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BI25M7: Energy for Life > Barrow: Carbohydrates > Flashcards

Barrow: Carbohydrates Flashcards

1
Q

What four things are carbohydrates useful for?

A

They are highly oxidisable (“high energy” H-atom associated electrons = major energy source for metabolism)

Storage of energy (starch in plants, glycogen in animals)

Structural and protective functions (plant cell walls, extracellular matrices around animal cells)

Cell-to-cell communication (eg: ABO blood groups)

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2
Q

How are carbohydrates stored long term (plants/animals)?

What structural and protective functions do carbs have?

A

As starch in plants, as glycogen in animals

Cell walls (plants), extracellular matrix (animals)

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3
Q

What is the name for six carbon sugars?

What are the three important ones in humans?

A

Hexoses

Glucose, galactose, fructose

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4
Q

Disaccharides: what is the covalent bond between the monosaccharides called?

What is an anomeric carbon? Which is it on glucose (and many others)? What two things make it important?

A

Glycosidic bond

Carbon on end of linear molecule if it wraps around on itself and joins together (carbon #1 on glucose) - stabilizes structure and it is the only residue that can be oxidised

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5
Q

Three important disaccharides in human biochemistry?

A

Maltose, lactose, and sucrose

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6
Q

What makes something a “reducing sugar”?

A

It has an anomeric carbon that is available for oxidation

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7
Q

Do we get maltose from the diet?

What is it a breakdown product of? Where is it therefore often found?

What two monosaccharides is it made from? Which type of glycosidic bond is it?

A

Not much

Starch (found in beer)

Alpha-D-Glucose and Beta-D-Glucose (Alpha 1,4)

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8
Q

Lactose: is it termed a reducing sugar?

What monosaccharides make it up?

A

Yes

Galactose and glucose (NB: remember the lactose part of galactose minus the g of glucose)

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9
Q

Common table sugar: what is the actual name?

How much % of dietary carbs does it make up?

What makes it? Also, is it a reducing sugar? Why/why not?

A

Sucrose

25%

Plants. No (no free anomeric C-1)

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10
Q

What is the name of molecule with lots of monosaccharides?

How are they classified? [4]

A

Polysaccharides

Identity of units (homopolysaccharide = one type of monomer, hetero = 2+ types), amount of branching, length of chains, and type of linkages

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11
Q

Starch

Made up of which monomers?

What are the names of the two polymers that make it up? How much of each are there? How do they differ?

A

Glucose

Amylose (20-25%) and Amylopectin (75-80%), former are linear with only alpha-1,4 linkages, whereas latter are also branched (every 24-30 residues) via alpha-1,6 linkages

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12
Q

Starch

What structure does it tend to form when the two components come together?

What does “non-reducing end” essentially mean?

A

Many non-reducing ends, few reducing ends, and believed to form alpha helices and a structure as seen in picture

Essentially just a nomenclature thing - it’s the end where stuff tends to get added on to.

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13
Q

Glycogen

How is glucose linked in this animal storage system?

Where is most of glycogen stored? How much is “most”? What different functions is it used for in these two places?

A

Alpha-1,4 linear with branches (alpha-1,6) every 8 to 12 residues

90% in liver (replenishes blood glucose) and skeletal muscles (catabolism produces ATP for contraction)

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14
Q

What three major reasons do we store glucose in glycogen?

A

Compactness (good for storage), many non-reducing ends (so can be formed/degraded quickly as needed), and it is a hydrated gel (not in solution = osmotically inactive = kept in cell for far lower energy cost)

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15
Q

What is the name of the proteins with carbohydrates covalently attached?

A

Glycoproteins

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16
Q

Glycoproteins

What are they?

Where are they commonly found?

What do the attached bits potentially do? [4]

A

proteins with carbohydrates covalently attached

Often attached to extracellular proteins

Increases protein solubility, influences folding/conformation, protects proteins from degradation, and acts as communication between cells.

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17
Q

Glycosaminoglycans

What did they used to be called? Where are they often found?

What are they?

A

Mucopolysaccharides (mucus and synovial fluid around joints)

Unbranched polymers made from repeating units of hexuronic acid and amino-sugar (sugar molecule with nitrogen on it)

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18
Q

Proteoglycans

What are they? What composes the majority of their structure?

How are they formed?

Where are they often found (in terms of cell and tissue)?

A

Protein + carbs (carbs dominant)

Formed from glycosaminoglycans attaching to proteins

Found on surface of cells or within extracellular matrix (so common part of connective tissue)

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19
Q

Glycoproteins

These are similar to proteoglycans. What’s the difference?

Where are they usually found? Where else can they be found?

A

Protein is dominant over carb

Usually found on plasma membrane and in ECM. Also: in blood and within cells in secretory system. Occasionally: cytoplasmic/nuclear proteins are glycoproteins

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20
Q

What are mucopolysaccharidoses?

What happens?

A

Genetic disorders caused by absence or malfunction of glycosaminoglycan breakdown enzymes

Over time, GAGs build up in connective tissue, blood, and cells -> damages cellular architecture and function -> dementia, heart and other endothelial structures (builds up between endothelial cells), stunted bones, joints inflamed/damaged

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21
Q

Can you remember the name of any mucopolysaccharidoses?

A

Hurler, Scheie, Hunter, and Sanfillipo syndromes

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22
Q

Hurler Syndrome: describe it

A

Mucopolysaccharidose leading to developmental defects (stop growing at 4, death by 10), clouding/degradation of cornea, arterial wall thickening, dementia (caused by build up of CSF and enlarged ventricles)

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23
Q

Digestion of carbohydrates. Run through what happens in…

… mouth…

… stomach…

… duodenum…

… jejunum [4]…

Main products?

A

Mouth: salivary amylase hydrolyses alpha-1,4 bonds

Stomach: nothing

Duodenum: pancreatic amylase (as mouth)

Jejunum: mucosal sell surface enzymes (isomaltase hydrolyses a-1,6; glucoamylase removes glucose from non-reducing ends; sucrase hydrolyses sucrose; lactase hydrolyses lactose)

Main products: glucose, galactose, fructose

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24
Q

Walk through absorption of glucose from the intestinal lumen into the blood

A

Glucose and Na+ symported into cell (driven by high EC Na+)

Sodium kept low (and potassium high) by acive pumping on basal surface of cell

Glucose (GLUT2) transporter allows glucose to pass into blood on basal side

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25
Q

Does glucose require ATP to be pumped through?

How does galactose differ?

How does fructose differ?

A

Indirectly - Na/K pump needed to maintain low sodium in cell to allow symporter on apical side of cell to function. This means glucose will enter cells even when its concentration is high.

It doesn’t

Binds to GLUT5 and moves down concentration gradient (high in gut, low in blood)

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26
Q

What is the use of cellulose and hemicellulose (plant oligosaccharides)?

What does break them down? What does this produce?

A

Can’t be digested, but increase faecal bulk and decrease transit time [too many/too few = unhealthy]

Gut bacteria - yields methane and hydrogen

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27
Q

How do you get disaccharidase deficiencies?

What are they characterised by?

What are the enzymes called for the three major disaccharides?

A

Genetic, severe intestinal infection, inflammation of gutlining, drugs injuring gut wall, surgical removal of intestine

Characterised by abdominal distention and cramps

Lactase, maltase, and sucrase

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28
Q

What is the most common disaccharidase deficiency?

Why do some people not have it? Which people?

What are the symptoms of deficiency? Why do they happen?

A

Lactose intolerance

Largely westerners: came from cattle domestication

Abdominal distension and cramps and the squits: undigested lactose broken down by gut bacteria (= gas build up and irritant acids), and lactose is osmotically active (= water into gut lumen -> squits)

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29
Q

What happens to glucose after it diffuses through the intestinal epithelium cells?

What happens to it when it reaches this point (or any other cell)? What effect does this have on the glucose?

A

Goes into portal blood and on to the liver

Hepatocytes (or other cells) phosphorylates it to G6P (which cannot diffuse out of cells - GLUT transporters won’t recognize it) [NB: also is first step in extracting energy from glucose]

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30
Q

What is the name of the enzyme catalyst that converts glucose to G6P?

How do the enzyme Km and Vmax differ between liver and other cells?

Why is this important in glucose metabolism?

A

Hexokinases (glucokinase in the liver)

Glucokinase (high Km/low binding, high vmax/rapidly processed), Hexokinases (low km/high binding, low vmax/slowly processed).

Liver only grabs up glucose if blood glucose is high (and it then does so quickly), whereas hexokinases elsewhere are constantly taking it in at lower levels.

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31
Q

Draw a diagram (involving blood, liver, and other tissues) that shows what happens to glucose after it is absorbed from the intestine.

A
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32
Q

What are the two main places where glycogen is stored? How much of it is found there?

A

Skeletal muscles and liver (90%)

33
Q

What is the name of the liver enzyme that turns G6P back into glucose? When does this happen?

What happens in skeletal muscles? Why?

A

Glucose-6-phosphatase (when blood glucose falls)

It goes through glycolysis and, in exercising muscles, is converted into lactate (because there is no phosphatase enzyme)

34
Q

What is the name of the protein that is necessary to begin the synthesis of glycogen?

What steps does it take before normal addition of glucose?

What is the name of the enzyme that, after this step, extends the glucose chain?

A

Glycogenin

It covalently binds approx. 8 glucose residues from UDP-glucose [Uracil-diphposphate-glucose]

Glycogen synthase

35
Q

Why do we have UDP-glucose?

A

It is a special pool of ‘tagged’ glucose that can be used for specific purposes (as opposed to being broken down) - for example, the initial synthesis of glycogen

36
Q

Glycogen synthase: what type of bonds are formed by this enzyme?

What is the name of the enzyme responsible for the branch points in glycogen? What type of bond does it form?

A

Alpha-1,4 glycosidic (covalent) bonds

Glycogen-branching enzyme, Alpha-1,6 glycosidic bonds

37
Q

Describe what glycogen looks like? How does it appear within cells?

A
38
Q

In the degradation/mobilisation of glycogen, what end are glucose monomers removed from, and in what form are they removed? What is the name of the enzyme?

A

Non-reducing ends (as Glucose-1-Phosphate) by glycogen phosphorylase

39
Q

Glycogen phosphorylase grinds to a halt at branch points. Why? What enzyme is used instead? What does it do?

A

Its active site is not configured to deal with them. Debranching enzyme takes over - stitches remaining glucose in branch to another non-reducing end (transferase activity), and then slices off alpha-1,6 link to release glucose monomer (glucosidase activity). Then glycogen phosphorylase can take over again.

40
Q

What happens to the glucose-1-phosphate once it is freed from glycogen? What then happens to it in the liver, and in the skeletal muscles?

A

It is converted to G6P. In the liver, glucose-6-phosphatase converts it to glucose, and it can be pumped into the blood. In the skeletal muscles, it undergoes glycolysis, creating ATP and lactate.

41
Q

What enzyme does von Gierke’s disease affect? Organs primary affected?

Symptoms?

Treatment?

A

Glucose-6-phosphatase. Liver (and kidney/intestines) affected.

High liver glycogen (not broken down), low blood glucose (fasting hypoglycaemia - because glycogen cannot be used), and high blood lactate (lacticacidaemia - lactate produced by skeletal muscle cannot be reconverted [Cori cycle] in the liver as G6Phosphatase is required)

Regular carb feeding every 3-4h throughout day and night

42
Q

What enzyme does McArdle’s disease affect?

Symptoms?

When do symptoms become apparent?

Treatment?

A

Skeletal muscle glycogen phosphorylase deficiency

High muscle glycogen (phosphorylase is used to break down glycogen), weakness and cramps post-exercise, no increase in blood glucose after exercise [not apparent at rest - other energy sources used - blood glucose and fatty acids]

20-30 years old

Avoid activity or use ‘second wind’ (exercise anaerobically, wait for pain to subside, and then continue)

43
Q

What feeds into glycolysis? What is the usual product?

A

6 carbon sugars (glucose), 3 carbon sugars (pyruvate) out

44
Q

Glycolysis is a _________ pathway that saves some potential energy from _______ by forming ___ through _________ _____ _______________ (and _______ electron carriers in limited numbers)

When it is the only way that energy can be made?

A

Catabolic, glucose, ATP, substrate level phosphorylation, reduced

In absence of oxygen (eg: exercising muscles) or in cells lacking mitochondria (eg: RBCs)

45
Q

Where in the cell does glycolysis occur? How many steps?

What occurs in the preparatory phase?

What happens in the payoff phase?

What is the net gain of glycolysis in terms of energy?

A

In the cytoplasm (10 steps)

Prep: Glucose converted into G3P and DHAP (which is converted to G3P = two molecules of G3P) at a cost of 2 ATP

Payoff: Each molecule of G3P is converted into a pyruvate (this produces 2 ATP via substrate level phosphorylation and 1 NADH [4ATP and 2 NADH in total]

2ATP + 2 NADH

46
Q

What is step 1 of glycolysis? Delta-G?

A

-16.7kJ/mol (irreversible essentially)

47
Q

What is step 2 of glycolysis? Delta-G?

A

1.7kJ/mol

48
Q

Step 3 of glycolysis? Delta-G?

What is special about this step? Why?

A

-14.2kJ/mol

1st committed step: product is solely destined for glycolysis

49
Q

Step 4 of glycolysis? Delta-g?

A

23.9kJ/mol (but negligible under cellular conditions)

50
Q

Step 5 of glycolysis? Delta-g?

A

Intraconversion of triose sugars (7.5kJ/mol)

51
Q

Step 6 of glycolysis? Delta-G? What is produced?

A

6.3kJ/mol (2 NADH produced)

52
Q

Step 7 of glycolysis? What is the delta-G? Which step is this coupled to? What is produced?

A

-18.5kJ/mol (coupled to step 6 = -12.2 overall), 2 ATP produced

53
Q

Step 8 of glycolysis? Delta-g?

A

4.4kJ/mol (even lower in cells)

54
Q

Step 9 of glycolysis? Delta-G?

A

7.5kJ/mol (lower in cells)

55
Q

Step 10 of glycolysis? Delta-G? What is produced?

A

-31.4kJ/mol (2 ATP produced)

56
Q

What are the non-reversible steps of glycolysis? How can you tell?

A

1, 3, and 10 (very negative delta-G)

57
Q

What do you need to make NADH? Where does this from from?

What happens to NADH in the conversion of pyruvate to lactate?

What is this conversion (back and forth) also known as?

A

NAD+ (Niacin - vitamin B3)

It is oxidised to NAD+

Redox balance

58
Q

What can happen to pyruvate after glycolysis? [3 pathways]

A
59
Q

What can generate ethanol from pyruvate?

It is a two step process. What enzymes are involved? What is the intermediate product?

A

Yeast and some other microorganisms

60
Q

In humans, when is pyruvate converted to lactate?

What enzyme is involved?

A

Cells lacking oxygen (exercising muscles) or mitochondria (RBCs)

61
Q

What is the name of the cycle that takes lactate from exercising muscles and converts it back to glucose? Where does the conversion happen?

A

Cori cycle (liver gluconeogenesis)

62
Q

What is pyruvate (3C) broken down to in the presence of oxygen? What else is formed?

Where does this occur?

What enzyme complex is involved?

A

Acetyl CoA [2C] (NADH also formed)

Mitochondria of cells

63
Q

Which tissues rely solely on glucose?

How much glucose does the whole body need per day? Just the brain?

How much free glucose in tissues? How much can be produced from glycogen stores?

A

Brain, nervous system, RBCs, testes, and embryonic tissues

160g (120g for the brain)

20g, 190g from glycogen stores

64
Q

What is the process of creating new glucose called? What is it generated from? Where does this usually occur, and what is it in response to?

A

Gluconeogenesis (from other non-carbs, occurring in the liver, in response to hormonal control)

65
Q

How are the three irreversible reactions of glycolysis reversed in gluconeogenesis?

A

They do not. There are four separate enzyme systems to bypass these steps (Pyruvate -> Oxaloacetate, oxaloacetate -> PEP [reverses step 10], Fructose 1,6-Biphosphate -> Fructose-6-Phosphate, G6P -> Glucose).

66
Q

Where do the four bypass reactions of gluconeogenesis take place?

A

Pyurvate -> Oxaloacetate -> PEP (mitochondria), others in cytosol

67
Q

Gluconeogenesis

Pyruvate -> Oxaloacetate -> PEP: which enzymes are involved when the substrate is pyruvate? And when it is lactate?

Which reaction series is more common?

A

More common: lactate as substrate

68
Q

Gluconeogenesis (reversing reaction 3 of glycolysis): what is the name of the enzyme? Is it a direct reversal?

A

Not direct reversal (doesn’t involve phosphate transfer to ADP - this would be energetically unfavorable)

69
Q

Gluconeogenesis (reversal of step 1 of glycolysis): what is occurring? What enzyme is involved? Is ATP produced?

A

Conversion of G6P to Glucose (phosphate just chopped off - as with bypass reaction 4->3, attaching it to ADP would be energetically unfavourable).

70
Q

What is the usual end point of gluconeogenesis? Why?

Where does the last bypass reaction of gluconeogenesis occur? Where is the enzyme (Glucose-6-Phosphatase) found?

A

Non-bypass mediated conversion of F6P to G6P (because it can then be trapped in the cell)

In the lumen of the ER (enzyme is bound to the membrane, thus allowing greater control over free glucose release)

71
Q

Where does galactose feed into glycolysis?

Where does fructose feed in? Which is more common? [adipose/liver]

A

Liver pathway

72
Q

What is the fructose pathway called?

How much ATP is used?

What are the enzymes involved? [2]

A

Fructose 1-Phosphate pathway (1 or 2 ATP for each fructose molecule) [Yellow boxes = glycolysis intermediates]

73
Q

What is galactose converted to?

Which intermediates (recycled) are involved?

A

Galactose -> Galactose-1-P -> Glucose-1-Phosphate

UDP-Galactose and UDP-Glucose

74
Q

What is the pentose phosphate pathway?

A

Produces NADPH, produces pentoses (ATP/RNA/DNA precursor), metabolizes pentoses from digestion

75
Q

NADPH produced through pentose phosphate pathway: how is it used in…

… liver…

… mammary gland…

adrenal cortex…

… and RBCs?

A

Liver: fatty acid synth, steroid synth, drug metabolism

Mammary: fatty acid synth

Adrenal cortex: steroid synth

RBCs: antioxidant

76
Q

Pentose Phosphate Pathway: how many phases? What are they called? Which is irreversible? What do they do?

A

Ox (irreversible): generates NADPH, converts G6P to pentose phosphate

Nonox: interconverts G6P and pentose phosphate to 3/4/5/6/7C sugars

77
Q

Main difference between NAD+ and NADP+

A

NAD: energy capturing processes to eventually create ATP

NADP: largely involved in passing energy from breakdown to buildup (catabolism -> anabolism)

78
Q

Drinking alcohol ________ gluconeogenesis. Why?

What does this lead to?

A

Reduces

Conversion of ethanol -> acetaldeyhyde -> acetate also converts NAD+ to NADH (and gluconeogenesis needs NAD+ for conversion of lactate to pyruvate)

Leads to hypoglycaemia and lacticacidaemia -> confusion -> unconsciousness -> death

79
Q

Which enzyme does Black Water Fever affect? Which pathway is this part of? What effect does it have? Any advantage?

A

G6P dehydrogenase (pentose phosphate pathway) - low RBC NADPH levels, allows free radicals and hydrogen peroxide to build up, and RBCs are unable to suffer normal insults (eg: infection). Protects vs malaria (cells burst on infection)

BI25M7: Energy for Life (8 decks)

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