Physiology Ii - Metabolism

Front 1

As general rule anarobic metabolism is associated with?

Back 1

storage (how so?)

also glycolysis and lactic acid
formation for making ATP

Front 2

metabolism is controlled by ?

Back 2

1. hormones (e.g. insulin and glucagon)
2. sympathetic nervous system via epi.& nor.
3. energy available (ratio of ATP to ADP)
4. sometimes if not taken up intermediates or metabolites inhibit from going forward

Front 3

are carbohydrates essential nutritients?

example of essential nutrient?

Back 3

No, because can be convert to make carbs; our body can make

some amino acids

Front 4

preferred energy source of tissues?

Back 4

glucose

Front 5

glucose dependent tissues?

Back 5

NERVOUS SYSTEM including neurons, retina, RBCs,
retina, renal medulla, gonads, fetus, lactation (milk production)

Front 6

first tissue/system to be affected by reduced glucose level?

Back 6

nervous system most sensitive to reduced glucose levels

Front 7

normal blood glc levels

at what lower level might have seizures? coma?

Back 7

80-120 mg Glc/dl

<50mg = seizures
<20mg = coma
death (spp. differences exist)

Front 8

process of releasing stored glucose

Back 8

glycogenolysis

Front 9

glycogenesis for ?

Back 9

storing (as glycogen)

Front 10

what happens if have insulinoma ?

common in what animal? why?

Back 10

excess insulin secreted, all tissues use glucose, get hypoglycemic

common in ferrets, b/c inbred and fed excess carbs

Front 11

Glucose enters cells via ?

Back 11

facilitated diffusion

Front 12

What unique about Glucose dependent tissues and Liver?

Back 12

GLUTs are ALWAYS part of their cell membranes
= facilitated diffusion (glucose uptake) is always active

Front 13

Are muscle,fat are examples of Glucose dependent tissues?

Back 13

No

Front 14

Where do Glucose independent tissues (eg muscle,fat) store/keep their GLUTs?

Back 14

GLUTs are stored intra-cellular

Front 15

What is required for GIT's (Glc. independent tissues) to express GLUTs on surface?

Back 15

= facilitated diffusion only when INSULIN present
- GLUTs detach when Insulin is absent

Front 16

What does insulin do?

Back 16

* when insulin present ALL TISSUES have free pass to use glucose!
- allows GLUTs to fuse with cell membranes
- now GIT's can use Glc

Front 17

Insulin is secreted in response to?

Back 17

- Insulin is secreted in response to hyperglycemia

Front 18

During Hypoglycemia what are insulin levels like in blood (or wherever it's secreted)?

Back 18

LOW

Front 19

Glucose Trapping : upon cell entry, glucose is ____?

Back 19

phosphorylated to Glc-6-P ->

Front 20

What's different about Glc-6-P...I mean in regard to its ability to move in and out cells of cells?

Is it reversible?

Back 20

glucose cannot diffuse out of cells;

irreversible except in liver, kidney and GI cells

Front 21

Fate of glucose depends on
the body’s energy situation:

What happens to GLUCOSE (which means Glu-6-P from now on unless otherwise stated) which has entered cells and O2 present?

Just give name of each cycle involved in order with major product/intermediate

Back 21

Glycolytic pathway -> pyruvate -> converted to acetyl gp. (acetyl CoA) -> enters Kreb's Cycle -> H+ ions -> ETC -> ATP

Front 22

What happens to GLUCOSE which has entered cells and w/o O2?

Back 22

Glycolytic pathway -> pyruvate -> Lactic Acid cycle

get 2 ATP, 2 pyruvate

Front 23

Why do we need Glycolytic pathway?

Back 23

glucose too big to enter mitochondria

pyruvate can enter mitochondria

Front 24

What happens to pyruvate as soon as enters mitochondria?

Back 24

carbon taken off (C3->C2), get acetyl gp., cofactor added to get acetyl CoA (activated to enter Kreb's cycle)

Front 25

Does Krebs Cycle have other functions aside from break down of glucose (pyruvate)?

Back 25

yes, involved in making non essential A.A. / glc (gluconeogenesis), and combusting FA & A.A.

Front 26

What happens to Citric Acid after going around cycle once?

What is lost?
In what form?

Back 26

; Citric acid undergoes a sequence of decarboxylations and dehydrations ending again in OAA

- 2 carbons brought in are lost as CO2 (waste product)

Front 27

Krebs cycle starts and
ends with ____?

Back 27

OAA (OXALOACETATE)

Front 28

What's OAA (OXALOACETATE) do?

Back 28

C2 (Acetyl CoA) joined by C4 (OAA) to form Citric Acid = C6

Front 29

After Kreb's Cycle turns once, what is produced?

Back 29

1 ATP, and NADH2, FADH

~most important outcome making its energy-rich hydrogen ions (NADH, FADH2) available for ETC

Front 30

How are NADH2 produced from aceyl CoA?

Back 30

- energy of acetyl gp. transferred onto cofactor NAD, 8 H+ from each acetyl gp. loaded onto NAD, to form NADH2 (FADH also created)

Front 31

where does ETC occur ?

Back 31

on inner wall of mitochondria membrane, H+ pumped in intermembrane space

Front 32

Where in metabolism is oxygen required ?

Back 32

ETC, oxygen is required as proton acceptor

Front 33

What kind of phosphorylation occurs in ETC?

Most important product?

Back 33

oxidation phosphorylation


ATP

Front 34

Aside from generating ATP, what is important function of ETC?

Back 34

re-generate electron acceptors NAD+ (and FADH+) for glycolysis and Krebs cycle

w/o those cofactors Krebs (and glycolysis to lesser extent) cannot happen

Front 35

How do anaerobic bacteria get rid of protons (cannot do ETC) to generate NAD+?

Back 35

load onto proprionate and butyrate to make methane

Front 36

What happens if O2 absent (overworked muscles) and NAD+ not generated by ETC?

Back 36

TCA (Krebs) stops, acetyl gp. pileup -> pyruvate accumulates -> glycolysis stops as well

Front 37

Can any ATP be generated in absense of O2?

Back 37

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

Front 38

How is pyruvate converted into lactic acid or lactate?

(skip until know everything else)

Back 38

2 H+ loaded onto central carbon of pyruvate (3-C) -> lactate or lactic acid

central carbon is keto- gp.

Front 39

How is lactate reabsorbed?

What does it form back into?

Back 39

taken by cells that have oxygen

H+ removed to form pyruvate -> enters TCA

Front 40

What enzyme responsible for converting lactate to pyruvate?

Is rxn reversible?

Back 40

LDH

Yes, whichever is higher concentration determining direction

Front 41

What tissue handle most of lactate accumulated?

Back 41

heart muscle and liver

(muscles have alot of LDH)

Front 42

What cells always in anaerobic conditions?

Back 42

RBC, no mitochondria, TCA, or ETC

so depend on glycolytic pthwy for 99% of energy

Front 43

why does glucose need to be stored as glycogen?

Back 43

because if remained as glucose in cell would increase osmolarity dramatically; too much H2O would accumulate

if condensed as 1 huge molecule, not as osmotically active

Front 44

Where can glycogen be made?

Which tissue produce/store most?

Back 44

every tissue can make but very little

only liver (up to 6% of weight) and muscle (up to 1%) can store a lot

Front 45

Structure of glycogen?

Back 45

endless chains of glucose, mostly condensed as α1-4 with some branches of α1-6 side chains

Front 46

enzyme encourages formation of glycogen?

Back 46

insulin

Front 47

What enzyme responsible for adding α1-6 chain?

What enzyme responsible for breaking off α1-6 chain?

Back 47

Branching enzyme: adds 1-6 side chain to very long α1-4 linkage

Debranching enzyme

Front 48

End product of glycogenolysis (w/debranching enzyme, etc)?

Back 48

makes Glc-6-P

note: cannot leave cell w/P

Front 49

process of synthesizing new glucose from precursors is

Back 49

gluconeogenesis

Front 50

Gluconeogenic precursors

Back 50

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

Front 51

What happens to these precursors?

Back 51

* usually have C4 or C5 backbone
* enter Krebs at half way point

Front 52

Precursors in Krebs cycle are pulled out into cytoplasm
as ____ -> enter gluconeogenesis (except glycerol).

Back 52

*OAA / Malate* pulled into cytoplasm to enter gluconeogenesis (except glycerol).

Front 53

Why can't we go directly backwards e.g. from precursor -> acetyl CoA -> pyruvate -> Glu-6-P? Is this possible with any precursors?

Back 53

- because some steps aren't reversible

- all precursor must enter TCA to form OAA/Malate w/exception of glycerol

Front 54

Both liver and kidney contain
_____ and release free
glucose into circulation.

Which releases more glucose?

Back 54

phosphatases

80% of glucose released into blood stream comes liver and 20% from kidney

Front 55

Where does glycerol come from?


Where do other precursors come from?

Back 55

According Dr. Zeigler:
* its precursor is one of products of glycolytic pathway

* often are A.A. precursors pulled from muscle tissue
* liver and kidney can also produce some
* proprionate (UFA) is major precursor in ruminants and hindgut fermenters
* lactate can be produced by any tissue

Front 56

When Gluconeogenesis is very active which intermediate is in highest demand?

Back 56

Malate (OAA can revert back to malate)

~this is major bottleneck in metabolism

Front 57

Lack of phosphatase enzyme common in what animal?

Back 57

dogs

Front 58

What is triglyceride?

Back 58

glycerol backbone + 3 FA's

Front 59

What bile acids are produced from?

Back 59

cholesterol

Front 60

what are lipoproteins?

Back 60

aggregations of lipids surrounded by a shell of hydrophilic proteins, phospholipids and specific receptor proteins = Apoproteins

Front 61

Two classes of lipoproteins:

Back 61

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

Front 62

why do fats form lipoproteins?

Back 62

combined with proteins so are soluble in water -> for transport in plasma

Front 63

how do cells take up VLDLs?

Back 63

cells have receptor which binds apoprotein in VLDLs

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

Front 64

what does LDL do?

Back 64

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

Front 65

What happens to components of VLDL after LDL has finished?

Back 65

FFA and glycerol components diffuse down concentration gradient into cell

if fat, components join again into triglyceride

Front 66

What cells store triglycerides?

Back 66

only fats cells

Front 67

what term describe break down of fat or release from storage?

Back 67

glycolysis or lipolysis

Front 68

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

Back 68

Hormone-Sensitive Lipase (HSL)

Front 69

chylomicrons are? what do they contain?

Back 69

are lipoproteins, have apoproteins

dietary fats after absorbed by enterocyte and go into blood stream

Front 70

lipoproteins (endogenous fats) made by liver cells known as ?

Back 70

VLDLs - very low density lipids

are same as chylomicrons, aside from their origin; are endogenous

Front 71

FFAs can originate from

Back 71

1. NEFAs
2. VLDLs
3.Chylomicrons

Front 72

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

Back 72

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

Front 73

after cell entry, FFAs enter mitochondria and undergo progressive release of C2 segments (Acetyl CoA) in process known as ???

Back 73

β-OXIDATION

Front 74

What happens to acetyl CoA after β-OXIDATION ?

Back 74

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

Front 75

Where does glycerol go?

Back 75

Diffuses into active tissues where can either:
1. enter glycolysis -> Krebs cycle -> ETC when ATP is needed
2. or enters GLUCONEOGENESIS when glucose is needed

Front 76

Excess glucose and amino acids can be <converted into FFAs> = ?

Back 76

LIPOGENESIS

glucose -> FFA

Front 77

Where does lipogenesis occur?

Back 77

(in Liver, Fat Tissue, Mammary Gland).

Front 78

True OR False: Lipogenesis is activated when stores of ATP, Glycogen and Labile Protein are full and Glc and AAs are still available.

Back 78

True

Front 79

True OR False: LIVER is a fat storage site?

Back 79

False *****!

LIVER: is not a fat storage site

Front 80

What does liver do with excess fat?

Back 80

Makes them into VLDLs, send into circulation for fat storage

Front 81

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

Back 81

Liver

Front 82

What occurs during lipogenesis?

Back 82

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