D lectures-GNG and times of plenty Flashcards

1
Q

What is glucose-1-phosphate activated by in glycogenesis?

A

Uridine triphosphate (UTP) to form UDP

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2
Q

What does UDP-glucose do?

A

Donates residues to growing molecule

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3
Q

What does the enzyme glycogen synthase do?

A

Initiates glycogen synthesis by synthesising primer molecule glycogenin (primer molecule-provides a scaffold) -glycogenin remains attached to glycogen molecule.

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4
Q

What is chain elongation synthesised by?

A

Glycogen synthase

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5
Q

What are the three stages of glycogen synthesis?

A

Initiation, elongation, branching

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6
Q

Where is glucose synthesised?

A

Primarily in the liver

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7
Q

When do we need to synthesise glucose?

A

During fasting and starvation,when glycogen is depleted, essential for maintenance of blood glucose, primary source of blood glucose about 8 hrs into post absorptive state. Slower response than glycogen breakdown

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8
Q

Which carbon skeletons provide a source for GNG?

A

Pyruvate, lactate, amino acids, glycerol

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9
Q

What is required for GNG?

A

NADH required and has to be transported out of mitochondria and ATP coming from beta oxidation

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10
Q

What is the enzyme taking place in reaction 1 of GNG?

A

Glucose-6-phosphatase (instead of hexokinase)

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11
Q

What is the enzyme taking place in reaction 10 of GNG?

A

Pyruvate carboxylase (instead of pyrivate kinase)

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12
Q

What fuels GNG?

A

Beta oxidation(ATP from it)

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13
Q

What is pathway of pyruvate determined by?

A

Energy levels of cell (level of Acetyl CoA)

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14
Q

What happens if there are high levels of Acetyl CoA in the cell? (allosteric regulation)

A

It will inactive pyruvate dehydrogenase complex and activate pyruvate carboxylate (anaplerotic enzyme) and channel pyruvate towards GNG.

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15
Q

How is pyruvate channeled towards formation of glucose?

A

By replenishing oxaloacetate

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16
Q

What do high levels of ATP mean for oxaloacetate?

A

Driven towards GNG

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17
Q

What do low levels of ATP mean for oxaloacetate

A

Driven towards CAC

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18
Q

What is special about the first bypass reaction and why does it happen?

A

pyruvate that forms oxaloacetate via pyruvate carboxylase cannot cross the mitochondrial membrane so oxaloacetate forms malate then the malate shuttle (protein carrier) transports malate out of mitochondira then malate is RECONVERTED into oxaloacetate which is THEN CONVERTED FINALLY INTO PEP.

  • THERE IS A NEED FOR NADH!!! and a lack of transporters
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19
Q

Which enzyme will be activated when ATP levels are high in bypass 2 (high energy)?

A

Fructose 1,6-bisphosphatase (times of high energy so body needs to make sure there isn’t energy wasted on a futile cycle.

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20
Q

Which enzyme will be activated when AMP levels are high in bypass 2 (low energy)?

A

Phosphofructokinase (PFK) to allow glycolysis to occur (low energy times so needs to produce energy)

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21
Q

What is the difference between glycolysis and GNG?

A

GNG occurs in the mitochondria to start, and pyruvate is starting point.REQUIRES high energy molecules at beginning (GTP ATP, NADH), only occurs in times of high energy, end product is glucose.

Glycolysis occurs in the cytoplasm, glucose is starting point, REQUIRES LOW energy molecules at beginning (ADP, Pi, NAD+), only occurs in times of LOW ENERGY, end product is pyruvate

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22
Q

What happens in GNG with lactate as a substrate?

A

THE CORI CYCLE: It gets transported out of the muscles (after vigorous activity) and goes to the liver via blood. Then GNG takes place with lactate as substrate. (ATP is needed). Glucose then transported back into the muscle where it is converted into glycogen.

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23
Q

How come there is no malate shuttle needed for the transportation of pyruvate (lactate–>pyruvate) into the liver mitochondria in the cori cycle?

A

Because from conversion of lactate to pyrvuate, NADH is formed which allows transportation across the membrane

24
Q

During exercise, what is the breakdown of muscleproteins channeled towards?

A

Channeled to form the ONE amino acid GLUTAMATE

25
Q

Why is glutamate then converted into alanine?

A

Because it is EASILY transported in blood to liver

26
Q

What happens once alanine is in the liver?

A

It is converted BACK into pyruvate. Pyruvate then indergoes GNG to form glucose which is then transported back into muscles for muslce contraction ENERGY

27
Q

What is the basic pathway of synthesising fatty acids?

A

Acetyl CoA–> malonyl CoA–> FAs

28
Q

Is synthesis of FAs reversile of Beta oxidation?

A

NOOO!! beta oxidation occurs in mitochondira whereas FA synthesis occurs in the CYTOSOL and has different enzymes.

29
Q

What is the first step of FA synthesis catalysed by?

A

Acetyl CoA carboxylase

30
Q

What is the second step of FA synthesis catalyed by?

A

Fatty acid synthase complex

31
Q

What does the Fatty acid synthase complex do?

A

Facilitates the 4 steps to add 2 carbon atoms on at a time.

32
Q

Where does beta oxidation occur in plants?

A

Perioxisomes

33
Q

How many cycles to SYNTHESISE palmitic acid?

A

7 cycles and 7 Acetyl CoA. Energy requiring.

34
Q

What are the two key enzymes in fatty acid synthesis?

A

AcetylCoA carboxylase and fatty acid synthase.

35
Q

Which electron carrier does the reductive biosynthesis of fats require?

A

NADPH

36
Q

Where can Acetyl CoA be sourced from?

A

Mitochondria (products of carbohydrate, lipid and protein catabolism), Acetyl CoA in mitochondria must be tranpsorted out. It is transported OUT of mitochondria as citrate. (via citrate carrier)

37
Q

Where is NADPH sourced from?

A

The PPP (pentose phosphate pathway) and the malic enzyme (malate—(malic enzyme)—> pyruvate +NADPH

38
Q

What is the PPP important for?

A

Generating NADPH and synthesising ribulose 5-phosphate which is critical for the synthesis of DNA.

39
Q

What happens when there is a lot of glucagon in fatty acid synthesis?

A

Inhibits acetylCoA carboxylase so preventing biosynthesis of fatty acids. (in starved state)

40
Q

What happens if there is a lot of insulin in cells? (fed state)

A

Inhibition from glucagon will be removed and will ENCOURAGE FATTY ACID SYNTHESIS (citrate lyase is activated by insulin!!)

41
Q

What is covalent inhibition of fatty acid synthesis?

A

Phosphorylation (adding phosphate group)

42
Q

What is the trigger to synthesise fatty acids?

A

Malonyl CoA

43
Q

What does Malonyl CoA inactivate?

A

inhibits the carnitine transporter (for beta oxidation) –prevents fatty acids from entering mitochondria

44
Q

What happens in untreated diabetes with the ketone body formation pathway?

A
  • Glucose uptake by cells is impaired
  • Malonyl CoA synthesis drops
  • FA oxidation increases
  • Increase in Acetyl CoA
  • Depleted CAC
  • Acetyl CoA chnneled towards ketone body formation
45
Q

What is the main ketone body produced in starvation?

A

Beta-hydroxybutarate

46
Q

Where does Ketogenesis occur?

A

Mitochondria in fasting state and untreatred diabetic state

47
Q

When does cholesterol synthesis occur?

A

In the fed state in the liver, enteriocyte; cellular in cytosol

48
Q

Where does the CA cycle occur?

A

In the fed and fasted states and occurs in the msucle; mitochondria

49
Q

In the liver of a well fed person, what happens?

A

Glucose is phosphorylated

50
Q

What is characteristic of low insulin levels?

A

Synthesis of ketone bodies

51
Q

In liver of well fed person, excess Acetyl CoA will be utilised to produce…

A

Cholesterol

52
Q

Metabolic pathways active in the adipocyte in the well fed state are:

A

Lipogenesis

53
Q

What does glucose-3-phosphate participate in?

A

Synthesis of triacylglycerols and PPP

54
Q

Which enzyme turns triacylglycerols into fatty acids?

A

Lipoprotein lipase

55
Q

What does a high G-6-P promote?

A

Glycogen synthesis

56
Q

What is the primary fuel for heart muscle?

A

Fatty acids, also CANT do anaerobic respiration, can’t store glycogen of fats (can also utilise glucose and ketone bodies in times of need)

57
Q

What happens when we are inbetween meals?

A

Must synthesise energy (no input of glucose)- All tissues will contribute to provide energy. Between meals glucagon predominates -tirgger to mobilise fats in adipocyte cells (beta oxidation). Glycerol is produced from molbilisation of lipids and undrgoes GNG to produce Glucose.