AC Lecture 60: Introduction to Metabolism Flashcards

1
Q

What is catabolism?

A

oxidative degradation of large nutrient macromolecules into smaller, simpler compounds
usually accompanied by the release of free energy (conserved as ATP)

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2
Q

What is anabolism?

A

the enzyme synthesis of larger molecular components of the cell from simple precursors
usually requires input of energy, often ATP

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3
Q

What are amphibolic pathways?

A

pathways that contain both catabolic and anabolic components

e.g Krebs citric acid cycle

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4
Q

How is metabolism regulated?

A

availability and concentration of substrates and cofactors
availability and need for energy/ATP
regulatory enzymes (allosteric effectors of some enzymes, end product feedback inhibition, etc.)
genetic control of rate of enzyme synthesis (e.g. by an enzyme substrate or a drug) determining the amount of active enzyme (constituative vs adaptive enzymes)
hormonal regulation (can act on regulatory enzymes or activate or repress gene expression)

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5
Q

Describe how insulin regulates metabolism of glucose.

A

regulates glucose and fatty acid metabolism in many tissues
produced in the beta cells of the pancreas (in response to high glucose levels)
promotes utilization of glucose in teh body

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6
Q

Describe how epinephrine regulates metabolism of glucose.

A

regulates glucose and fatty acid metabolism in many tissues

epi is produced in the adrenal glands in response to stress

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7
Q

Describe how glucagon regulates metabolism of glucose.

A

regulates glucose and fatty acid metabolism in the liver and adipose tissue
produced in the alpha cells of the pancreas (in response to low glucose levels)
promotes production of glucose by the liver

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8
Q

What is Type I DM?

A

associated with lack of insulin production due to destruction of pancreatic beta cells due to autoimmune attack

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9
Q

What is Type II DM?

A

increased resistance to the actions of insulin

insulin is produced but its effectiveness in enhancing utilization of glucose is decreased

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10
Q

What metabolic problems are caused by DM?

A

energy production from glucose is impaired
fat metabolism is elevated to provide energy
much of the fat is oxidized to ketone bodies (causing ketosis)
high levels of circulating glucose react improperly and result in modified proteins with altered functions
results in aldose reductase to sorbitol (results in increased osmotic pressure)

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11
Q

How does glucagon promote glucose production in the liver?

A
  1. stimulation of glucose synthesis (gluconeogenesis)

2. stimulation of glycogen breakdown

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12
Q

What functions does glucagon perform?

A

promote glucose production in the liver

increase fatty acid release from triglycerides stored in adipose tissue

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13
Q

How does glucagon perform its functions?

A
  1. stimulating the activities of critical enzymes involved in synthesis of glucose and breakdown of glycogen
  2. transcriptionally activating the genes for such critical enzymes
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14
Q

How does insulin promote the utilization of glucose?

A

stimulating glycolysis
stimulating glucose uptake into some tissues (muscle, adipose)
stimulating glycogen formation
stimulating fatty acid synthesis from glucose
stimulating protein synthesis (several amino acids can be produced from glucose)

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15
Q

What is the general rule regarding epi, glucagon, and insulin and phosphorylation.

A

glucagon: promotes phosphorylation of enzymes by activating cAMP-dependent PKA
epi: promotes phosphorylation of enzymes by activating cAMP-dependent PKA
insulin: promotes dephosphorylatin of enzymes by activating certain phosphatases

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16
Q

How are glucagon (or epi) signals turned off?

A

hydrolysis of GTP by GTPase activity of alpha-GTP subunit resultin gin reassociation of the beta-gamma subunit with the alpha-beta (inactive GDP-bound G protein)

17
Q

Through what mechanism do epi, glucagon, and insulin act?

A

G-protein coupled receptor

18
Q

How is glucose transported into cells?

A

Liver, RBC, brain, pancreas, and most cells: pssive carrier-mediated glucose transport via glucose carriers (GLUT1 and GLUT3; liver and pancreas also have GLUT2)
Muscles: GLUT4
GI and Kidney: GLUT5 (catalyzes active transport of fructose; weak glucose uptake activity); SGLUT1 and SGLUT2 (active uptake of glucose linked to NA+ transport)

19
Q

How does insulin affect glucose carriers?

A

no effect on GLUT 1, 2, or 3

increases the number of GLUT 4 carriers on plasma membrane of muscle and fat cells (increases glucose uptake)