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MEH > Energy storage > Flashcards

Energy storage Flashcards

1
Q

tissues that have an absolute requirement for glucose as an energy source

A
  • red blood cells
  • neurtrophils
  • innermost cells of kidney medulla
  • lens of eye
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2
Q

what is glycogen

A

highly branched polymer of glucose residues linked together by α1-4 and α1-6 glycosidic bonds in 10:1 ratio

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3
Q

structure of glycogen

A
  • highly branched structure (α1-6 bonds form branch points) provides many sites where glucose can be added or removed so rapid synthesis and degradation
  • large molecule so many glucose molecules stored with minimal osmotic effect in the tissue
  • highly polar molecule that attracts a lot of water
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4
Q

major energy stores in a 70kg man

A
  • triacylglycerols 15kg
  • glycogen 0.4 kg
  • muscle protein 6kg
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5
Q

how is glycogen stored

A

granules

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6
Q

glycogen in liver vs muscle

A

liver
- ~100g glycogen
- G6P converted to glucose and exported to blood
- buffer of blood glucose levels

muscle
- ~300g glycogen
- lacks glucose-6-phosphatase enzyme
- G6P enters glycolysis for energy production for muscle

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7
Q

glycogenesis (glycogen synthesis)

A
  1. glucose + ATP → glucose-6P + ADP hexokinase (glucokinase in liver)
  2. glucose-6P ↔ glucose-1P phosphoglucomutase
  3. glucose-1P + UTP + H2O → UDP-glucose + Pi G1P uridyltransferase
  4. glycogen (n) + UDP-glucose → glycogen (n+1) + UDP glycogen synthase(α 1-4 glycosidic bonds) or branching enzyme(α 1-6 glycosidic bonds)
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8
Q

what is UTP

A
  • structurally similar and energetically equivalent to ATP
  • UDP-glucose considered highly activated form of glucose
  • important intermediate in synthesis of sugar-containing molecules
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9
Q

when does glycogenolysis occur

A
  • in skeletal muscle in response to exercise
  • in liver in response to fasting or stress
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10
Q

glycogenolysis (glycogen degradation)

A
  1. glycogen (n) + Pi → glucose-1P + glycogen (n-1) glycogen phosphorylase (α 1-4 glycosdic bonds) or de-branching enzyme (α 1-6 glycosidic bonds)
  2. glucose-1P ↔ glucose-6P phosphoglucomutase
    in muscle, glucose-6P enters glycolysis for energy production
  3. in liver: glucose-6P + H2O → glucose + Pi glucose-6-phosphatase
    in liver, glucose released into blood and transported to tissues
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11
Q

how is glycogen metabolism regulated

A
  • controlling activities of rate limiting enzymes (glycogen synthase and glycogen phosphorylase)
  • allosteric control
  • covalent modification in response to hormone levels (reversible phosphorylation)
  • enzymes controlled reciprocally
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12
Q

allosteric control of glycogen metabolism

A

AMP activates muscle glycogen phospphorylase but not liver form

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13
Q

hormonal regulation of glycogen metabolism

A

glucagon and adrenaline increase phosphorylation of enzymes
- glycogen synthase inhibited
- glycogen phosphorylase activated

insulin increases dephosphorylation of enzymes
- glycogen synthase activated
- glycogen phosphorylase inhibited

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14
Q

glycogen storage diseases

A
  • inherited diseases
  • arise from deficiency or dysfunction of enzymes in glycogen metabolism
  • severity depends on which enzyme/tissues is affected
  • 12 distinct types
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15
Q

clinical consequences of glycogen storage diseases

A
  • excess glycogen storage causes tissue damage
  • diminished glycogen stores cause hypoglycaemia and poor exercise tolerance
  • liver and/or muscle are affected
  • glycogen structure may be abnormal
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16
Q

2 examples of glycogen storage diseases

A
  • von Gierke’s disease - glucose-6-phosphate deficiency
  • McArdle disease - muscle glycogen phosphorylase deficiency
17
Q

time course of glucose utilisation

A
  • glucose from food ~2 hours
  • glycogenolysis 8-10 hours
  • gluconeogenesis 8-10 hours onwards
18
Q

where does gluconeogenesis occur

A
  • liver
  • kidney cortex (lesser extent)
19
Q

precursors of gluconeogenesis

A
  • lactate from anaerobic glycolysis in exercising muscle and RBC (Cori cycle)
  • glycerol released from adipose tissue breakdown of triglycerides
  • amino acids mainly alanine and those whose metabolism involves pyruvate
  • acetyl Co-A can’t be converted to glucose because the PDH reaction is irreversible
20
Q

gluconeogenesis

A

irreversible steps 1, 3 and 10 of glycolysis are bypassed by thermodynamically spontaneous reactions

10.pyruvate + ATP + CO2 → oxaloacetate + ADP + Pi pyruvate carboxylase
oxaloacetate + GTP → phosphoenolpyruvate + GDP + CO2 PEPCK

3.fructose-1,6-bisphosphate + H2O → fructose-6-phosphate + Pi fructose 1,6-bisphosphatase

1.glucose-6-phosphate + H2O → glucose + Pi glucose-6-phosphatase

21
Q

regulation of gluconeogenesis

A

glucagon, cortisol stimulates gluconeogenesis
- increased amount of PEPCK
- increased amount and activity of fructose 1,6-bisphosphatase

insulin inhibits gluconeogenesis
- decereased amount of PEPCK
- decreased amount and activity of fructose 1,6-bisphosphotase

insulin:glucagon determines rate of gluconeogenesis

22
Q

triacylglycerols

A
  • highly efficient energy store
  • energy intake in excess of requirements converted to TAGs for storage
  • TAGs are hydrophobic so stored in anhydrous form in adipose tissue
  • utilised in prolonged exercise, stress, starvation, pregnancy
  • storage under hormonal control (promoted by insulin and reduced by glucagon, adrenaline, cortisol, GH, thyroxine)
23
Q

adipocytes

A
  • ~0.1mm in diameter
  • cells expand as more fat added
  • average adult has ~30 billion fat cells wieghing 15kg
  • increase in size about fourfold before dividing and increasing number of cells
  • don’t lose adipocytes on weight loss
24
Q

overview of dietary triacylglycerol metabolism

A
  • TAG → fatty acids + glycerol by pancreatic lipase in small intestine
  • reform into TAGs in intestinal epithelial cell and packaged into chylomicron
  • chylomicrons drain into lacteal system which drains into lymphatic system
  • chylomicrons into bloodstream via thoracic duct
  • TAGs either stored in adipose tissue or utilised by tissues
  • TAG in adipose broken down by hormone sensitive lipase and fatty acids transported from adipose to tissues bound to albumin
  • fatty acid oxidation for energy in tissues
25
Q

what is fatty acid synthesis (lipogenesis)

A

fatty acids are synthesised from acetyl-CoA (drived from catabolism of carbohydrates and amino acids) using ATP and NADPH

26
Q

liver lipogenesis

A
  • NADPH produced in cytoplasm from pentose phosphate pathway
  • glucose → pyruvate in cytoplasm (glycolysis)
  • pyruvate enters mitochondria and forms acetyl-CoA + oxaloacetate which condense to form citrate (TCA cycle)
  • citrate cleaved in cytoplasm releasing acetyl-CoA and oxaloacetate
  • oxaloacetate converted back to pyruvate, making NADPH in process
  • acetyl-CoA carboxylase converts acetyl-CoA to malonyl-CoA (3C)
  • fatty acid synthase complex builds fatty acids by sequential addition of 2 carbon units provided by malonyl-CoA with loss of CO2
27
Q

regulation of liver lipogenesis

A

allosteric regulation of acetyl-CoA carboxylase
- citrate activates
- AMP inhibits

hormonal regulation of acetyl-CoA carboxylase
- insulin activates by dephosphorylating enzyme
- glucagon and adrenaline inhibit by phosphorylating enzyme

28
Q

lipolysis (fat mobilisation)

A
  • hormone senstive lipase breaks down TAGs in adipose tissue to release glycerol and fatty acids into blood
  • glycerol travels to liver and used for gluconeogenesis
  • fatty acids travel bound to albumin to mucscle and other tissues for β oxidation
29
Q

regulation of lipolysis

A
  • glucagon and adrenaline lead to phosphorylation and activation of hormone-sensitive lipase
  • insulin leads to dephosphorylation and inhibition of hormone-sensitive lipase
30
Q

why is it beneficial for degradative (catabolic) and biosynthetic (anabolic) pathways to have different routes

A
  • greater flexibility - substrates and intermediates can be different
  • better control - can be controlled independently or co-ordinately
  • thermodynamically irreversible steps can be by-passed
31
Q

fatty acid oxidation VS fatty acid synthesis

A

fatty acid oxidation (β oxidation)
- cycle of reactions that remove C2
- C2 atoms removed as acetyl CoA
- produces acetyl CoA
- occurs in mitochondria
- separate enzymes in mitochondrial matrix
- oxidative - produces NADH and FADH2
- requires small amount of ATP to activate fatty acid
- intermediates linked to CoA
- regulated indirectly by availability of fatty acids in mitochondria
- glucagon and adrenaline stimulate
- insulin inhibits

fatty acid synthesis
- cycle of reactions that add C2
- C2 atoms added as malonyl CoA
- consumes acetyl CoA
- occurs in cytoplasm
- multi-enzyme complex in cytoplasm
- reductive - requires NADPH
- requires large amount of ATP to drive process
- intermediates linked to fatty acid synthase by carrier protein
- regulated directly by acetyl-CoA carboxylase activity
- glucagon and adrenaline stimulate
- insulin stimulates

MEH (26 decks)

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