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Nutrition And Metabolism > Metabolism > Flashcards

Metabolism Flashcards

1
Q

Glycolysis events (4 stages)

A
  1. Activation (2 phosphorylation costing 2 ATP)
  2. splitting 6c to 3c (produces 1ATP)
  3. Oxidation
  4. Synthesis of ATP (2ATP produced) Times 2 because 2 biphosphoglycerate
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2
Q

Reaction catalyze by lactate dehydrogenase (liver and muscle)

A

In muscle: pyruvate to L-lactate using NADH In liver: l lactate to pyruvate

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3
Q

Control mechanism associated with phosphofructokinase

A

Enzyme responsible for activating glucose. Inhibited by citrate and ATP and stimulated by AMP

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4
Q

Definition of TCA cycle

A

Oxidation of acetyl coA to carbon dioxide and water

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5
Q

The link reaction (and bond between CoA and carboxylic acid)

A

Pyruvate to acetyl CoA Catalized by pyruvate dehydrogenase

Produces NADH

Coenzyme A forms thioester bond with carboxylic acid

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6
Q

Condensation reaction of TCA cycle product

A

Citrate

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7
Q

Isomerisation reaction of TCA cycle

A

Citrate to isocitrate

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8
Q

First loss of CO2 (products)

A

Ketoglutarate Carbon dioxide NADH

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9
Q

Second loss of CO2

A

Succinyl CoA NADH CO2

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10
Q

Succinyl CoA to oxaloacetate reaction

A

Succinate Fumarate Malate Oxaloacetate

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11
Q

Products of TCA cycle

A

3 NADH (2.5) 1 FADH2 (1.5) 1 GTP

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12
Q

Other biosynthetic roles of aspartate and ketoglutarate

A

Amino acids, purines, purimidines via transamination

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13
Q

Chain reaction products that produce pyruvate

A

Oxaloacetate Malate

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14
Q

3 functions of fat

A

1 cell membrane 2. Precursor of hormone 3. Long term fuels

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15
Q

Breakdown of tryacylglycerol

A

TAG lipase to DAY lipase DAG lipase to MAG MAG lipase to glycerol Each time fatty acid travels in plasma bound to albumin Glycerol diffuses in blood stream

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16
Q

Metabolism of glycerol fate

A

Converted to pyruvate the TCA Or converted to glucose by gluconeogenesis

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17
Q

Transport of fatty acrylic CoA info mitochondria

A

Enters outer membrane binds to carnitine passes through inner membrane and is transferred back to fatty acyl CoA

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18
Q

B oxidation steps (4)

A

Loses 2 H as FADH2 Gains H2O Loses 2H as NADH Loses 2 carbons, making pyruvate and fatty acyl CoA

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19
Q

Regulation of b oxidation

A

Glucagon activates release of fatty acid Rate determined by availability of water and carbon dioxide

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20
Q

Glycogen synthesis

A
  1. Glucose to glucose 6 phosphate 2. Glucose phosphate with UTP makes UDP glucose ( glycogen synthase): 3. Branching enzymes ads branches to glycogenin
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21
Q

Regulation of glycogen synthatse

A

Activated by protein phosphatase Inactivated by protein kinase Opposite for glycogen phosphorylase

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22
Q

Breakdown of glycogen

A

Glycogen phosphorilase breaks 1,4 bonds, debranching breaks 1,6 bonds

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23
Q

Synthesis of glucose from glucose 1 phosphate (product of glycogen breakdown)

A

Mutase enzyme to glucose 6 phosphate glucose 6 phosphatase to glucose

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24
Q

Control of glycogen breakdown in liver

A

Initiated by glucagon which activates cAMP with activate glycigen phosphorylase kinase which activate glycogen phosphorylase

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25
Q

Normal blood glucose

A

3.9 to 6.2 mM

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26
Q

Definition of gluconeogenesis

A

Production of glucose from non carbohydrate percursos (not fatty acids)

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27
Q

Regulation of gluconeogenesis

A

Mobilisation of substrate Activation of enzymes by insulin or glucagon

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28
Q

Amino acid pool

A

Free amino acids, in low concentrations

29
Q

Protein turnover

A

The idea that protein breakdown rate should be equal to the rate of protein synthesis. N intake= n excretion

30
Q

Nitrogen balance

A

N intake = n excretion

31
Q

Deamination

A

Removal of a amino group as ammonia uses coenzyme

32
Q

Transamination

A

Movement of an amino group to keto acid, making different amino acid

33
Q

Fate of deaminated amino acids (keto acids) and ammonia

A

Ammonia secreted in urine

Glucogenic go into Krebs and can be made into glucose

Ketogenic can be made into acetyl CoA and Krebs cycle or fat

34
Q

Protein degradation in most proteins

A

Removed by ubiquitin breakdown system , giving amino acids

35
Q

Protein degradation of foreign/ exogenous proteins

A

Taken into vesicles by endocytosis or autophagocytosis and degraded by proteolytic in lysosome

36
Q

Importance of glutamine and glutamate

A

Transports 2 ammonia in blood to liver

37
Q

Importance of aspartate

A

Plays a role in urea cycle and transport of ammonia

38
Q

Fatty acid synthesis location

A

Cytoplasm of hepatocytes

39
Q

First step of fatty acid synthesis

A

Citrate to oxaloacetate and acetyl CoA

40
Q

Lipid synthesis 2nd step

A

Acetyl CoA to malonyl CoA with acetyl CoA carboxylase

41
Q

Regulation of acetyl CoA carboxylase Citrate Insulin Long chain FA Glucagon

A

Citrate and insulin stimulate Long chain FA and glucagon inhibit

42
Q

Lipid synthesis 3rd step

A

Malonyl CoA to fatty acid with fatty acid synthase

43
Q

Transport molecule for TAG

A

VLDL

44
Q

What LDL and HDL and chylomicrons transport

A

LDL: mainly cholesterol to tissues HDL: cholesterol from tissue to liver Chylomicrons: mostly dietary TAG

45
Q

Importance of HMG CoA reductase and what inhibit it

A

Rate limiting step of cholesterol synthesis, inhibited by statins

46
Q

Risk factors for secondary hyperlipoproteinaemias

A

Obesity Diabetics type 2 Cholesterol Dietary fatty acid Alcoholism

47
Q

What biosynthetic reactions are driven by:

ATP

UTP

GTP

A

ATP: pumps, tansporters, pathways…

UTP: Synthesis of complex sugars

GTP: synthesis of proteins

48
Q

Summary of TCA cycle events (In terms of # carbons and CO2 loss and name of intermediates)

A
49
Q

Roles of glucose

A

Energy

Pentose sugars for DNA

Source of carbon for other sugars

Source of NADP

50
Q

Processing of glucose in:

Skeletal muscle

Heart/ Brain

Adipose

Erythrocyte

Liver

A

Skeletal muscle: anaerobic + aerobic, glycogen storge and degradation

Heart/ Brain: Glycolisis and TCA

Adipose: glycolysis for glycerol in TAG

Erythrocytes: glycolysis and pentose phosphate pathway

Liver: Everything

51
Q

Lipoprotein a and it’s association with disease

A

High concentrations in plasma are associated with increased risk of CHD.

52
Q

Formation of an atherosclerotic plaque

A

Contains connective tissue and cholesterol rich lipid, accumulates foam cells which are macrophages filled with lipid.

53
Q

Importance of LDL receptors in controlling blood cholesterol

A

LDL transports cholesterol into cells, by binding to B-100 receptors that cause receptor-mediated-endocytosis.

Deficiency of these receptors can cause hypercholesterolaemia

54
Q

PEM: protein energy malnutrition describe the diseases:

Marasmus

Kwashiorkor

Marasmic Kwashiorkor

A

Marasmus: malnourishement -> low weight (bad immunity, muscle wasting, loss of intestinal mucosa)

Kwashiorkor -> malnutrition causes lack of protein (can cause oedemas, liver enlargement, retardation)

Marasmic Kwashiorkor: combination of 2 above

55
Q

DIetary requirement for Iron, Zinc and copper

A

Iron:

Zinc: 2-3 mg/day

Copper:

56
Q

Locations where iron is stored

A

Liver, reticuloendothelial macrophages, RBC, bone marrow, muscle

57
Q

How iron is stored and how is it transported

A

Iron is taken into endothelial cells of intestines and then stored in intracellular proteins called ferretin. It is transported in a protein called transferrin

58
Q

Describe deferoxamine to treat iron overdose

A

Deferoxamine is a chelating agent (can have several bonds with a metal ion) that binds to iron to reduce it’s amount.

59
Q

Zinc function in the body and storage

A

For many different enzymes, protects against toxins.

Many channels involved in storage and processing of zinc

60
Q

Islets of Langerhans -> where they are and what they produce

A

Located in the pancreas, produce insulin (beta cells), glucagon (alpha cells) and somatostatin (delta cells)

61
Q

Effects of the following on insulin secretion

Glucose:

Amino acid in blood:

Secretin:

Glucagon:

Adrenaline:

A

Glucose: increase

Amino acid in blood: increase

Secretin: increase

Glucagon: increase

Adrenaline: decreases/ inhibits

62
Q

Insulin receptor and secondary messenger action

A

Insulin has 2 beta and 2 alpha subunits. Causes activation of Akt/protein kinase B protein. this causes

1) activation of Glycogen synthase kinase (muscle, liver)
2) translocation of Glut4 channels (Muscle, liver)
3. activation of phosphodiesterase, chich inhibits TAG releasing pathway (adipocyte).

63
Q

Effects of adrenaline and cortisol on metabolism in the body

A

Adrenaline: released during stress, glycogenolysis (liver), FA release (adipose)

Cortisol: released for long term requirements, aa mobilisation, gluconeogenesis, FA release from adipocytes.

64
Q

What happens to fats, glucose and AAs in the fed state (2-3h after meal)

A

glycolysis is activated through glucokinase (low km not to compete with the brain)

65
Q

Enzymes activated for the following reactions to occur:

Glycogen synthesis

Glycolysis

Fatty acid metabolism and tag synthesis

Storage of TAG

A

LIVER

Glycogen synthesis: glycogen synthase

Glycolysis: phosphofructokinase and pyruvate kinase

Fatty acid metabolism and TAG synthesis: Acetyl-CoA carboxylase, malonyl CoA (inhibits carnitine transferase)

Adipose Tissue

Esterification an storage of TAG: lipoprotein lipase

66
Q

Response of body to fasting (early and late)

A

Early: glycogen breakdown, FA oxidation to acetyl Co A, breakdown of TAG

Late: gluconeogenesis (from lactate, glycerol and AA)

67
Q

Explain importance of pyruvate dehydrogenase (pyruvate to acetyl CoA) in fasting and why FA are not gluconeogenic products

A

Pyruvate dehydrogenase must be inhibited (by glucagon) during fasting so that you keep Pyruvate (needed for gluconeogenesis) and not acetyl CoA.

FA oxidation makes acetyl coa straight, which can’t be made back to pyruvate for gluconeogenesis.

68
Q

What happens to the excess ketone bodies produced by oxidation of fatty acids in the fasting state?

What are their effects on protein and lipid breakdown

A

They are oxidised by most tissues (except erythrocytes).

It stimulates release of insulin, causing slowing down of protein and lipid breakdown, so that brain can use more KB instead of glucose.

69
Q

Main pathways of metabolism in starvation

A

Nutrition And Metabolism (2 decks)

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