Energy storage Flashcards

1
Q

name some cells with an absolute requirement for glucose as main source of energy.

A
  • RBC
  • Neutrophils
  • innermost cells of kidney medulla
  • lens of eye (as blood disrupts vessels)
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2
Q

name some consequences of hypoglycaemia.

A
  • confusion
  • weakness, nausea
  • muscle cramps
  • brain damage and death
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3
Q

what is the body’s response for the issue of keeping stable blood glucose levels?

A
  • store of glucose known as glycogen.
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4
Q

where is glycogen stored in the body?

A
  • muscle as intra and intermyofibrillar glycogen.

- liver as granules in hepatocytes.

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5
Q

describe the structure of glycogen.

A
  • glucose polymer, with many glucose residues.
  • a 1-6 glycosidic bonds join the branches every 8-10 residues and a 1-4 glycosidic bonds join the chains.
  • branched structure originating from primer core dimer protein glycogenin that converts glucose to glycogen.
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6
Q

how is glycogen stores utilised in liver?

A
  • G6P converted to glucose and exported to blood.

- liver glycogen is a buffer of blood glucose levels.

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7
Q

how is glycogen utilised in muscle?

A
  • muscle lacks Glucose-6-phosphotase to convert G6- into glucose so enters glycolysis.
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8
Q

what is the rate limiting enzyme for glycogenesis?

A
  • glycogen synthase
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9
Q

what is the rate limiting enzyme for glucogenolysis?

A
  • glycogen phosphorylase
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10
Q

what happens to the two pathways at high levels of glucagon/adrenaline?

A
  • glycogenesis decreases and increases.

* muscle cells do not have glucagon receptors so unaffected by high glucagon levels.

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11
Q

what happens to the two pathways at high levels of insulin?

A
  • glycogenesis increases and glycogenolysis decreases.
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12
Q

why do glycogen storage diseases arise?

A
  • inborn errors of metabolism, inherited.
  • deficiency or dysfunction of enzymes of glycogen.
  • excess glycogen storage leads to tissue damage.
  • diminished stores lead to hypoglycaemia and poor exercise tolerance.
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13
Q

what are some examples of glycogen diseases?

DEFICIENCY NOT LACK

A
  • von gierkes disease : G6-phosphatase deficiency

- mcardle disease : muscle glycogen phosphorylase deficiency.

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14
Q

why is it necessary for gluconeogenesis to take place?

A
  • beyond 8h, liver glycogen starts to deplete so alternative source needed.
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15
Q

what are the precursors of gluconeogenesis?

A
  • lactate : from anaerobic in cori cycle
  • glycerol : adipose breakdowns triglycerides
  • amino acids : mainly alanine
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16
Q

what are the key enzymes in gluconeogenesis? and what are the main control sites of pathway?

A
  • phosphoenolpyruvate carbocykinase (PEPCK)
  • oxaloacetate to glycolysis pathway intermediate.
  • fructose 1-6, bisphosphatase
  • as phosphofructokinase irreversible.
  • glucose-6-phosphatase
  • hexokinase irreversible.

PEPCK and fructose 1-6, bisphosphatase control sites.

17
Q

when is gluconeogenesis regulated?

A
  • starvation
  • prolonged exercise
  • stress
  • stimulated by glucagon and cortisol.
  • inhibited by insulin.
18
Q

how are lipids stored?

A
  • glycerol and fatty acids stored as triacylglycerols.
  • TAG hydrophobic so stored an anhydrous adipose.
  • utilised in exercise, starvation, stress and pregnancy.
  • storage and mobilisation under hormone control.
19
Q

describe structure of adipose/

A
  • large lipid drops filled with TAG or cholesterol with organelles pushed to side.
  • 30 billion fat cells - 15kg.
20
Q

What is lipogenesis?

A
  • fatty acid synthesis mainly in liver, carbon from pyruvate.
21
Q

what is the key regulatory enzyme in lipogenesis?

A
  • acetyl-CoA carboxylase which is increased in activity by insulin and citrate allosterically, and decreased by glucagon and adrenaline and AMP allosterically.
22
Q

compare B-oxidation and FA synthesis.

A
  • remove C2 vs add C2
  • in mitochondria vs in cytoplasm
  • oxidative vs reductive
  • insulin inhibits vs insulin stimulates