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biochemistry Flashcards

1
Q

what is glycogenesis?

A

They synthesis of glycogen from glucose

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2
Q

what is glucogenolysis?

A

The breakdown of glycogen to form glucose

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3
Q

what is gluconeogenesis?

A

The synthesis of glucose from non-carbohydrate precursors

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4
Q

what is glycogen?

A

The storage form of glucose

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5
Q

describe how glycogen releases glucose (glycogenolysis) including enzymes.

A

STEP 1: Glycogen -> G1P, by glycogen phosphorylase
STEP 2: G1P -> G6P, by phosphoglucomutase
STEP 3: Either:
in liver: G6P -> glucose to enter blood
in muscle: G6P -> glucose for glycolysis to give energy

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6
Q

what must be present for a glucose molecule to form glycogen?

A

can only be added to an existing chain

glycogen prime containing at least 4 glucose residues attached to glycogenin (protein)

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7
Q

describe gluconeogenesis.

A

Non-carbohydrate precursors form glucose via a pathway similar to the reverse of glycolysis BUT there are three unfavourable steps which must be overcome by unique liver enzymes

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8
Q

why is gluconeogenesis needed?

A

During periods of starvation to maintain blood glucose levels

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9
Q

where is glycogen found?

A

liver and muscle cells

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10
Q

what are the 3 sources of blood glucose?

A 
dietary glucose (maintains levels after a meal)
glycogenolysis (active inbetween meals)
gluconeogenesis (active during prolonged fasting)
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11
Q

what are liver and muscle glycogen used for?

A

Liver glycogen is broken down to maintain blood glucose levels
Muscle glycogen is broken down to produce energy during physical activity

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12
Q

when is glycolysis used?

A

In muscle cells to provide energy

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13
Q

which type of bonds hold glucose molecules together and which bond branches in glycogen?

A

Held together by alpha 1-4 glycosidic links

Branched by alpha 1-6 glycosidic links

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14
Q

describe the pathway of glycogenesis (glycogen synethesis) including enzymes involved.

A

STEP 1: glucose -> G6P, by hexokinase, 1ATP is used
STEP 2: G6P -> G1P, by phosphoglucomutase
STEP3: G1P -> UDP-glucose, by UDP-glucose pyrophosphorylase
STEP 4: UDP-glucose -> [glucose]n+1 + UDP, by glycogen synthase.

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15
Q

what is the role of UTP in glycogenesis?

A

G1P cannot form glucose alone, needs to bind to UTP. UDP is recycled to UTP by ATP which donates it a phosphate allowing UTP to continue to bind to G1P to make UDP-glucose

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16
Q

what is the rate limiting step of glycogenesis?

A

glycogen synthase

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17
Q

what is the rate limiting step in glycogenolysis?

A

glycogen -> G1P, by glycogen phosphorylase

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18
Q

where does gluconeogenesis occur?

A

in the liver, some in the kidney

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19
Q

which precursors can be used for gluconeogenesis and where do they come from?

A

Lactate: generated by skeletal muscle under anaerobic conditions
Amino acids: from muscle proteins by proteolysis
Glycerol: from triglycerides by lipolysis in adipose tissue

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20
Q

How is the precursor lactate synthesised and reaches the liver for use in gluconeogenesis?

A

synthesised by skeletal muscle under anaerobic conditions/heavy exercise
Reaches the liver via Cori cycle.

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21
Q

describe the Cori cycle and its aim.

A

Cori cycle describes how lactate is transported in the blood to the liver where it is converted to glucose which is then converted back to the skeletal muscle through the blood.
Its aim is to shift the metabolic burden from muscle to other organs and redistrubute the carbon precursors

22
Q

what are the 3 unfavourable steps which must be overcome in gluconeogenesis and what enzymes allow their bypass?

A

pyruvate kinase by PEPCK enzyme
phosphofructokinase by fructose 1-6 biphosphate
hexokinase by glucose-6-phosphate

23
Q

describe the pathway of gluconeogenesis.

A

STEP 1: Oxaloacetate is synthesised in the mitochondria
STEP 2: TCA in reverse until pyruvate part where PEPCK enzyme is used to bypass
STEP 3: Moves up reverse of glycolysis till phosphofructokinase step which is overcome by fructose 1-6 biphosphate
STEP 4: Hexokinase step is bypassed by glucose-6-phosphate
STEP 5: Glucose is made

24
Q

how are glyolysis (breakdown) and gluconeogenesis (synthesis) regulated hormonally?

A

Glucagon signals the starved state: stimulating gluconeogenesis and inhibiting glycolysis
Insulin signals the fed state: stimulating glycolysis and inhibiting gluconeogenesis

25
Q

where is insulin released from and why?

where is glucagon released from and why?

A

Insulin:
- released from pancreatic beta-cells in response to increased blood glucose levels
Glucagon:
- released by pancreatic alpha cells in response to decreased blood glucose levels

26
Q

how are glyolysis (breakdown) and gluconeogenesis (synthesis) regulated cellularly?

A

High AMP or ADP = low energy so gluconeogenesis is inhibited (as requires lots of energy)
High ATP means high energy so gluconeogenesis is stimulated
High fructose 2,6-bisphosphate is high in fed state, low in starved state
Citrate, alanine, acetyl CoA are high when intermediates or building blocks are abundant.

27
Q

how does the body gain energy from fats and fatty acids?

A

via lipolysis

28
Q

why is fat needed?

A

energy source
for essential fatty acids (ones which cannot be generated within the body)
fat soluble vitamins A, D, E and K

29
Q

what does beta oxidation of fatty acids produce?

A

1 acetyl-CoA, 1 FADH2, 1 NADH + H+, 1 fatty acyl-CoA shortened by 2 carbon atoms

30
Q

describe how fats are metabolised (lipolysis) and transported from adipose tissue to the liver?

A

STEP 1: stored fat is cleaved by hormone sensitive lipases releasing free FA’s and glycerol
STEP 2: FA’s + CoA -> acyl-CoA. Occurs in cytoplam and need energy
STEP 3: Further oxidation, but in mitochondrial matrix so carnitine shuttle is used to transport
STEP 4: Beta oxidation
STEP 5: TCA cycle

31
Q

how are ketone bodies produced?

A

they are formed in the liver mitochondria from acetyl-CoA produced by beta oxidation. They then diffuse into bloodstream to peripheral tissues

32
Q

what are the function of ketone bodies?

A

Important for energy metabolism for the heart muscle and renal cortex where they are converted back to acetyl-CoA which enters the TCA cycle

33
Q

how are ketone bodies normally used vs what happens in diabetes and starvation?

A

Normally:
- FA oxi gives acetyl-CoA which enters TCA cycle IF fat and carbohydrate degradation are balanced. This depends on oxaloacetate which is needed to form citrate.
IN STARVATION/DIABETES:
- Oxaloacetate is used for gluconeogenesis. So FA’s are oxidised to provide energy but acetyl-CoA cannot enter the TCA as there isn’t enough oxaloactetate so are converted to ketone bodies.
High levels of ketone bodies are toxic and cause severe acidosis

34
Q

how are amino acids from dietary protein or from cellular protein turnover degraded?

A

they are broken down in the liver to form ammonia and ammonium ions. These are then converted to urea to be excreted safely from the body

35
Q

how is protein digested?

A

proteolytic enzymes in the stomach and small intestine break them down into single amino acids and di and tri-peptides. There are then absorped

36
Q

why does ammonia need to be converted to urea?

A

because ammonium ions are toxic to the body at high concentrations, therefore it needs to be excreted

37
Q

describe how ammonia is converted to urea

A

STEP 1: Transamination: amino acid -> glutamic acid by aminotransferases, this occurs in tissues, is transported to liver by forming alanine and glutamine (carriers of N)
STEP 2: De-amination: glutamic acid -> ammonium ion - occurs in liver
STEP 3: Urea cycle: aspartate + ammonium ions -> urea. - this requires energy

38
Q

how are the carbon skeletons left over from amino acid degredation used for energy generation?

A

By being converted to glucose or oxidised in TCA

  • ketogenic amino acids are degraded to acetyl-CoA or acetoacetyl-CoA which can give rise to ketone bodies or fatty acids
  • glucogenic amino acids are degraded to pyruvate or TCA cycle intermediates OR can be converted to glucose
39
Q

why does FA synthesis occur?

A

during excess energy intake

40
Q

what happens when excess carbohydrate is taken in and how are they transported?

A

Produces acetyl-CoA which is converted to FA’s and trigylcerides in the cytoplasm of the liver. Free FA’s are transported in plasma bound to albumin. Triglycerides formed in the liver are transported to adipose tissue by VLDL for storage

41
Q

in fatty acid synthesis how does the precursor, acetyl-CoA enter the cytoplasm from the mitochondria where it is generated?

A

citrate is used to transport the acetyl groups into the cytoplasm from the mito

42
Q

what is the vital first step in fatty acid synthesis?

A

acetyl-CoA MUST be converted to malonyl-CoA by acetyl-CoA carboxylase. Malonyl-CoA then donates carbon atoms to the new lipid.

43
Q

what is the purpose of fatty acid synthase?

A

to catalyse the synthesis of saturated long chain fatty acids from malonyl-CoA, acetyl-CoA and NADPH
NOTE: It contains an acyl-carrier protein (ACP)

44
Q

what 4 steps does fatty acid synthase use to form fatty acids?

A

condensatioin, reduction, dehydration and reduction and release

45
Q

what is the purpose of fatty acid synthase?

A

to catalyse the synthesis of saturated long chain fatty acids from malonyl-CoA, acetyl-CoA and NADPH (electron donor) by adding 2 carbons per cycle. They chain is attached to ACP to hold it in place. Chain is released when C16 is reached
NOTE: It contains an acyl-carrier protein (ACP)

46
Q

how is fatty acid synthesis regulated?

A

insulin: stimulates FA synthesis
Citrate: stimulates FA synthesis
Glucagon: inhibits FA synthesis
Palmitoyl-CoA: inhibits FA synthesis

47
Q

what is alcaptouria?

A

an inherited disorder affecting amino acid degradation by blocking degradation of phenylalanine and tyrosine

48
Q

what is maple syrup urine disease?

A

an inherited disorder affecting amino acid degradation by blocking the degradation of valine, isoleucine and leucine. (Urine smells like maple syrup, causes mental and physical retardation)

49
Q

what is phenylketonuria?

A

an inherited disorder affecting amino acid degradation where phenylalanine accumulates in all body fluids leading to severe mental retardation if untreated

50
Q

What would a defect in urea cycle enzyme lead to?

A

accumulation of urea cycle intermediates, increasing glutamine levels in circulation.
A-ketoglurarate is no longer regenerated so levels become too low to fix more free ammonium ion so toxic levels of ammonium ions build up in the blood

GI (11 decks)

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