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GI First half > biochem - feast/starve cycle > Flashcards

biochem - feast/starve cycle Flashcards

1
Q

brain derives energy from…

A

glucose and ketone bodies only

cannot use FA

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2
Q

glucose levels for

  • normal
  • renal threshold
  • diabetic coma
  • overnight fast
  • hypoglycemia
A

-normal 8 mM
-renal threshold at 10mM –> glucosuria, excess urination
-diabetic coma 60 mM
-overnight = 5 mM
-

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3
Q 
after a meal
glucose from where 
0-4 hrs
up to 24 hrs
starting at 8 hrs
A

gut
liver glycogen
gluconeogenesis - dominant process at 16 hrs

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4
Q

insulin

A

polypeptide secreted by beta cells in pancreas in response to elevated blood glucose
SIGNALS well fed state and promotes increased transport of glucose into adipose and muscle, glycogen synthesis, de novo TG synthesis, deposition of fat, and protein synthesis
-inhibits breakdown of fat, protein, and glycogen

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5
Q

glucagon

A

made from alpha cells in pancreas in response to low blood glucose, low insulin
signals fasting state and promotes glycogenolysis, lipolysis, and gluconeogenesis

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6
Q

where is there no glucagon receptor (so no effect on)?

A

muscle

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7
Q

in pancreas glucose binds and causes

A

glucagon to go down, and insulin to go up

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8
Q

liver fat production

A

in liver glucose can be converted to triacylglycerols and packged into VLDLs and released into blood –> FAs of VLDLs are stored in adipose tissue

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9
Q

intestinal triacylglycerol absorption

A

packaged into chylomicrons and secreted into lymph into blood

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10
Q

insulin activates which transporter?

A

GLUT4 on muscle and fat tissue

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11
Q

RBCs require

A

glucose
oxidize it to pyruvate and lactate
no mitochondria

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12
Q

what vessel transports aa and glucose to liver

A

hepatic portal vein

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13
Q 
in liver, what activates...
1- glucose transport
2-glycogen storage
3-glycogen breakdown
4-FA synthesis
5- FA oxidation
6-glycolysis
7 - gluconeogenesis
A

1 - insulin and glucagon both have no effect on transport
2 - insulin activates glycogen storage
3 - glucagon activates glycogen breakdown
4 - insulin activates FA synthesis
5 - glucagon activates FA oxidation
6 - insulin activates glycolysis
7 - glucagon acivates gluconeogenesis

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14
Q

in adipose, what inhibits
1- glucose transport
2 - TG deposition
3- TG mobilization

A

1 - glucagon inhibits glucose transport in fat
2 - glucagon inhibits TG deposition in fat
3 - insulin inhibits TG mobilization; glucagon ACTIVATES TG mobilization

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15
Q 
in muscle, what enzyme works? what is its effect on...
glucose transport
glycogen synthesis
glycogen breakdown
protein synthesis
protein breakdown
A

insulin only

activates - glucose transport, glycogen synthesis, protein synthesis

inhibits - glycogen breakdown and protein breakdown

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16
Q

TGs of chylomicrons and VLDL

where are each produced? and where are they digested/by what?

A

chylomicrons are made from dietary fat and VLDL is made from glucose in liver
digested in capillaries by lipoprotein lipase to form FAs and glycerol –> stored by adipose as TGs

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17
Q

as blood glucose decreases…insulin? and glucagon?

A

insulin decreases and glucagon increases –> stimulating release of stored fuels into blood

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18
Q

when in fasting state, the liver…

A

supplies glucose and KB to the blood

it maintains blood glucose via glycogenolysis and gluconeogenesis and makes ketone bodies from FAs of adipose

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19
Q

2 ketone bodies?

A

B-hydroxybutyrate

acetoacetate

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20
Q

ketone bodies have a _____ ______ effect

A

protein sparing

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21
Q

what happens 2-3 hrs after a meal to release glucose into blood

A

glycogenolysis - glycogen is broken down;

glycogen stores deplete within 30 hrs

22
Q

what happens 4-6 hrs after a meal?

A

gluconeogenesis

23
Q

gluconeogenesis carbon sources

A

lactate from RBCs or exercising muscle
glycerol from TGs of adipose breakdown
AAs (alanine) from muscle protein
propionate from oxidation of odd chain FAs

24
Q

ketone body formation

A

adipose tissue breaks down TGs in response to rising glucagon
FAs and glycerol are released
B oxidation converts the FAs to acetyl coA which is used in liver to make KBs

25
Q

muscle release ____ in fasting state

A

aa

the carbons are used for gluconeogenesis and the nitrogen is converted to urea

26
Q

in starvation…

A

muscles decrease use of KBs so KB [ ] in blood goes up and brain can use them for energy so that it requires less glucose
gluconeogenesis slows down which spares muscle protein and produces less urea than an overnight fast!
body uses mostly fat when in starvation

27
Q

two places where gluconeogenesis occur?

A

liver and kidney cortex

28
Q

cori cycle

A

cycling of Lactate produced by red blood cells during anaerobic respiration in the muscles back into glucose.

The lactate produced by the muscle anaroebic glycolysis (glucose to lactate to produce atp) is cycled into the liver through the blood. In the liver it is converted to pyruvate by lactate dehydrogenase. The pyruvate is then cycled back into glucose by gluconeogenesis (using atp) and recycled back into the blood for use by red blood cells and muscles.

The Cori Cycle is significant two fold; it is neccesary to prevent lactic acidosis and in the conservation of oxygens being carried by erythrocytes(red blood cells). Because erythrocytes do not contain mitochondria, any aerobic respiration they would undertake would require the use of the oxygen they are transporting, which would negate the transport.

29
Q

major gluconeogenesis precursors?

A

aa
lactate
glycerol

30
Q

things that cant be converted to glucose

A

acetyl coA
even chain FAs
KBs
ethanol

31
Q

how is gluconeogenesis different from glycolysis

A

not just a simple reversal

3 irreversible steps are bypassed (all are kinases)

32
Q

the three irreversible steps of glycolysis

A

glucokinase (glucose + atp –> G6p + adp)
pfk-1 (f1p + atp –> F16BP + adp)
pyruvate kinase (PEP + adp –> pyr + atp)

33
Q

where is alanine converted to pyruvate?

A

mito matrix

34
Q

In gluconeogenesis, pyruvate carboxylase converts….what to what and where?

A

pyruvate –> oxaloacetate in the mitochondrion

35
Q

in gluconeogenesis, oxaloacetate is converted to either ____ or _____ by what?

A

malate by malate dehydrogenase

aspartate by transaminase

36
Q

in gluconeogenesis, malate/aspartate travel _____ where they_____

A

to cytosol

reconverted to oxaloacetate

37
Q

there is no transporter for ____ so ___ is used

A

oxaloacetate

malate-aspartate shuttle

38
Q

biotin

A

cofactor that carries activated CO2 during two step reaction of pyruvate carboxylase

39
Q

two step reaction of pyruvate carboxylase

and net

A

E-biotin + ATP + CO2 + H2O –> E-carboxybiotin + ADP + Pi
E-carboxybiotin + pyruvate –> oxaloacetate + E biotin

Net = ATP + pyruvate + CO2 + H20 –> oxaloacetate + ADP + Pi

ATP is driving force

40
Q

key regulatory enzyme of gluconeogenesis

what does it reqiure?

A

pyruvate carboxylase

-requires acetyl coA as a positive allosteric activator

41
Q

what is the positive allosteric activator of pyruvate carboxylase?

A

acetyl CoA

in live: fasting –> elevated acetyl coa –> gluconeogenesis is activated

42
Q

PEPCK

A

phosphoenolpyruvate carboxykinase
converts oxaloacetate to phosphoenol pyruvate (PEP)

first bypass reaction pyruvate to PEP

43
Q

PEP forms…

is made by

A

F 1,6 BP by reversal of glycolysis

PEPCK from oxaloacetate

44
Q

second bypass reaction

A

F16BP –> fructose 6 phosphate
by fructose 16bisphosphatase

F6p can then become g6p

45
Q

third bypass reaction

A

glucose 6 phosphate –> glucose

by glucose 6 phosphatase

46
Q

importance of glucose 6 phosphatase

A

allows liver to export glucose

g6p cannot leave cell since it isnt recognized by GLUT transporter

47
Q

what enzymes are inactive during gluconeogenesis

A

pyruvvate dehydrogenase
pyruvate kinase
PFK1
glucokinase
–these are the 4 used in glycolysis that are bypassed
—ensures that pyruvate becomes glucose and avoids futile cycle

48
Q

only sounds of energy during gluconeogenesis to liver?

A

oxidation of FA

glycolysis is inactive to avoid futile cycle

49
Q

synthesis of 1 mol glucose requires ____ mol lactate? and ____ mol ATP?

A

2 mol lactate

6 mol atp

50
Q

gluconeogenesis starting with aa

A

aa –> pyruvate —(pyruvate carboxylase)-> OAA
OAA —-(PAP carboxykinase) —->PEP
PEP ——> G3P (glyceraldehyde 3 phosphate)
glycerol –> G3P –> DHAP
DHAP /G3P ——> Fructose 1,6 Phosphate
F16P —(fructose 1,6 bisphosphotase) —-> F6P
F6P —->G6P
G6P —(glucose 6 phosphotase) —-> glucose

GI First half (8 decks)

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