Brain Metabolism Flashcards

1
Q

oxygen flow to the brain is regulated by

A

neuronal activity and cerebral blood flow

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2
Q

diagnostic functional imaging is done on what substrate

A

glucose

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3
Q

how much of the bodys O2 consumption is done by the brain

A

20%

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4
Q

what are the fuels of the brain?

A

glucose, and under prolonged fast ketone bodies

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5
Q

where does the brain use its energy

A

to power Na-K ATPase which maintains membrane potential

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6
Q

does the brain store glycogen?

A

yes very little

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7
Q

below what level of glucose leads to brain dysfunction

A

<2-2.5mM

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8
Q

how much energy is used by glial cells ?

A

17%-40%

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9
Q

the brain has metabolic compartmentation, what does this mean?

A

presence in a tissue of more than one distinct

pool of a given metabolite.

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10
Q

uses of compartmentation

A

Separate pools of a metabolite are not in rapid equilibrium with one another,
but rather maintain their own integrity and turnover rates.
• Compartmentation makes metabolism in the brain complex and continuous
interactions of neurons and glial cells essential for brain function.

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11
Q

what makes up the blood brain barrier

A
  • endothelium
  • basement membrane
  • astrocytes
  • pericytes
  • vasculr smooth muscle cells
  • microglia
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12
Q

what is the function of the blood brain barrier selectivity

A

To establish a stable ionic environment ensuring appropriate firing of neurons and
propagation of membrane potentials

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13
Q

what can pass the BBB by passive diffusion

A
small molecules: H2O, O2
, CO2
, NH3
, ethanol
- soluble lipids: steroid hormones
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14
Q

what can pass through carrier mediated transport

A

glucose using GLUT2 (insulin independant)

amino acids

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15
Q

what role do astrocytes have in the BBB

A
  • tightening of tight junctions (physical barrier)
  • modulation of expression and polarized localization of transporters (transport barrier)
  • controlling specialized enzyme systems (metabolic barrier)
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16
Q

what are the major nutrient transporters in the BBB

A

GLUT1, MCT1 (monocarboxylc acid transporter)

17
Q

side note on MCT1

A
High amounts of MCT1 are present
in the brain microvasculature during
nursing/suckling, and decline
significantly after 14 days of age (in
the rat brain), with a concomitant
dramatic increase in the GLUT1
content.
• This phenomenon is paralleled by a
metabolic switch to glucose as the
predominant energy fuel of the
brain.
18
Q

levels of x and y increase with cerebral maturation and synaptogenesis

A

GLUT1 GLUT3

19
Q

in a neonate what does the brain use for metabolism?

A

ketone bodies

20
Q

what are ketone bodies?

A

the acetyl-CoA produced by fatty acid oxidation in liver mitochondria is
converted to acetone, acetoacetate and b-hydroxybutyrate (ketone bodies)
−These are transportable forms of fatty acids
−In starving state oxaloacetate is mainly used in gluconeogenesis, therefore acetyl
CoA produced by b-oxidation cannot enter TCA
−Source of fuel for brain, heart and muscle (major energy source for brain during
starvation)

21
Q

is succinyl-coA present in the liver

A

no

22
Q

an increase in glucose metabolism during brain maturation is accompanied by

A

increased oxidation of glycolytically derived pyruvate via the TCA cycle.

23
Q

in the brain, what is the % of glucose and oxygen extraction?

A

glucose: 10%
O2: 50-70%

24
Q

neurovascular coupling has 2 subsets

A

Cerebral autoregulation: ensures constant cerebral blood flow over a wide range of arterial
pressures (60-150 mmHg).
Functional hyperemia: ensures rapid delivery of oxygen and glucose to active neurons

25
Q

net uptake of glucose is x on plasma glucose concentration

A

independant, it is transported by facilitated diffusion. It has a significant tissue glucose [].

26
Q

is there glycogen in the brain?

A
  • yes, very little
  • glycogen granules are only present in the astrocytes of adult animals.
  • glycogen phosphorylase in in astrocytes only
27
Q

brain glycogen metabolism is affected by

A
  • vasoactive intestinal peptide, noradrenaline, insulin
28
Q

glycogen [] increases

A
s in conditions of decreased
electrical activity (e.g., deep pentobarbital anesthesia)
29
Q

glycogen [] and its enzymes are modulated by

A

sleep deprivation

30
Q

glycogen is needed for

A

maintaining intense firing in an isolated axon