Metabolism in the fed and starved states Flashcards

1
Q

What determines the switch between the fed and fasting state

A

The molar ratio of insulin to glucagon in the blood.

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2
Q

outline the fed state

A

during meals and for several hours afterwards characterized by high insulin and low glucagon

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3
Q

outline the fasting state

A

6-12 hours after a meal, anythings after 12 hours is starvation, characterized by low insulin and high glucagon.

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4
Q

What are the different metabolic processes in the fed state

A

increase in insulin to glucagon ratio
glucose converted to glycogen, TAG and secreted as VLDL, some enter the Krebs cycle
glycerol from peripheral tissues are converted to TAG’s and excess amino acids are converted to pyruvate

LPL activity is greatly affected by high insulin to glucagon ratio.

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5
Q

Outline metabolism in the early fasting state

A

there is low insulin to glucagon ratio
During fasting, the liver switched from glucose-utilizing to a glucose producing organ, there is more glycogenolysis than glycogen synthesis, gluconeogenesis is also occurring
fatty acids from lipolysis produce energy via beta-oxidation

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6
Q

Outline metabolism in the early fasting state in adipose tissue

A

the entry of glucose into adipose tissue via GLUT 4 is reduced as a response to low insulin,
TAG’s are mobilised in response to the reduced insulin to glucagon ratio and fatty acids are used directly within the tissue to produce energy.

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7
Q

Outline metabolism in the early fasting state in the muscles

A

Glucose entry via GLUT-4 is reduced, glycogenolysis doesn’t occur as there are no glucagon receptors in skeletal muscle to cause activation.

muscles and other peripheral tissue switch to fatty acid oxidation as a source of energy which inhibits glycolysis and glucose utilisation

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8
Q

Outline metabolism in the early fasting state in the brain

A

Continues to take up glucose due to high affinity of GLUT-1 & GLUT-3, Glucose continues to be metabolised as other cells start using fatty acids as fuel and the liver starts exporting glucose.

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9
Q

Outline metabolism in the starved state

A

chronic low insulin and high glucagon decreased metabolic rate, free fatty acids become the major energy source and the production of ketone bodies as an alternative fuel source

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10
Q

Outline metabolism in the starved state in the liver

A

no glucose enters the liver, plasma glucose is dependant on gluconeogenesis from lactate, glycerol and alanine from fat and protein breakdown.

fatty acids enter the liver and provide energy to support gluconeogenesis with excess acetyl CoA being converted to ketone bodies

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11
Q

Outline metabolism in the starved state in the adipose tissue

A

Little glucose entry
the body switches to using fatty acids from TAG’s to supply all the energy needs of the major tissues, glycerol exported to the liver to support gluconeogenesis.

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12
Q

Outline metabolism in the starved state in the muscles

A

little glucose entry, switch to fatty acids as a fuel.
ketone bodies are also used to generate acetyl-CoA.
protein breakdown stimulated and the longer starvation continues the more muscle tissue you lose.

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13
Q

Outline the glucose fatty acid cycle

A

not actually a cycle, mobilisation of fatty acids as a response to glucagon, excess CoA converted to citrate in the Krebs cycle which inhibits PFK-1 which is converting F6P to F1,6BP, the build-up of G6P inhibits hexokinase and prevents glucose phosphorylation and therefore conserves glucose.

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14
Q

Outline metabolism in the starved state in the brain

A

Ketone bodies can cross the blood-brain barrier where fat cannot and can be utilised by the brain as an energy source.

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15
Q

state 4 hormones that have control over gluconeogenesis and glycogenolysis.

A

activators- Glucagon, adrenaline, cortisol (response to stress),
inactivator- insulin

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16
Q

Outline reciprocal regulation of phosphorylase and glycogen synthase by phosphorylation

A

Glucagon and adrenaline activate cAMP dependant PK, which inactivates glycogen synthase b and activates phosphorylase kinase (can be mimicked by calcium ions via muscle contraction). phosphorylase kinase phosphorylates glycogen phosphorylase which drives glycogen breakdown.

in the presence of insulin, it activates phosphatase 1 which deactivates phosphorylase kinase and activates glycogen synthase.