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Clinical Chemistry II - 4378 > Sugar-advanced metabolism > Flashcards

Sugar-advanced metabolism Flashcards

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1
Q

a sum of enzyme-catalyzed reactions by which a living cell perpetuates and
replicates itself

A

Metabolism

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2
Q

Intermediary/Energy metabolism:

A SET OF REACTION concerned with..

A
  1. generation or storing energy and with
  2. using that energy for biosynthesis of small molecules.
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3
Q

Metabolism is associated with maintenance of cellular ______ & blood _______ levels

A

ATP, glucose

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4
Q

using energy
derived from
catabolic
pathways;
endergonic
process

A

Anabolic process biosynthesis pathway

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5
Q

Oxidative breakdown
of complex larger
molecules that
results in energy
release captured by
formation of high
energy compounds
(ATP); exergonic
process

A

catabolic

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6
Q

a metabolic pathway that can be both, catabolic and anabolic

A

Amphibolic

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7
Q

sugars with names containing the suffix -ose.

A

Saccharides

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8
Q

Monosaccharides are stereoisomers:
* All monosaccharides in humans are…

A

D-stereoisomers

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9
Q

Most stable confirmation of saccharides are ring structures.
What are the ring structures?

A

Six member rings (pyranose) & five membered ring (furanose)

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10
Q

OH- group at position 1 in saccharides can adapt in ____or ____ confirmation.

which is more stable?

A

α or β

The β confirmation is more stable in glucose but polysaccharides (starch) and glycogen have glucose linked in the α confirmation.***

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11
Q

Which complex carbohydrates is nutritionally most important?

A

Disaccharides

-maltose(glucose+glucose)
-lactose(glucose+ galactose)
-sucrose( glucose+ fructose)

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12
Q

Complex carbohydrate that contain 2 to 10 monosaccharide units

A

Oligosaccharides

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13
Q

Complex carbohydrate that is greater than 10 monosaccharide units

A

Polysaccharides

-Cellulose
* Starch
* Glycogen
* Glucan: Polysaccharide of D-glucose monomers

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14
Q

What are the other (minor) carbohydrates?

A

glycogen, alcohol, lactic acid, pectin & dextran

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15
Q

Polysaccharide starch: source of ___% of monosaccharides

A

80

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16
Q

When does amylase action begin? end?

A

Starts in the mouth, continues in stomach to hydrolyze starch into maltose and other small polymers of glucose.

ends in about an hour, gastric secretions inhibit activity.

after chyme enters duodenum, pancreatic amylase is added.

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17
Q

Disaccharides & oligosaccharides need to be converted to ___________ before absorption.

A

monosaccharides

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18
Q

Chyme enters jejunum and ileum where four enzymes are located in the brush border of cells
lining the intestine, which are… ?

A

lactase, sucrase, maltase, & α-dextrinase.

–Monosaccharides are immediately absorbed into the portal blood.

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19
Q

What are the Glucose transporters used to get glucose across cell membranes?

A

GLUT-1, GLUT-2, GLUT-3, GLUT 4 & GLUT-5

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20
Q

Glucose transporter that…

has low affinity (high Km) to glucose.
* Found in areas with high glucose concentrations.
* Involved in insulin-independent glucose in small intestines, renal tubules &
liver

A

GLUT-2

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21
Q

Glucose transporter that…

has a high affinity (low Km) to glucose.
* Found in glucose-sensitive, insulin independent cells of the brain & RBC.

A

GLUT-1, GLUT-3 & GLUT-5

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22
Q

Glucose transporter that…

has an intermediate affinity to glucose
* Found in insulin-dependent muscle & adipose cells.

A

GLUT-4

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23
Q

storage form of glucose in muscle &liver

A

Glycogen (Polymeric glucose)

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24
Q

major source of energy & primary form of nutrition

A

Monosaccharide

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25
Q

Monosaccharides can be transformed into what metabolites?

A
  • Glucose to ribose
    – Glucose to oxidized / reduced forms, such as mannitol, glucuronic acid
    –> important constituents of complex polysaccharides
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26
Q

Other functions of carbohydrates?

A

» Long chains of hyaluronic acid and keratin sulfate makeup components of synovial
fluid and connective tissue
» Heparin
» Integral proteins
» Secreted proteins

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27
Q

Fructose is Primarily metabolized in…

A

liver, kidney, and small intestine

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28
Q

In the liver, fructose is converted to?
In other tissues?

A

-fructose-1-p by fructokinase

-Phosphorylated by hexokinase

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29
Q

What are three disorders of fructose metabolism?

A

-Essential fructosuria
-Hereditary fructose intolerance
-Hereditary fructose-1,6-bisphosphatase deficiency

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30
Q

this disorder of fructose metabolism won’t effect glycolysis

A

Hereditary fructose-1,6-bisphosphatase deficiency

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31
Q

What is known as false diabetes mellitus?

A

Essential fructosuria

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32
Q

Disorder of fructose metabolism:

results from a deficiency of
fructokinase in the liver

A

Essential fructosuria

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33
Q

Disorder of fructose metabolism:

results from a
deficiency of fructose-1-p aldolase of liver, kidney cortex and small intestine

A

Hereditary fructose intolerance

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34
Q

What are the disorders of Galactose metabolism?

A

-Classic galactosemia
-Galactosemia due to loss of galactokinase (GALK)
-Epimerase deficiency (GALE)

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35
Q

Disorders of Galactose metabolism:

due to loss of uridylyltransferase
(GALT)

A

Classic galactosemia

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36
Q

Disorders of Galactose metabolism:

Galactosemia due to loss of galactokinase (GALK)
- Both are lactose intolerant, can lead to blindness and fatal liver damage

A

Galactosemia due to loss of galactokinase (GALK)

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37
Q

Disorders of Galactose metabolism:

– 2 forms,
1) benign, 1) similar to transferase deficiency

A

Epimerase deficiency (GALE)

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38
Q

the liver controls blood glucose concentrations, how?

A

-Via glycogen levels
* Converts intestinally absorbed galactose & fructose to glucose
* Produces glucose via gluconeogenesis (glucose-6-phosphatase activity)

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39
Q

Liver also responsible for producing important glucose metabolites, like?

A

-Ribose
-Oxidizes/reduces to form complex monosaccharides

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40
Q

What is the primary energy source used by the brain?

A

Sugar

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41
Q

Glucose can make up to ___ pyruvate and _____ Acetyl CoA.

A

2, 2

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42
Q

Building up to glucose is called?
And breaking down glucose is called?

A

gluconeogenesis (Using non-carb sources to make glucose)

glycolysis

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43
Q

which is limited? which is unlimited storage?

A

glycogen storage is limited!
-not all Acetyl CoA can be processed to the TCA cycle

fat storage is unlimited

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44
Q

what is the storage form of glucose?

A

Glycogen

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45
Q

How is ATP and ADP related?

A

ATP/AMP:ADP:P* ratio

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46
Q

What influences the metabolic rate?

A

ATP levels

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47
Q

What is a major difference in HDL and LDL?

A

HDL-moves cholesterol to liver to be cleared

LDL-moves cholesterol to peripheral circulation

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48
Q

What is the starting point of the TCA cycle?
What is it also important for?

A

oxaloacetate

gluconeogenesis

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49
Q

Where is NAD+ and NADH mainly found?

A

NAD+- mitochondria
NADH- cytosol

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50
Q

What is the difference between alpha and beta confirmations?

A

?
If carbon #1 and carbon #5 is linked by oxygen —> alpha confirmation.

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51
Q

How can you distinguish D-glucose from L-glucose?

A

-Look at the second to last carbon
-OH group on the right side —> D-glucose
-OH group on the left side —> L-glucose

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52
Q

What is maltose made up of?

A

2 glucose

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53
Q

What is lactose made up of?

A

glucose and galactose

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54
Q

What is sucrose made up of?

A

glucose and fructose

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55
Q

Only ___________ form of sugar can enter the cells.

A

monosaccharide

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56
Q

a minor carbohydrate that can be used as a blood thinner. It is very large and can also be used for patients with low blood volume.

A

dextran

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57
Q

If the first carbon has the OH group on top it is alpha or beta confirmation?

A

Beta

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58
Q

Km =

A

1/2 Vmax

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59
Q

What are the two processes involving glycogen?

A

-Glycogenesis
-Glycogenolysis

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60
Q

What are the two processes involving glucose?

A

-Glycolysis
-Gluconeogenesis

*Hexose MonoPhosphate Shunt

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61
Q

___________ produces the storage form of glucose: high MW polysaccharide composed of glucose.

A

Glycogenesis

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62
Q

Glycogenesis:
linked with a _______ glycosidic bonds and branches with ________ glycosidic bonds (every 10 untis*)

A

α (1–>4)

α (1–>6)

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63
Q

Where does glycogenesis occur?

A

cytoplasm (liver and muscle)

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64
Q

What is step #1 of glycogenesis?

A

glucose-6-phosphate is catalyzed by phosphoglucomutase to glucose-1-phosphate

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65
Q

What is step #2 of glycogenesis?

A

glucose is activated with UTP which is catalyzed by UDP-glucose pyrophosporylase to UDP-glucose

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66
Q

What is step #3 of glycogenesis?

A

glycogen synthase adds UDP-glucose to growing glycogen molecule.

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67
Q

What can glycogen synthase (GS) be controlled by?

A

by phosphorylation or dephosphorylation

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68
Q

Glycogen synthase (GS) is regulated by?

A

cAMP-dependent PKA phosphorylation

-GS activity inhibited by PKA phosphorylation***

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69
Q
  • Hormones that increase cAMP (___________& __________) activate PKA. [inhibit glycogen formation]
A

glucagon, epinephrine

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70
Q

**GS activity is ___________ if phosphate is removed.

A

increased

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71
Q

Branching enzyme attaches ___ to __glucose units to glycogen via α (1–>6) glycosidic bonds

A

5, 6

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72
Q

________________ phosphatase removes phosphate group & as cAMP concentrations decline, glycogen
formation is increased

A

Insulin-regulated

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73
Q

What is the major point of regulation for glycogen synthesis?

A

Branching enzyme***

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74
Q

The process involved in producing glucose from glycogen?

A

Glycogenolysis

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75
Q

Glycogenolysis:

What cleaves glycogen to glucose-1-phosphate

A

Glycogen phosphorylase

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76
Q

Glycogenolysis:

Glycogen phosphorylase activity is increased following phosphorylation by ___________ which activated by ______.

A

phosphorylase kinase

PKA

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77
Q

Glycogenolysis:

*What does hormones that increased cAMP (glucagon and epi) do to PKA?

A

activates PKA so that glucose-1-phosphate formation increases

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78
Q

Glycogenolysis:

______________ converts glucose-1-phosphate into glucose-6-
phosphate

A

Phosphoglucomutase

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79
Q

Glycogenolysis:

__________________ removes phosphate in glucose is free to diffuse from liver into the circulation

A

(liver) glucose-6-phosphatase

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80
Q

-This is an old metabolic pathway, fully functional under Anaerobic conditions
-Essential for cells unable to function aerobically (have no mitochondria)

A

Glycolysis

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81
Q

What cells rely on glycolysis?

A

**RBC & some cells in the eye (lenz and retina)

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82
Q

What cells/organism undergo glycolysis?

A

all types

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83
Q

Where does glycolysis take place?
Hoe much energy does it extract from glucose?

A

cytosol

less than 5%

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84
Q

What are the three enzymes needed for glycolysis? **

A

(Steps 1,3, and 10) step 6 is the connecting point?

-Hexokinase
-phosphofructo-kinase-1
-pyruvate kinase

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85
Q

Is glycolysis reaction #1-phosphorylation reversible or irreversible?

A

irreversible

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86
Q

liver or brain?

Hexokinase-
glucokinase-

A

Hexokinase-body
glucokinase-liver?

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87
Q

Glycolysis Reaction #1:

Catalyzed by Glucokinase in the _____ or Hexokinase in ______.

A

liver, muscle/fat

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88
Q

Glycolysis Reaction #1:

– Traps glucose inside the cell – charge at physiological pH
– Conserves metabolic energy
– Phosphates interact with enzyme active sites and lower activation energy
-Mg used as a cofactor

A

cf. Phosphorylation:

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89
Q

Glucokinase (Liver) is highly specific for ________.

A

Glucose

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90
Q

Glucokinase has a ___ Km for glucoase (about ___mM)

A

high, 10

-Not saturated at physiological blood glucose concentration
(4-5mM)

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91
Q

Glucokinase is inhibited by __________, but NOT __________.

A

fructose-6-phosphate

glucose-6-phosphate

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92
Q

Glucokinase is induced by __________.

A

insulin

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93
Q

What is the specificity of hexokinase?

A

Low specificity – phosphates most relevant hexoses
(Glucose, Fructose, Mannonse)

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94
Q

hexokinase has a _____ Km (___mM): saturated at all plasma glucose
concentrations

A

low, 0.1 (increased affinity)

-x100 lower than glucokinase

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95
Q

Hexokinase is inhibited by..,

A

glucose-6-phosphate (fructose and others?)

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96
Q

What effect does insulin have on hexokinase?

A

little effect on expression

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97
Q

*** In RBCs, rates of glycolysis is regulated by _________.

A

ATP/AMP+ADP

-Increased ATP or not enough ADP, glycolysis will shutdown*

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98
Q

Regulation of Glycolysis:

  2. 3.
A
  1. Hexokinase/Glucokinase
  2. Phophofructokinase-1 (PFK-1)
  3. Pyruvate Kinase
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99
Q

Regulation of Glycolysis, Phophofructokinase-1 (PFK-1):

activated by:
inhibited by:

A

activated by: AMP, F-2, 6-BP

inhibited by: ATP, citrate

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100
Q

Regulation of Glycolysis, Pyruvate Kinase:

activated by:
inhibited by:

A

activated by: F-1, 6BP

inhibited by: ATP, Acetyl CoA, Alanine

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101
Q

Glycolysis reaction #6:

  1. Anaerobic conditions:
  2. Aerobic conditions:
A
  1. Anaerobic conditions: conversion of pyruvate to
    lactate by lactate dehydrogenase
  2. Aerobic conditions: by Shuttles which passes H+ to
    the mitochondrion.
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102
Q

What are the two major shuttles under aerobic conditions?

A

-Glycerol phosphate shuttle
-Malate-Aspartate shuttle

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103
Q

What is the reverse pathway of glycolysis?

A

Gluconeogenesis

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104
Q

gluconeogenesis is a process that produces glucose-6-phosphate from what three things?

A

-AA
-FA
-glycerol and lactate

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105
Q

Gluconeogenesis:

Glucose is only formed in ______ and ______: Glucose-6-phosphatase

A

*** liver, kidney

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106
Q

What are the primary pursers for glucose synthesis?

A

– Glucose only formed in liver & kidney: Glucose-6-phosphatase

– Lactate goes pyruvate,
– Alanine goes to pyruvate,
– Glycerol goes to glyceraldehyde-3-phosphate

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107
Q

*** Hexose Monophosphate Shunt
Pentose Phosphate Pathway:

produces ______ in two-step pathway.
-Oxidative & non-oxidative steps

A

ribose

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108
Q

Why is ribose and NADPH needed from the pentose phosphate pathway?

A

*Ribose used to produce nucleotides and nucleic acid
*Pathway produces NADPH which is important reducing agent for biosynthetic process ex) FA & Cholesterol synthesis

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109
Q

“Alternative glucose oxidation pathway”

A

Hexose Monophosphate Shunt
Pentose Phosphate Pathway

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110
Q

Hexose Monophosphate Shunt
Pentose Phosphate Pathway:

Which tiesues?

A
  1. Active in FA & steroid synthesis: adrenal gland, liver, adipose tissue &
    mammary gland
  2. RBCs: Maintain their membrane integrity.
  3. Rapidly dividing cells: require DNA synthesis
    (Length of survival depends on this pathway)
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111
Q

Pentose phosphate pathway can be divided into what two parts?

A

1) Oxidative and 2) non-oxidative “A kind of “recycle pathway”

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112
Q

What are the organs and glands involved in hormonal regulation of carbohydrates?

A

-Pancreas
* Insulin (hypoglycemic)
* glucagon
* somatostatin
– Adrenal gland
* Cortisol
* epinephrine
– Thyroid
* thyroxine
– Pituitary (anterior)
* Growth hormones

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113
Q

Insulin-dependent diabetes is which type ____

A

1

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114
Q

Where is insulin synthesized from?

A

islet of Langerhans β cells of pancreas as preproinsulin.
-packaged in beta granules

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115
Q

Insulin:

➢ Enzymatic cleavage of pre-proinsulin first forms proinsulin
✓ goes to….

A

insulin + C-peptide

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116
Q

INSULIN consists of an α & β chain connected by _____ bonds

A

s-s

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117
Q

Insulin released from β cells after what stimulations?

A

neural, dietary or hormonal stimulation (GIP, Somatostatin, Bombesin)

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118
Q

Glucose, amino acids increase _____________ peptide which increase insulin.

A

gastric inhibitory

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119
Q

What are the major target organs of insulin action?

A
  • Liver which decreases proteolysis, lipolysis, gluconeogenesis, and
    glycogenolysis
  • Muscle which increase protein synthesis
  • Fat which increases triglyceride synthesis
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120
Q

Glucagon is Synthesized in islet of Langerhans ___ cells of the pancreas

A

alpha

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121
Q

what increases glucagon release?

A

AA & exercise

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122
Q

Secretion of glucagon is potent & irreversibly regulated by…

A

[glucose]blood

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123
Q

Increased glucagon increases what?

A

-increased glycogenolysis: activates PKA & phosphorylase kinase
–increased gluconeogenesis,
– ketogenesis by inhibiting
storage of TG in liver
– Fat increases lipolysis

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124
Q

Synthesized in islets of Langerhans δ cells of pancreas

A

Somatostatin (GI paracrine)

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125
Q

what is the circulatory half-life of somatostatin (GI paracrine)?

A

short, about 2 min

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126
Q

What is somatostatin released with?

A

[glucose]blood, AA, FA & GI hormones

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127
Q

Somatostatin acts locally to __________ insulin and glucagon secretion.

A

decrease
-The effect is to increase for period of time which did nutrients are
assimilated into the bloodstream

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128
Q

Cortisol:
glucocorticoid is released from the adrenal ________.
The secretion is regulated by ______.

A

cortex

ACTH

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129
Q

Cortisol results in increased blood glucose due to….

A

-increased gluconeogenesis in the liver
–increased enzymes in GLUCONEOGENESIS pathway
– Mobilization of AA from extra hepatic tissue

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130
Q

Epinephrine released from ___________ after stimulation
of SYMPATHETIC NERVES

A

adrenal medulla

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131
Q

How does epinephrine result in increased blood glucose?

A

-decreased insulin secretion

-increased glucagon secretion
-increased glycogenolysis
-increased
gluconeogenesis

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132
Q

Thyroxine (T4) results in an overall ________ in protein synthesis. What else does it increase?

A

protein

-in glucose uptake
-in glycolysis
-gluconeogenesis
-rate of glucose absorption from intestinal tract
-Also results in increased
insulin but a secondary to
increasing
blood glucose

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133
Q

What is an important effect of thyroxine (T4)?

A

increased rate of glucose absorption from intestinal tract***

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134
Q

*** GH counteracts “in general” the effects of…

A

insulin on glucose & lipid
metabolism, but shares protein anabolic properties with insulin.

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135
Q

GH results in an overall increase in blood glucose as a result of….

A

-decreased utilization glucose for energy
- increased in glycogen deposition in cells
-decreased uptake of glucose by cells —> increase blood glucose

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136
Q

What is the enzyme used for oxidative decarboxylation?

A

Pyruvate dehydrogenase complex
Lipoate, TPP, FAD

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137
Q

Is oxidative decarboxylation reversable?

A

no

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138
Q

Oxidative Decarboxylation:

Involves both, oxidation-reduction and decarboxylation.

What agent always participates?

A

✴ NAD+ & NADP+ or other oxidizing agent always participates.

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139
Q

Is Oxidative Decarboxylation endergonic or exergonic?

A

always exergonic ΔG< 0

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140
Q

_____________________ always participates in oxidative decarboxylation &
often in simple decarboxylations

A

Thiamine pyrophosphate

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141
Q

Oxidative Decarboxylation:

The overall reaction is ____________ : FA cannot be converted into carbohydrate

A

irreversible

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142
Q

What is the allosteric regulation of PDH?

A

– Inhibition by ATP, acetyl-CoA and NADH
– Activation by AMP, CoA and NAD+

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143
Q

What is the covalent regulation of PDH?

A

– Activation by dephosphorylation [PD phosphatase]
– Inhibition by phosphorylation of E1(pyruvate dehydrogenase)
(by PD Kinase activated by ATP)

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144
Q

REFREASH TCA CYCLE

A

!

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145
Q

What is the prime site of the TCA cycle?

A

oxaloacetate

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146
Q

What are the three enzymes that regulate the TCA cycle?

A

-Citrate synthase
-Isocitrate dehydrogenase
-α-Ketoglutarate dehydrogenase

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147
Q

Key sites of Regulation of TCA:

Citrate synthase is inhibited by…

A

ATP, citrate, NADH and succinyl-CoA

148
Q

Key sites of Regulation of TCA:

Isocitrate Dehydrogenase is inhibited by…

A

ATP, alpha ketoglutarate, and NADH

149
Q

Key sites of Regulation of TCA:

α– Ketoglutarate dehydrogenase is inhibited by…

A

ATP, GTP, succinyl-CoA and NADH

150
Q

Can pyruvate ONLY get into the TCA cycle through
decarboxylation?

A

No. Anaplerotic pathways.

-pyruvate carboxylase —> oxaloacetate (ATP-dependent carboxylation reaction)
-Malic enzyme —–> Malate (pro- and eukaryotes)
-oxaloacetate —> PEP by PEP-CK, heart and skeletal muscle (phosphoenolpyruvate carboxykinase)

151
Q

Oxaloacetate is very important for…

A

gluconeogenesis

152
Q

Where does gluconeogenesis mainly take place?

A

liver, not muscle

153
Q

Gluconeogenesis:

7 out of 10 reactions are the reverse of __________.

A

glycolysis

154
Q

The highly exergonic nature of the glycolysis is due to what reactions?

A

HK/GK, PFK-1, and pyruvate kinase reactions.
Three reaction cannot be reversible

155
Q

Gluconeogenesis must get around the three irreversible reactions by a new set of exergonic reactions that drive the process in the _________ direction.***

A

opposite

156
Q

What are the gluconeogenesis substrates?

A

-Lactate (pyruvate) – Cori cycle
-Glucogenic AA (all, except leu & Lys)
-Glycerol (from the breakdown of TG)
-All TCA intermediates

157
Q

Is acetyl-CoA a TCA intermediate?

A

NO

158
Q

What AA do NOT give you intermediates that fit into the TCA cycle?

A

leu and Lys

159
Q

How is lactate (pyruvate) continuously produced?

A

-RBC metabolism
-excising muscles

160
Q

Where are the majority of the enzymes responsible for gluconeogenesis are found?

A

cytosol, although some precursors are generated in the mitochondria

161
Q

Cori cycle summary

A

[ Liver ] 2 lactate ->2 pyruvate –>(6) glucose
————>
[ Muscle ] glucose (2ATP) –> 2 pyruvate –> 2 lactate

back to liver (by blood)

Net consumption of 4 ATPs

162
Q

The Cori cycle is very energy ___________.

A

inefficient

163
Q

How is pyruvate converted to PEP?
first reaction…

A

A biotin-dependent carboxylation of pyruvate by pyruvate
carboxylase to yield oxaloacetate

primes the TCA cycle

164
Q

How is pyruvate converted to PEP?
second reaction…

A

A decarboxylation by phosphorenolpyruvate carboxykinase
(PEPCK) to produce PEP

165
Q

Conversion of OAA to PEP can occur through the action of cytosolic or mitochondrial PEP-CK

What is it for Ala?
What is it for Lac?

A

Alanine- cytosolic
Lactose-mitochondrial

166
Q

Gluconeogenesis, which occurs in the cytosol, requires _______

A

NADH

NADH “must” be generated in the cytosol or imported from the mitochondria

167
Q

How is NAD+ supplied for glycolysis?

A
168
Q

What is important for regulating gluconeogenesis pathway?

A

-PEPCK
-fructose 1,6 bisphosphatase
???

169
Q

PEP is converted to ______ by the glycolytic enzymes acting in reverse.

A

F-1,6-BP

170
Q

The PFK-1 reaction is bypassed in by a simple hydrolytic reaction
catalyzed by ______________________.

A

Fructose 1,6 Bisphosphatase

***This step represents the “major site of regulation” of gluconeogenesis

171
Q

The irreversible GK reaction is reversed by the action of ________________ (a simple hydrolysis).
➢ G-6-phosphatase is present in the liver & kidney.

  • Glucose can thus leave the liver and enter the blood.
A

Glucose-6-phophatase

172
Q

Gluconeogenesis:

***Carbon atoms for the synthesis of glucose are provided from ________ or _________.
This is why protein wasting is a prominent phenomenon during starvation
or Type 1 diabetes

What provides the necessary energy required by gluconeogenesis?

A

lactate, amino acids

*Lipid oxidation

173
Q

What is the major regulation site of gluconeogenesis?

The major allosteric modulator of the activities?

A

PFK-1/Fructose-1,6 Bisphophatase couple

Fructose-2,6 bisphosphate

174
Q

Phosphorylated PFK-2 (inhibited)- decreased levels of F-2,6 BP =

A

Inactivating PFK-1 & activating Fructose-1,6 Bisphosphatase

175
Q

disease associated with increased production and metabolism of glucose
What are the types?

A
  • Type I
    – Type II
    – Secondary
    – Gestational
176
Q

Type 1 diabetes accounts for ____% of all cases of diabetes and is usually diagnosed before the age of ____.

A

5-10, 20

177
Q

Causes of type 1 diabetes?

A

inherited, autoimmune or infection

178
Q

What are the complications of type 1 diabetes?

A

Retinopathy, Neuropathy, Nephropathy,
Angiopathy*

Hyperlipidemia, Ketoacidosis, increased susceptibility to infection & lactic acidosis

179
Q

Clinical presentation of ketoacidosis patients?

A

low HCO3-, normal pCO2, high anion gap and [glucose]blood —> Low pH

180
Q

What is the difference in type 1 diabetic and starvation induced ketoacidosis?

A

presence of hyperglycemia in type I diabetics and hypoglycemia in starvation.

181
Q

____________ causes type I diabetes to use FA as an alternative

A

Insulinopenia

FA mobilized —-> increases acetyl-CoA
Excess AcCoA!acetoacetyl CoA –> HMG CoA

182
Q

Type II diabetes accounts for _______ % of all diagnosed cases of diabetics

A

90-95

2% of Americans

often obesity related but appears to have a hereditary component

183
Q

Onset of type II diabetes is usually after ____ years of age.

A

40

184
Q

Type II diabetes is characterized by hyperglycemia and “presence of _________”

A

insulin

185
Q

Diabetic ketoacidosis primarily occurs in type….

A

I diabetics; however,
can occur in type II diabetics

186
Q

Gestational diabetes occurs in ____ % of pregnancies.

What causes it?

A

2-5

inability to secrete insulin towards the 4x increase in demand

187
Q

What is the risk of gestational diabetes?

How is it treated?

A

-Hyperglycemia increases the risk of spontaneous abortion & birth defects

-Treated with insulin or hypoglycemia agents

188
Q

What is the primary structural change in a protein happening with high blood glucose?

A

Covalent bonding of carbohydrates to proteins produced in presence of excess carbohydrates

elevation of GHb

189
Q

The elevation of GHb occurs about ___ wks after sustained
elevation in blood glucose, and last ____ months

A

3, 2-3

190
Q

What is used to assess adherence to insulin treatment?

A

Percent of glycosylated Hb (HbA1c)

191
Q

What conditions/diseases is testing of HbA1c not good for? why?

A

-cystic fibrosis
-gest. diabetes
-pt. with chronic liver or kidney disease
-sickle cell anemia

because RBC turnover is too fast

192
Q

Normal HbA1c %?

A

below 5.7%*

193
Q

Prediabetes HbA1c %?

A

5.7-6.4%*

194
Q

Diabetes HbA1c %?

A

6.5% or above*

195
Q

HbA1c:***
* Child:
* Good diabetic control:
* Fair diabetic control:
* Poor diabetic control:

A
  • Child:1.8-4%
  • Good diabetic control: 7%
  • Fair diabetic control: 10%
  • Poor diabetic control:
    13-20%
196
Q

What is normal Glucose level range?

A

70-110 mg/dL

197
Q

Decreased blood glucose concentration can result in mild to severe coma, seizures and death.
* Occurs when blood glucose is less than ____ mg/dL

A

50

Cf. According to ADA, less than 70 mg/dl

198
Q

What are causes of hypoglycemia?

A
  • Excess insulin
    – Liver disease
    – Alcoholism
    – Renal insufficiency
    – Malignancy (beta cell tumor)
    – Infection
    – Pregnancy
    – malnutrition
199
Q

Treatment for hypoglycemia

A

IV glucose

200
Q

NADH Ethanol Metabolism…

A

-alcohol dehydrogenase converts, in the cytosol, EtOH to acetaldehyde & produces
NADH
* Acetaldehyde enters mitochondria and is oxidized by acetaldehyde
DH to acetate and generates NADH

201
Q

The capacity to metabolize EtOH is dependent upon the ability to shuttle ______ into mitochondria.

A

NADH

202
Q

In NADH ethanol metabolism, increased NADH inhibits….

A

gluconeogenesis, FA oxidation, &
glycerophosphate DH***

203
Q

Hepatic Ethanol Toxicity:

NADH increases pyruvate to lactate, thus inhibiting pyruvate conversion to

A

glucose

(Inhibiting gluconeogenesis)

204
Q

How does hepatic ethanol toxicity lead to “fatty liver” and hyperlipidemia?

A

-Acetate converted to acetyl-CoA, can’t be oxidized in TCA so converted to fat

-Inhibited glycerophosphate DH leads to more glycerophophate which
is a backbone of TGs,

205
Q

Hepatic Ethanol Toxicity:

_______________ forms adducts with proteins, nucleic acids, leading to acute toxic effects
* EtOH inserted into membranes altering action potentials and depressing CNS function.

A

Acetaldehyde

206
Q

Heparin is a type of

A

Is a mix of sulfonated polysaccharides

207
Q

Glucuronic acid

A

helps remove harmful substances from the body

Is ethier a oxidized or reduced form of glucose

208
Q

Galactose to

A

—-galactose kinase–> galactose 1 phosphate

  • type two galactosemia
209
Q

Galactose 1 phosphate

A

—uridylyltransferase with UDP-gal-glu-1-P—> glucose 1 phosphate

type one galactosemia

210
Q

Glucose 1 phosphate to

A

—phosphoglucomutase–> glucose 6 phosphate

211
Q

Glucose 6 phosphate–>

A

G-6-P—>F-6-P—>F-1,6-BP

212
Q

Lactose goes to what and then what

A

Galactose then glucose 1 phosphate

213
Q

Maltose goes to what and then what

A

Glucose and then glucose 6 phosphate

214
Q

Mannose goes to what and then what

A

Mannose 6 phosphate and then fructose 6 phosphate

215
Q

Sucrose goes to either what or what or what

A

Fructose—> fructose 6 P

Glucose—> Glucose 6 P

Fructose—> fructose 1 P—> Dihydroxyacetone or glyceraldehyde

216
Q

Glycerol goes to what

A

A glycerol phosphate then Dihydroxyacetone-P

217
Q

Fructose to F-6-P by

A

Hexokinase in other tissues

218
Q

Glucose to

A

Glucose—> G-6-P—-> F-6-P—-> F-1,6 BF

219
Q

Fructose in liver by Fructose kinase pathway

A

1.) Fructose—> Fructose 1 phosphate by Fructose Kinase and ATP is converted into ADP

2.) Fructose 1 Phosphate——> either Glyceraldehyde or DHAP by enzyme Fructose 1-P aldolase

3A.) Glyceraldehyde—-> Glyceraldehyde 3 phosphate by enzyme Triose kinase and ATP to ADP

3B.) DHAP—> Glyceraldehyde 3 phosphate with enzyme TIM

220
Q

Glucose to G-6-P to

A

F-6-P—> F,1,6 BP

221
Q

Glucose 1 phosphate—> UTP to PPi and enzyme UDP-glc pyrophosphorylase to UDP- glucose

A

1.) UTP to PPi and enzyme UDP-glc pyrophosphorylase to UDP- glucose

2.)

222
Q

Ribose is a

A

Glucose metabolite

223
Q

Glycogenesis

A

The formation of glycogen from sugar

224
Q

Gluconeogenesis

A

The making of sugar from non carb sources

225
Q

Glycogeneisis

A

Produces the storage form of glucose

High MW polysaccharide composed of glucose

226
Q

Glycogen is linked

A

Linked with a (1–>4) glycosidic bond and branches with a (1—>6) glycosidic bond (every 10 units)

227
Q

Mutase

A

Catalyses the movement of a functional group from one location to another

228
Q

Kinase

A

Transfers of a phosphate group from a ATP molecular to another another molecule

229
Q

Transferase

A

Catalyzes the transfer of a group from one molecule to another

230
Q

Pyrophosphorylase

A

Catatalyses the nterconversion of glucocose 1 phosphate and Uridine triphosphate (UTP) to inorganic phosphate and UDP glucose

231
Q

Glycogenin

A

Involves in the Convertion glucose to glycogen

232
Q

Pyruvate to blank in aerobic conditions

A

Acetyl COA

233
Q

Pyruvate to blank in anaerobic conditions

A

Lactate in RBC’s

234
Q

NAD+ and FAD+ are special what

A

Proton acceptors

235
Q

Oxidative form

A

NAD+ and FAD+

236
Q

Reduced form

A

NADH and FADH

237
Q

what is added to make NAD+ into NADH

A

a hydride ion H* + and a -

238
Q

what are kinases

A

Recall that kinases are enzymes that catalyze the transfer of the terminal phosphoryl group from ATP to an acceptor nucleophile.

239
Q

Step one glycolysis

A

one phosphate group are attached to one molecule of glucose 6 phosphate, ATP is converted to ADP with the help of Mg2+ and G10=-16.7 kj/mol

240
Q

Hexokinases and magnesium

A
  • The acceptor in the case of hexokinase is a hexose, normally D-glucose
  • hexokinase also catalyzes the phosphorylation of other common hexoses, such as D-fructose and D-mannose.
  • Hexokinase, like many other kinases, requires Mg2+ for its activity, because the true substrate of the enzyme is not ATP4- but the MgATP2- complex. Mg2+ shields the negative charges of the phosphoryl groups in ATP, making the terminal phosphorus atom an easier target for nucleophilic attack by an –OH of glucose.
241
Q

Where are hexokinases

A
  • Hexokinase is present in all cells of all organisms. Hepatocytes also contain a form of hexokinase called hexokinase IV or glucokinase, which differs from other forms of hexokinase in kinetic and regulatory properties.
  • Two enzymes that catalyze the same reaction but are encoded in different genes are called isozymes.
242
Q

Preparatory phase of glycolysis step two

A

Glucose -6-phosphate is converted into fructose-6-phosphate with the help of Mg2+. G10=1.7 kj/mols; The reaction proceeds readily in either direction,as might be expected from the relatively small change in standard free energy

243
Q

The enzyme phosphohexose isomerase

A

catalyzes the reversible isomerization of glucose 6-phosphate, an aldose, to fructose 6-phosphate, a ketose.

244
Q

The PFK-1 enzyme

A

catalyzes the transfer of a phosphoryl group from ATP

245
Q

PFK-is

A

is essentially irreversible under cellular conditions, and it is the first“committed” step in the glycolytic pathway; glucose6-phosphate and fructose 6-phosphate have other possible fates, but fructose 1,6-bisphosphate is targeted for glycolysis.

245
Q

The PFK-1 reaction

A

is essentially irreversible under cellular conditions, and it is the first“committed” step in the glycolytic pathway; glucose6-phosphate and fructose 6-phosphate have other possible fates, but fructose 1,6-bisphosphate is targeted for glycolysis.

246
Q

PFK is considered what

A

PFK-1 was considered the rate-limiting enzyme, because it was known to be closely regulated by fructose 2,6-bisphosphate and other allosteric effectors.

247
Q

some bacteria and protists and perhaps all plants have

A

PFK catalyzes the phosphorylation of fructose-6-phosphate into fructose-1,6-biphosphate also using Mg2+ to convert a ATP into ADP G10=-14.2 Kj/mol

248
Q

More one PFK-1

A

Phosphofructokinase-1 is a regulatory enzyme, one of the most complex known.

  • It is the major point of regulation in glycolysis.
  • The activity of PFK-1 is increased whenever:
  • the cell’s ATP supply is depleted
  • when the ATP breakdown products, ADP and AMP (particularly the latter), are in excess.
  • The enzyme is inhibited whenever the cell has ample ATP and is well supplied by other fuels such as fatty acids.
248
Q

The activity of PFK-1 is increased when

A
  • the cell’s ATP supply is depleted
  • when the ATP breakdown products, ADP and AMP (particularly the latter), are in excess.
248
Q

The enzyme fructose 1,6 bisphosphate aldolase often called aldolase is

A

catalyzes a reversible aldol condensation

249
Q

Fructose 1,6 bisphosphate is cleaved to yield

A

two different triose phosphates, glyceraldehyde3-phosphate, an aldose, and dihydroxyacetonephosphate, a ketose

250
Q

Although the aldolase reaction has a strong positive standard free energy change

A

in the direction of fructose1,6-bisphosphate cleavage, at the lower concentrations of reactants present in cells, the actual free-energy change is small and the aldolase reaction is readily reversible

250
Q

step 4 of glycolysis

A

Fructose 1,6-bisphosphate <–> dihydroxyacetone + glyceraldehyde 3-phosphate.

Uses an aldolase enzyme.

251
Q

Only one of the two triose phosphates formed by aldolase, Glyceraldehyde-3-phasphate can

A

can be directly degraded in the subsequent steps of glycolysis.

252
Q

The other product, DHP is rapidly and reversibly converted to

A

glyceraldehyde 3-phosphate by the fifth enzyme of the sequence, triose phosphate isomerase

252
Q

Step 5

A

Dihydroxyacetonephosphate <–> glyceraldehyde 3-phosphate

Uses triose phosphate isomerase enzyme.

253
Q

Step 5 characteristics

A

This reaction completes the preparatory phase of glycolysis. The hexose molecule has been phosphorylated at C-1 and C-6 and then cleaved to form two molecules of glyceraldehyde 3-phosphate.

254
Q

The payoff phase

A

Remember that one molecule of glucose yields two molecules of glyceraldehyde 3-phosphate; both halves of the glucose molecule follow the same pathway in the second phase of glycolysis. The conversion of two molecules of glyceraldehyde 3-phosphate to two molecules of pyruvate is accompanied by the formation of four molecules of ATP from ADP

255
Q

The first step of the payoff phase

A

glyceraldehyde 3-phosphate to 1,3-bisphosphoglycerate, catalyzed by glyceraldehyde 3-phosphate dehydrogenase

256
Q

The acceptor of hydrogen in the glyceraldehyde 3-phosphate dehydrogenase is

A

is NAD

257
Q

Because cells maintain only limited amounts of NAD

A

glycolysis would soon come to a halt if the NADH formed in this step of glycolysis were not continuously oxidized

257
Q

Step 6

A

Glyceraldehyde 3-Phosphate + Pi <–> 1,3-biphosphoglycerate.

Uses G3P dehydrogenase enzyme.

NAD+ <–> NADH

258
Q

step 7

A

1,3-bisphosphoglycerate + ADP <–> 3-phosphoglycerate + ATP+ mg2+

Uses phosphoglycerate kinase enzyme.

258
Q

The enzyme phosphoglycerate kinase

A

transfers the high-energy phosphoryl group from the carboxyl group of 1,3-bisphosphoglycerate to ADP, forming ATP and 3-phosphoglycerate

259
Q

Steps 6 and 7 are

A

exothermic together

260
Q

Step 8

A

3-phosphoglycerate <–> 2-phosphoglycerate

Uses phosphoglycerate mutase enzyme and Mg2+

261
Q
A
262
Q

2,3 BPG

A

s initially phosphorylated by phosphoryl transfer from 2,3-BPG, which is required in small quantities to initiate the catalytic cycle and is continuously regenerated by that cycle.

263
Q

Step 9

A

2-phosphoglycerate <–> Phosphoenolpyruvate (PEP)

Uses enolase enzyme.

Dehydration reaction (loss of water).

263
Q
A
264
Q

Enolase promotes

A

reversible removal of a molecule of water from 2-phosphoglycerate to yield phosphoenolpyruvate (PEP)

265
Q

Step 10

A

PEP + ADP –> Pyruvate + ATP

Uses pyruvate kinase enzyme + mg2+ and K+.

266
Q

TCA cycle step one

A

Oxaloacetate( 4C) + Acetyle CoA( 2C) –> Citrate

267
Q

Too much citrate can be used to make

A

Fatty acid steroid synthasis

268
Q

Citrate to

A

Isocitrate by enzyme Aconitase

269
Q

Isocitrate to

A

a-ketoglutarate by Isocitrate dehydrogenase

270
Q

a-ketogluterate to

A

Succinyl CoA by a-ketoglutarate dehydrogenase

271
Q

A-ketogluterate can be used

A

for AA synthesis

272
Q

Succinate to

A

Fumarate by Succinul dehydrogenase

273
Q

Malate to

A

Oxaloacetate by malate dehydrogenase

274
Q

Oxaloacetate to

A

PEP by PEP carboxykinase

275
Q

PEP to either

A

Glucose of AA

276
Q

Phosphatase

A

Dephosphatase in liver and kidneys

277
Q

More glycogen becomes

A

Fat

278
Q

Long chain fatty acids to

A

–> FA spiral–> Acetyl CoA by B-oxidation

279
Q

16FA –>

A

8 Acetyl coA

280
Q

16FA –>

A

8 Acetyl coA

281
Q

Insulin has a

A

Anabolic function Inhibits fat burning

282
Q

Acetyl coA–>

A

lipogenesis–> FAs

283
Q

Amminoacids–>

A

Nitrogen pools

284
Q

Nitrogen pool–>

A

-Pyruvate
- Acetyl coA
- NH3–> Urea cycle

285
Q

ATP/AMP:ADP: P ratio is decreased

A

FA metabolism is stimmulated

286
Q

Vegans dont eat meat

A

receptor hit BV and then cholestral can be internalized

287
Q

Cholesterol is a

A

Steroid hormone

288
Q

Endogenous cholesterol synthesis pathway

A

your body can make Cholesterol

289
Q

Pentose phosphate pathway will

A

Reduce Oxidative damage

290
Q

Too much NADH and FADH then citrate will exit the mitochondria and make

A

FAT

291
Q

Citrate is exergonic products or endergonic products –>

A

products are endergonic

292
Q

Acetyl coA + oxaloacetate to citrate is

A

Catabolic and exergonic

293
Q

A high NADH can

A

fight Oxidative damage

294
Q

NADH=

A

Redox potential elevated

295
Q

As we age

A

Increase in NAP+ and FAP2+

296
Q

Alpha confirmation

A

OH on bottom

297
Q

Beta confirmation

A

OH is on top

298
Q

Km values indicate how strong

A

Interaction of molecules

299
Q

Velocity vs what

A

Substrate

300
Q

Vmax is

A

Maximum velocity of reactions

301
Q

Km is

A

is Substrate concentration that is required to make speed to reach 1/2 vmax

302
Q

lower kM=

A

high affinity

303
Q

Higher kM

A

lower affinity

304
Q

too much glucose in cells

A

apoptosis

305
Q

glucose is important in

A

regulating osmo

306
Q

Obligatory glycolysis

A

Lack of mitochondria= RBC

307
Q

Glucuronic acid is important in

A

clearing bilirubin

308
Q

Heparin is a

A

Anti-oxidant

309
Q

there is no heparinized

A

Serum

310
Q

Integral proteins

A

Glycolysalated proteins

311
Q

Fructose 1-6 Bisphosphatase will influence what

A

Gluconeogenesis

312
Q

GLycogen to

A

Glucose 1 phosphate

313
Q

UDP gal for

A

UDP glucose

314
Q

1- benign form of epimerase deficiency

A

only in RBC and WBC

315
Q

transferace form of epimerase defciency

A

whole body

316
Q

Glucose UDP to

A

glycogen-G-G-G glycogen synthase

317
Q

Epipinephere

A

Sympathetic nervous system- HR increase- ATP increase– ADP and AMP increase

318
Q

Glycogen synthase activity is increased if blank is removed

A

Phosphate

319
Q

PKA inhibits glycogen synthesis but enhances

A

Glycogenolysis

320
Q

regulation of Pyruvate dehydrogenase

A

-Allosteric regulation
inhibited by ATP, acetyl coA, and NADH
Activated by AMP, CoA, and NAD+
- Covalent regulation
Activated by Dephosphorylation (PD phosphatase)
Inhibited by phosphorylation of E1(pyruvate dehydrogenase) ( by PD kinase activated by ATP)

321
Q

Pyruvate with enzyme Pyruvate dehydrogenase –>

A

Acetyl coA with lose of CO2

322
Q

Only small FA can

A

be used to go into the mitochondria and make acetyl coA

323
Q

Pyruvate dehydrogenase complex cofactors

A

Lipoate, FAD+, and TPP

324
Q

Pyruvate dehydrogenase complex

A

E1= real pyruvate dehydrogenase
E2= Dyhydrolipamide transferase
E3= Dihydrolipoamide dehydrogenase= is the dehydrogenase

325
Q

Thiamine pyrophosphatase is needed in

A

Oxidative decarboxylation and simple decarboxylation

326
Q

gluconeogenisis components

A

Glyceral, AA, and lactate
lactate= to pyruvate
alanine= to pyruvate
glyceral= to glyceraldehyde 3 phosphate

327
Q

thrid name for Pentose phosphate pathway

A

Alternative glucose oxidation pathway

328
Q

Glucose becomes ribose through

A

hydrolysis

329
Q

Ribose is used in

A

Nucleotides and nucleic acids-utilization of pentose

330
Q

PPP=NADPH=

A

used in FA and cholesterol synthesis

331
Q

liver=

A

lipogenesis FA and cholestral synthesis

332
Q

Mammary gland

A

FA storage

333
Q

NAPDH can be a source of hydrogen for

A

Oxidized glutathione

334
Q

Lenghts of survival of cells depend on

A

Pentose phos pathway

335
Q

glucose can get into cells by

A

Glucose transportors

336
Q

PPP= glucose 6-phosphate-2 pathways

A

1.) glucose 6 phosphate–> glycolysis–> 2 pyruvate or NADH or 2 ATPs–> lactate dehydrogenase–> Lactate+NAD+
**The second pathway is the Pentose phosphate pathway
2.) 1. glucose 6-phosphate–> Glucose 6 phosphate dehydrogenase–> 2NADP+ to NADPH–> Glutathione reductase–> 3a- 2GSH to GSGS–> 3B. 2GSH–> glutathione peroxidase–> H202 to 2H20

337
Q

OH- is a strong source of

A

hemolysis

338
Q

ROS is built up

A

Heiz bodies

339
Q

Pentose phosphate pathway oxidative step one

A

1.) Glucose 6 phosphate is oxidized with enzyme G6PDH and NADP to NADPH—> 6- phosphogluconolacetate

340
Q

The pentose phosphate pathway is divided into two steps

A

Oxidative and non-oxidative

341
Q

PPP step three oxidative

A

6-phosphogluconate with enzyme 6-phosphogluconate DH with NADP+, NADPH, CO2—-> Ribulose 5-phosphate

342
Q

Ribulose-5 phosphate oxidative to

A

Non oxidative reactions

343
Q

PPP oxidative step two

A

6 phosphogluconolactone is hydrolized( h20–>OH+H) with enzyme gluconolactonase —> 6 phosphogluconate.

344
Q

step one of PPP oxidative in word form

A

G-6-P is oxidized to 6-phosphogluconolactone by G-6-PDH
- 1 molecule of NADPH is generated by reducing NADP

345
Q

Step two of PPP oxidative in word form

A

The lactone is hydrolyzed by a lactonase to 6-phosphogluconate

346
Q

Step three of PPP oxidative in word form

A

6-phosphogluconate is oxidatively decarboxylated
by 6-phosphogluonate dehydrogenase to ribulose-5-phophate and CO2
And an additional molecule of NADPH

347
Q

Step 4,5,6 PPP oxidative in word form

A

4) Ribulose-5-P Ribose-5-P [Phosphopentose isomerase]DNA and RNA synthesis
5) Unneeded ribose-5-Ps are recycled back to hexose-6-Ps thought a series transketolase & transaldolase- catalyzed reactions
6) The resulting hexose phosphates are either recycled through the pentose phosphate pathway or through glycolysis

348
Q

Non oxidative PPP

A

recycled pathway

349
Q

PPP non oxidative steps

A

ribose 5 P made and goes to DNA and RNA synthesis
- if we don’t need Ribose 5 P then R5P goes to Glyceraldehyde 3 P in step 6 of Glycolysis
- Fructose 6 P can go to step 2 in Glycolysis
- glucose 6 P can go to step one of glycolysis

350
Q

Non-oxidative steps of PPPcan be connected to the

A

glycolytic pathway

351
Q

activators of TCA enzymes

A

Substrates, AMP and ADP, and NAD+

352
Q

Oxaloacetate is really important for gluconeogenesis

A

Oxaloactate–> PEP–> either AA or glucose

353
Q

TCA cycle- Pyruvate—> oxaloacetate is catalyzed by what

A

ATP dependent reaction with pyruvate carboxylase

354
Q

what activates Pyruvate carboxylase

A

Biotin and acetyl coA

355
Q

Muscle response to exercise

A

Glycogen synthesis decreased,

glycolysis increased

increased degradation

356
Q

Glycerol phosphate shuttle

A

1A.(1/2) glucose —> glyceraldehyde 3 phosphate
2A. Glyceraldehyde 3 phosphate with glyceraldehyde 3PDH—> 1,3 BPG
2B. NAD–>NaDH
2C. glycerol 3 phosphate with glycerol 3 PDH–> DHAP
2D. FAD with glycerol 3 PDH–> FADH2
3A- 1,3 BPG–> pyruvate
4A- pyruvate–>acetyl coA

357
Q

Malate-aspartate shuttle

A

1A.(1/2) glucose —> glyceraldehyde 3 phosphate
2A. Glyceraldehyde 3 phosphate with glyceraldehyde 3PDH—> 1,3 BPG
2B. NAD–>NaDH
2C. OAA with MDH enzyme—> Malate
2D. malate–>a-ketoglutarate
3A. 1,3 BPG–> pyruvate
4A. Pyruvate–> Acetyl coA

358
Q

Malate aspartate shuttle and glycerol phosphate Shuttle work under what conditions

A

Aerobic conditions

359
Q

The Alanine cycle

A

Glucose—> 2pyruvate—> alanine muscle

Alanine—> pyruvate—> glucose liver

6atps consumed

Alanine—> NH2–> urea

4atps are consumed

Clinical Chemistry II - 4378 (28 decks)

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