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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
Normal blood glucose
3.9 to 6.2 mM
26
Definition of gluconeogenesis
Production of glucose from non carbohydrate percursos (not fatty acids)
27
Regulation of gluconeogenesis
Mobilisation of substrate Activation of enzymes by insulin or glucagon
28
Amino acid pool
Free amino acids, in low concentrations
29
Protein turnover
The idea that protein breakdown rate should be equal to the rate of protein synthesis. N intake= n excretion
30
Nitrogen balance
N intake = n excretion
31
Deamination
Removal of a amino group as ammonia uses coenzyme
32
Transamination
Movement of an amino group to keto acid, making different amino acid
33
Fate of deaminated amino acids (keto acids) and ammonia
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
Protein degradation in most proteins
Removed by ubiquitin breakdown system , giving amino acids
35
Protein degradation of foreign/ exogenous proteins
Taken into vesicles by endocytosis or autophagocytosis and degraded by proteolytic in lysosome
36
Importance of glutamine and glutamate
Transports 2 ammonia in blood to liver
37
Importance of aspartate
Plays a role in urea cycle and transport of ammonia
38
Fatty acid synthesis location
Cytoplasm of hepatocytes
39
First step of fatty acid synthesis
Citrate to oxaloacetate and acetyl CoA
40
Lipid synthesis 2nd step
Acetyl CoA to malonyl CoA with acetyl CoA carboxylase
41
Regulation of acetyl CoA carboxylase Citrate Insulin Long chain FA Glucagon
Citrate and insulin stimulate Long chain FA and glucagon inhibit
42
Lipid synthesis 3rd step
Malonyl CoA to fatty acid with fatty acid synthase
43
Transport molecule for TAG
VLDL
44
What LDL and HDL and chylomicrons transport
LDL: mainly cholesterol to tissues HDL: cholesterol from tissue to liver Chylomicrons: mostly dietary TAG
45
Importance of HMG CoA reductase and what inhibit it
Rate limiting step of cholesterol synthesis, inhibited by statins
46
Risk factors for secondary hyperlipoproteinaemias
Obesity Diabetics type 2 Cholesterol Dietary fatty acid Alcoholism
47
What biosynthetic reactions are driven by: ATP UTP GTP
ATP: pumps, tansporters, pathways... UTP: Synthesis of complex sugars GTP: synthesis of proteins
48
Summary of TCA cycle events (In terms of # carbons and CO2 loss and name of intermediates)
49
Roles of glucose
Energy Pentose sugars for DNA Source of carbon for other sugars Source of NADP
50
Processing of glucose in: Skeletal muscle Heart/ Brain Adipose Erythrocyte Liver
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
Lipoprotein a and it's association with disease
High concentrations in plasma are associated with increased risk of CHD.
52
Formation of an atherosclerotic plaque
Contains connective tissue and cholesterol rich lipid, accumulates foam cells which are macrophages filled with lipid.
53
Importance of LDL receptors in controlling blood cholesterol
LDL transports cholesterol into cells, by binding to B-100 receptors that cause receptor-mediated-endocytosis. Deficiency of these receptors can cause hypercholesterolaemia
54
PEM: protein energy malnutrition describe the diseases: Marasmus Kwashiorkor Marasmic Kwashiorkor
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
DIetary requirement for Iron, Zinc and copper
Iron: Zinc: 2-3 mg/day Copper:
56
Locations where iron is stored
Liver, reticuloendothelial macrophages, RBC, bone marrow, muscle
57
How iron is stored and how is it transported
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
Describe deferoxamine to treat iron overdose
Deferoxamine is a chelating agent (can have several bonds with a metal ion) that binds to iron to reduce it's amount.
59
Zinc function in the body and storage
For many different enzymes, protects against toxins. Many channels involved in storage and processing of zinc
60
Islets of Langerhans -\> where they are and what they produce
Located in the pancreas, produce insulin (beta cells), glucagon (alpha cells) and somatostatin (delta cells)
61
Effects of the following on insulin secretion Glucose: Amino acid in blood: Secretin: Glucagon: Adrenaline:
Glucose: increase Amino acid in blood: increase Secretin: increase Glucagon: increase Adrenaline: decreases/ inhibits
62
Insulin receptor and secondary messenger action
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
Effects of adrenaline and cortisol on metabolism in the body
Adrenaline: released during stress, glycogenolysis (liver), FA release (adipose) Cortisol: released for **long term** requirements, aa mobilisation, gluconeogenesis, FA release from adipocytes.
64
What happens to fats, glucose and AAs in the fed state (2-3h after meal)
glycolysis is activated through glucokinase (low km not to compete with the brain)
65
Enzymes activated for the following reactions to occur: Glycogen synthesis Glycolysis Fatty acid metabolism and tag synthesis Storage of TAG
**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
Response of body to fasting (early and late)
Early: glycogen breakdown, FA oxidation to acetyl Co A, breakdown of TAG Late: gluconeogenesis (from lactate, glycerol and AA)
67
Explain importance of pyruvate dehydrogenase (pyruvate to acetyl CoA) in fasting and why FA are not gluconeogenic products
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
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
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
Main pathways of metabolism in starvation

Nutrition And Metabolism (2 decks)

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