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Metabolism > Week 2 > Flashcards

Week 2 Flashcards

0
Q

Why is our dietary intake of carbohydrates 300g per day, and yet only 1% of our body weight is carbohydrates?

A

We oxidise carbohydrates to use them as fuel in the tissues, or store them as triacylglycerols once glycogen stores are full.

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1
Q

What is a carbohydrate?

A 
General formula (CH2O)n
Contains an aldehyde or ketone, and multiple hydroxyl groups.
Mono, Di or Poly saccharides
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2
Q

What are the natural stereoisomers of monosaccharides?

A

D

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3
Q

Name two important properties of sugars

A

Hydrophilic - can’t cross plasma membranes, water soluble

Partially oxidised - need less oxygen than fatty acids

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4
Q

What are the main dietary disaccharides, and what disaccharide is formed during the breakdown of polysaccharides?

A

Lactose (galactose and glucose)
Sucrose (fructose and glucose)
Maltose (glucose and glucose)

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5
Q

What makes a sugar non reducing?

A

If the ketone/aldehyde groups of both monosaccharides are involved in forming the glycosidic bond (eg sucrose)

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6
Q

What is starch?

A

Polymer of glucose found in plants

Mixture of amylose (alpha 1-4 linkages) and amylopectin (alpha 1-4 and alpha 1-6 linkages)

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7
Q

What is cellulose?

A

Polymer of glucose found in plants. Glucose joined by beta 1-4 linkages - no enzymes in human gut can break bonds.
Major component of dietary fibre

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8
Q

Describe the extracellular metabolism of dietary polysaccharides to glucose.

A

Polysaccharides are broken down by glycosidases (salivary and pancreatic amylase) this releases glucose, maltose and dextrins.
Maltose, dextrins, and fructose and lactose are broken down into monosaccharides (lactase, glycoamylase, sucrase/isomaltase, which are large glycoprotein complexes attached to the brush border membranes of epithelia in the duodenum and jejunum.

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9
Q

What is the consequence of a deficiency of lactase?

A

Lactose intolerance - lactose persists into the colon, and is then broken down by bacteria - releases carbon dioxide, methane and hydrogen causing bloating
Osmotic pressure causes diarrhoea.

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10
Q

How does glucose arrive in the tissues?

A

Glucose is actively transported from gut into epithelial cells. Diffuses down concentration gradient into blood, then down concentration gradient via transporter molecules (GLUT 1-5), whose relative affinities for glucose reflect the requirements of the tissues for glucose

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11
Q

What is the committing step of glycolysis?

A

Step three - phosphorylation of fructose 6 phosphate to fructose 1,6 bisphosphatase
First reaction unique to glycolysis

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12
Q

What is the purpose of phosphorylation glucose?

A

Makes it anionic which prevents it leaving the cell.
Adds a high energy phosphate group which allows substrate level phosphorylation of ADP further along the pathway.
Increases reactivity - can enter many pathways - glycogenolysis, pentose phosphate etc

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13
Q

What is the role of lactate dehydrogenase?

A

Regenerates NAD+ when glycolysis must occur anaerobically, converts pyruvate to lactate.

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14
Q

What is the net yield of ATP during glycolysis?

A

2 moles per mole of glucose (two invested to phosphorylate glucose and fructose - phosphate.

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15
Q

Name two important substances produced from intermediates of glycolysis

A

2,3 Bisphosphoglycerate produced from 1,3 Bisphosphoglycerate. Regulates affinity of haemoglobin for oxygen
Glycerol phosphate is required for synthesis of triacylglycerols - liver has enzyme glycerol kinase, absent from adipose.

16
Q

What is the role of myokinase?

A

Enzyme in muscle that catalyses:

2ADP -> AMP + ATP

17
Q

What enzyme catalyses the rate limiting step of glycolysis?

A

Phosphofructokinase

18
Q

How is the activity of phosphofructokinase regulated?

A

In the muscle is regulated allosterically. It is inhibited by heigh [ATP] and stimulated by high [AMP]
In the liver it is regulated hormonally insulin stimulates and glucagon inhibits.

19
Q

What is the fate of lactate produced during anaerobic respiration?

A

It is transported to the liver, heart muscle and kidney and converted back to pyruvate.
In the heart muscle it is then oxidised to carbon dioxide
In the liver and kidney it enter ps gluconeogenesis.

20
Q

At what concentration does plasma lactate cause problems and why?

A

5mmol - exceeds renal threshold, affects buffering capacity of blood - lactic acidosis.

21
Q

What may cause an increase in plasma lactate?

A

An increase in production due to strenuous exercise, hearty eating, shock and congestive heart disease
Decrease in utilisation during alcohol metabolism, or due to liver disease or thymine deficiency

22
Q

What is galactose required for?

A

Synthesis of glycolipids and glycoproteins such as blood group antigens

23
Q

Describe the metabolism of galactose including enzymes.

A

Galactose -> Galactose 1-phosphate (galactokinase)
Galactose 1-phosphate + UDP glucose -> Glucose 1-phosphate + UDP-galactose (galactose 1-phosphate uridyl transferase)
(UDP glucose is regenerated by epimerase from UDP-galactose)
Glucose 1-phosphate -> glucose 6-phosphate (phosphoglucomutase)

24
Q

What is an important role of epimerase?

A

Allows galactose to be synthesised from glucose during lactation.

25
Q

What is galactosaemia?

A

Lack of one of the enzymes involved in galactose metabolism.
Lack of kinase is rare, accumulation of galactose
Lack of galactose 1-phosphate uridyl transferase is more common and more serious - accumulation of galactose and galactose 1-phosphate.
Galactose is reduced to galactitol by aldosterone reductase, depletes NADPH.
This means NADPH no longer maintains free SH groups in the lens of the eye, proteins cross link - causes cataracts. Worsened by non enzymatic glycosylation of proteins.
Accumulation of glucose and galactitol in the eye -> glaucoma
Accumulation of galactose 1-phosphate causes brain, liver and kidney damage.

26
Q

How is fructose metabolised?

A

Metabolised in the liver by soluble enzymes to glyceraldehyde 3-phosphate, enters glycolysis.

27
Q

What is the function of the pentose phosphate pathway?

A

Produce NADPH - reducing power for anabolism, maintain free SH groups, detoxification.
Produce ribose sugars for DNA and RNA synthesis.

28
Q

Where is the pentose phosphate pathway most important?

A

Red blood cells, bone marrow, liver, adipose

29
Q

What are the differences between glycolysis and the pentose phosphate pathway?

A

Glycolysis doesn’t produce carbon dioxide, it produces ATP. The pentose phosphate pathway produces carbon dioxide and doesn’t produce ATP.

30
Q

What is phase one of the pentose phosphate pathway?

A

Glucose 6-phosphate undergoes oxidative decarboxylation to a five carbon sugar, catalysed by glucose 6-phosphate dehydrogenase and 6 phosphogluconate dehydrogenase.

31
Q

What is phase 2 of the pentose phosphate pathway?

A

Complicated reactions that convert C5 sugar phosphates to the intermediates of glycolysis - 2 fructose 6 phosphates and a glyceraldehyde 3 phosphate.

32
Q

What controls the rate of the pentose phosphate pathway. How?

A

Control the rate of glucose 6-phosphate dehydrogenase.

Controlled by the NADP+/NADPH ratio.

33
Q

What is G6PD deficiency?

A

X linked genetic defect - more prevalent in Mediterranean people, and black Americans
Point mutations resulting in low activity of the enzyme
Low NADPH, disulphide bridges form, glutathione system saturates.
Heinz bodies, haemolysis.
Acute episodes precipitated by antimalarials, sulphonamides, glycosides in broad beans.

34
Q

What is PDH? What cofactors are required?

A

Pyruvate dehydrogenase -multienzyme complex catalyses pyruvate to Acetyl CoA, lose carbon dioxide, makes NADH.
Four b vitamins - pantothenic acid in CoA, niacin in NAD+, riboflavin in FAD, thiamine in thiamine pyrophosphate
Lipoic acid is a cofactor

35
Q

What are the consequences of the PDH reaction being irreversible?

A

Loss of carbon dioxide irreversible.

Acetyl coA cannot be converted to pyruvate therefore cannot be used as a substrate for gluconeogenesis.

36
Q

How is the activity of PDH regulated?

A

Inhibited by Acetyl CoA, so if fatty acids are being oxidised they will be used preferentially
Sensitive to energy state - inhibited by NADP and ATP, activated by ADP (allosterically)
Activated by insulin when blood sugar high, by dephosphorylation.

Metabolism (9 decks)

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