Carbohydrates Flashcards

1
Q

What is the general structure of a carbohydrate?

A

(CH2O)n - aldehyde or ketone group and multiple hydroxyl groups

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2
Q

What are monosaccharides? Give examples.

A

Singular units of sugar - glucose, fructose, galactose

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3
Q

What are disaccharides? Give examples.

A

Sugars with two subunits - maltose (2 x glucose), sucrose (glucose + fructose), lactose (glucose + galactose)

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4
Q

What are oligosaccharides?

A

Sugars with 3-10 subunits - e.g. dextrins

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5
Q

What are dextrins?

A

Smaller carbohydrates of up to 10 subunits. Formed when polysaccharides are cleaved by enzymes in digestion

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6
Q

What are polysaccharides? Give examples.

A

10’s - 1000’s of subunits - starch, glycogen, cellulose

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7
Q

What is the function of carbohydrates?

A

They are metabolised to produce energy and provide useful intermediates for use in other biochemical pathways. Required for formation of glycoproteins, glycolipids, etc.

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8
Q

What is the first step in the digestion of carbohydrates?

A

Amylase in the salivary glands breaks down polysaccharides like starch and glycogen into dextrins

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9
Q

Where does salivary amylase stop working?

A

In the stomach due to the acidic conditions

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10
Q

What is the role of the pancreas in the digestion of carbohydrates?

A

It releases bicarbonate into the duodenum to neutralise stomach acid which creates an environment for pancreatic amylase (and other pancreatic enzymes) to work in

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11
Q

What is the role of disaccharidases and where are they located?

A

They break down remaining disaccharides into monosaccharides and are found on the membrane of the small intestine

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12
Q

How is glucose absorbed into the blood?

A
  • Via secondary active transport
  • Sodium potassium pump - pumps out 3 Na+ and pumps in 2 K+ which creates a conc. grad.
  • Less Na+ in epithelial cell that in lumen of SI
  • Na+ moves down conc. gradient co-transporting glucose in via protein carrier
  • blood flow maintains a conc. gradient of higher glucose in cell than in blood so glucose moves into blood via F.D.
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13
Q

What does phase 1 of catabolism involve?

A

The breakdown of molecules into building blocks. It is extracellular

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14
Q

Why isn’t cellulose digested in the human GI tract?

A

Cellulose contains BETA 1,4 linkages that result in a more rigid and elongated shape of molecule than ALPHA 1,4 linkages. This means it doesn’t fit the shape of the active sites of the enzymes that break down the alpha 1,4 linkages in starch and glycogen.

IMPORTANT = ALPHA AND BETA GLYCOSIDIC BONDS ARE DIFFERENT

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15
Q

What causes lactose intolerance?

A

Lactase deficiency

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16
Q

Why is lactase deficiency normal in some populations?

A

When being BF, we have lots of lactase but as weaned off it, lactase levels drop. This is normal as there is less lactose in the diet so high lactase levels unnecessary

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17
Q

Why can people in many populations continue to consume lactose after being weaned off breast milk?

A

We continue to consume lactose in higher quantities so have developed a lactase persistence phenotype, preventing the drop off

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18
Q

What is primary lactase deficiency?

A

Where there is an absence of lactase persistence allele. It occurs in adults and is common in Northwest Europe

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19
Q

What is secondary lactase deficiency?

A

Where there is damage to the GI tract so lactase enzyme in membrane of SI not effective. This is reversible as the damaged area recovers and can be seen in infants and adults. It is caused by gastroenteritis, Crohn’s, UC, Coeliac disease

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20
Q

What is congenital lactase deficiency?

A

Extremely rate and caused by a defect in the lactase gene. Cannot digest breast milk

21
Q

Which cells are more dependent on glucose and why?

A
  • RBC’s, lens of eye, innermost cells of kidney medulla as all don’t have mitochondria so rely on glycolysis for ATP production
  • Neutrophils as often found in areas with low oxygen so need to respire anaerobically via glycolysis
  • Cells of brain prefer glucose - can use other sources but it takes time to adapt so can’t switch rapidly
22
Q

What is glycolysis?

A

Phase 2 of carbohydrate metabolism where it’s broken down into important metabolic intermediates

23
Q

What are the key features of glycolysis?

A
  • Occurs in cytoplasm
  • Oxidative
  • Provides key intermediates for other processes such as formation of fatty acids
  • Irreversible
24
Q

What are the 2 phases to glycolysis?

A
  • First primes glucose through phosphorylation, making it negatively charged so it cannot pass back through plasma membrane
  • Second is payback as gives 4x ATP for a net gain of 2 via substrate-level phosphorylation
25
Q

What are the products of glycolysis?

A
  • Net gain of 2 ATP (4 formed but 2 used to phosphorylate glucose)
  • 2 NADH (reducing power)
  • 2 pyruvate molecules
26
Q

What are the key enzymes in glycolysis?

A
  • Hexokinase which phosphorylates glucose to G6P using ATP (glucokinase isoform in liver)
  • Phosphofructokinase - further phosphorylates using ATP to form fructose - 1,6 - bisphosphate - key control enzyme
27
Q

What key metabolites are derived from glycolysis?

A
  • Some amino acids formed from intermediates
  • Glycerol phosphate is formed from intermediate in glycolysis and used for lipid synthesis
  • Intermediate can form important molecule in erythrocytes that regulate oxygen affinity
28
Q

How is fructose metabolised?

A
  • in liver
  • enzymes catalyse conversion to glyceraldehyde 3-phosphate which is an intermediate in glycolysis
29
Q

How is galactose metabolised?

A
  • galactose can be primed for glycolysis or used to form glycogen
  • requires 3 enzymes
  • deficiency in any one can cause galactosaemia
30
Q

Why is lactic acid production necessary in anaerobic respiration?

A
  • NAD+ required for continued glycolysis but needs to be recycled as conc. in cells is constant
  • LDH enzyme catalyses reduction of pyruvate to lactate with use of NADH
  • producing oxidised NAD+
31
Q

How is blood concentration of lactic acid controlled?

A
  • in heart lactate converted back to pyruvate by LDH and pyruvate then used to produce energy
  • in liver + kidneys can occur as above but the pyruvate can also be used in gluconeogenesis
32
Q

What is galactosaemia?

A
  • a deficiency in any of 3 enzymes involved in galactose digestion
  • different types depending on which enzyme is deficient
  • galactokinase deficiency is rare and causes galactose to build up
  • transferase deficiency is more common and galactose and galactose-1-P both build up
33
Q

What are the problems associated with galactosaemia?

A
  • as galactose builds up it enters other pathways forming galactitol which requires NADPH
  • NADPH essential in cells especially to prevent against oxidative stress
  • cataracts form in eye as lens undergoes oxidative damage
  • build of galactose-1-P causes issues with liver, kidneys and brain
34
Q

How is galactosaemia treated?

A
  • no dietary lactose
35
Q

What are key features of the pentose phosphate pathway?

A
  • uses G6P from glycolysis
  • forms NADPH - needed to maintain GSH levels, for fatty acid production
  • produces ribose 5-P - for production of nucleotides
  • No ATP
  • Produces CO2
36
Q

What is the rate limiting enzyme is pentose phosphate pathway?

A
  • glucose 6-phosphate dehydrogenase
37
Q

Why is the pentose phosphate pathway especially important in some tissues?

A
  • main source of NADPH in some tissues
  • e.g. RBC’s
  • lack of NADPH would leave these tissues at risk of oxidative damage
38
Q

What is G6PD deficiency?

A
  • deficiency in glucose 6-phosphate dehydrogenase means pentose phosphate pathway cannot occur
  • leads to a lack of NADPH in cells
39
Q

What is the effect of G6PD deficiency?

A
  • lack of NADPH leaves cells at risk of oxidative damage as GSSG not reduced back to GSH
  • proteins become damaged
  • haemoglobin particularly at risk as pentose phosphate pathway is only source of NADPH and role as O2 carrier
  • ROS cause crosslinkage by disulphide bonds and form insoluble aggregates called Heinz bodies and this leads to haemolysis
40
Q

What precipitates effects of G6PD deficiency?

A

Some drugs e.g. antimalarials deplete cells of NADPH and this in combination with an already reduced amount causes oxidative stress

41
Q

What is the main regulatory enzyme of glycolysis?

A

Phosphofructokinase

42
Q

How is phosphofructokinase regulated?

A
  • hormonal - insulin stimulates phosphofructokinase and glucagon inhibits it
  • allosteric - stimulated by high AMP and high fructose 2,6 bisphosphate and inhibited by high ATP and high citrate
43
Q

What is the role of pyruvate dehydrogenase in glucose metabolism?

A
  • catalyses conversion of pyruvate to acetyl CoA in an irreversible reaction
  • key site of regulation for entry into TCA cycle
  • activated by high pyruvate, CoA, NAD+, ADP, insulin, dephosphorylation (phosphatase)
  • inhibited by high acetyl CoA, NADH, ATP, citrate, phosphorylation (kinases)
  • first step that breaks C-C bond
  • reaction in mitochondrial matrix
44
Q

What is the important of the TCA cycle?

A
  • central pathway in catabolism of sugars, fatty acids, ketone bodies, AA’s, alcohol
  • generates reducing power (NADH, FADH2) from oxidation of acetyl CoA
  • produces some energy directly as GTP
  • produces precursors for biosynthesis
45
Q

What are some key points of the TCA cycle?

A
  • acetyl CoA is oxidised in series of reactions
  • occurs in mitochondria
  • acetyl converted to 2CO2
  • NADH + FADH2 produced - reducing power
  • important intermediates
  • 2 cycles per glucose
  • tightly coupled to ETC so doesn’t function in absence of O2
46
Q

How is the TCA cycle regulated?

A
  • ATP/ADP ratio and NADH/NAD+ ratio
  • isocitrate dehydrogenase regulates one of irreversible steps allosterically - inhibited by NADH (high energy signal) and activated by ADP (low energy signal)
47
Q

What are the key features of oxidative phosphorylation?

A
  • occurs in mitochondria
  • NADH2 and FADH2 reoxidised
  • O2 utilised
  • Forms H2O
  • large amount of energy produced (ATP)
  • 2 processes - ETC and ox phos
48
Q

What happens in ETC?

A
  • NADH and FADH2 bind to protein carriers on inner mitochondrial membrane called proton translocating complexes
  • electrons move along series of PTC’s via intermediates
  • process releases free energy
  • 1/2O2 is bound to final PTC and becomes terminal electron acceptor
  • free energy used to pump hydrogen ions into intermembranal space against its electrochemical gradient
  • lots of energy also lost as heat
  • generates proton motive force - electrochemical gradient
49
Q

What happens in ATP synthesis part of ox phos?

A
  • H+ ions move down electrochemical gradient
  • only way in is via ATP synthase so movement of H+ ions drives ATP synthesis
  • oxygen, electron and H+ come together to form H2O