KETONE BODIES (=Ketoacids)

Front 27

Ketone Bodies are a physiological and very important energy source for many tissues when glucose levels are ___?

What is advantage here?

Back 27

low

ketone bodies are readily taken up and easily metabolizable

Front 28

Can liver reverse ketone formation: ketone back to acetyl gp.?

Back 28

no, not reversible in liver

apparently other tissue e.g. muscle has no problem chopping in half back to acetyl gp. for energy production

Front 29

what is A.A. called if remove amine gp. ?

Back 29

ketone analog

(don't confuse with ketone bodies)

Front 30

if deaminate _____ get pyruvate

Back 30

alanine (3-C) - NH2 = pyruvate

so pyruvate is keto-analog of alanine

Front 31

if deaminate glutamate get ?

Back 31

alpha ketoglutarate

Front 32

True or False: keto-analog can enter Krebs Cycle?

Back 32

True

Front 33

Amino-Transferases are found i.p. in ?

What if found where not suppose to be

Back 33

Amino-Transferases are found i.p. in muscle tissue and liver:

they are intracellular enzymes!

Increases in plasma levels of these enzymes are of diagnostic value..pathological!

Front 34

Name 2 major Amino-Transferases

Back 34

ALT (alanine a.t.) and AST (aspartate a.t.).

Front 35

ALT (alanine a.t.) increase in plasma indicates?

Back 35

problem with liver
(ALT is liver specific in small animals)
- has "L" in it

Front 36

if AST (aspartate a.t.). increase in plasma but not ALT, indicates?

Back 36

problem with muscle
(AST found in muscle and liver tissue)

Front 37

what happens to nitrogen products of deamination?

Back 37

if amino groups are not needed -> liver converts excess potentially
toxic ammonia to UREA -> renal excretion

Front 38

Accumulation of NH3, e.g. due to liver failure -> ?

Back 38

-> interference with GABA a/o glutamate nt's -> neurotoxicity
-> depression, neurological deficits, coma, death
= HEPATIC ENCEPHALOPATHY
(very sad, animal depressed, head pressing, go into coma, and die)