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Difference between revisions of "Schoenfeld 2023 MiP2023"

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{{MiP header page name}}
{{Abstract
{{Abstract
|title=[[Image:MiPsocietyLOGO.JPG|left|100px|Mitochondrial Physiology Society|MiPsociety]] Brain's difficult relationship to burning fatty acids.
|title=[[File:Schoenfeld.png|left|100px|Schoenfeld Peter]] A view on brain's problem with fatty acid burning.
|info=[[MiP2023 Obergurgl AT]]
|info=[[MiP2023 Obergurgl AT]]
|authors=Schoenfeld Peter
|authors=Schoenfeld Peter
|year=2023
|year=2023
|event=MiP2023 Obergurgl AT
|event=MiP2023 Obergurgl AT
|abstract=Authors: Schönfeld P, Reiser G
|abstract='''Authors:''' [[Schoenfeld Peter|Schönfeld P]], [[Reiser G]]<br><br>
Distinct hypothalamic neurons sense blood levels of fatty acids (FA) and, thereby regulate caloric intake. Astrocytes have some capacity of β-oxidation. But, there are ongoing discussions on this question: Do neurons generally burn FA for energy generation?
Distinct hypothalamic neurons sense blood levels of fatty acids (FA) and, thereby regulate caloric intake. Astrocytes have some capacity of β-oxidation. But, there are ongoing discussions on this question: Do neurons generally burn FA for energy generation?


Respiration and membrane potential of mitochondria of rat brain (RBM) and, for comparison, of liver (RLM) were measured without and with octanoate (l-octanoylcarnitine). In addition, H2O2 generation was measured with Amplex Red.
Respiration and membrane potential of mitochondria of rat brain (RBM) and, for comparison, of liver (RLM) were measured without and with octanoate (l-octanoylcarnitine). In addition, H<sub>2</sub>O<sub>2</sub> generation was measured with Amplex Red.


In line with previous studies, we found no evidence for a noteworthy β-oxidation of FA by RBM. This fits with theoretical considerations (1) and values obtained for capacities of enzymes of β-oxidation (2). But, these results contradict those of a previous study (3), reporting that RBM incubated with mixtures of FA (carnitine derivatives) plus other substrates (e.g. succinate) show substantial β-oxidation.   
In line with previous studies, we found no evidence for a noteworthy β-oxidation of FA by RBM. This fits with theoretical considerations (1) and values obtained for capacities of enzymes of β-oxidation (2). But, these results contradict those of a previous study (3), reporting that RBM incubated with mixtures of FA (carnitine derivatives) plus other substrates (e.g. succinate) show substantial β-oxidation.   
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What could be possible reasons for disregarding FA as energy substrates by neurons? These are mainly: (a) Harmful activities of non-esterified long-chain FA on mitochondria. (b) Burning of FA costs more oxygen than glucose burning with respect to the energy yield. (c) FA oxidation by mitochondria is associated with more sites of superoxide generation. (d) Neurons are equipped with poor antioxidative capacity. In conclusion, burning of FA would expose neurons to intolerably high oxidative stress.
What could be possible reasons for disregarding FA as energy substrates by neurons? These are mainly: (a) Harmful activities of non-esterified long-chain FA on mitochondria. (b) Burning of FA costs more oxygen than glucose burning with respect to the energy yield. (c) FA oxidation by mitochondria is associated with more sites of superoxide generation. (d) Neurons are equipped with poor antioxidative capacity. In conclusion, burning of FA would expose neurons to intolerably high oxidative stress.


References
<small>
 
# Speijer D (2011] Oxygen radicals shaping evolution: Why fatty acid catabolism leads to peroxisomes while neurons do without it. https://doi.org/10.1002/bies.201000097
[1] Speijer D., Bioessays 2011, 33, 88–94
# Yang SY, He XY, Schultz H (1987) Fatty acid oxidation in rat brain is limited by the low activity of 3-ketoacyl-coenzyme A thiolase. https://doi.org/10.1016/S0021-9258(18)45161-7
 
# Panov A, Orynbayeva Z, Vavilin V, Lyakhovich V (2014) Fatty acids in energy metabolism of the central nervous system. https://doi.org/10.1155/2014/472459
[2] Yang SY et al., J Biol Chem 1987, 262: 13027–13032
</small>
 
[3] Panov A et al., Biomed Res Int. 2014, :472459
schoenfeld
2023-03-23 06:31
|mipnetlab=DE Magdeburg Schoenfeld P
|mipnetlab=DE Magdeburg Schoenfeld P
}}
}}
== Affiliation ==
::::Otto-von-Guericke Universität, 39120 Magdeburg, Germany
:::: Corresponding author: peter.schoenfeld@med.ovgu.de
{{Labeling
{{Labeling
|area=Respiration
|organism=Rat
|tissues=Nervous system, Liver
|topics=Fatty acid
|event=Oral
|event=Oral
}}
}}

Latest revision as of 10:14, 16 May 2023

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Schoenfeld 2023 MiP2023

Schoenfeld Peter
A view on brain's problem with fatty acid burning.

Link: MiP2023 Obergurgl AT

Schoenfeld Peter (2023)

Event: MiP2023 Obergurgl AT

Authors: Schönfeld P, Reiser G

Distinct hypothalamic neurons sense blood levels of fatty acids (FA) and, thereby regulate caloric intake. Astrocytes have some capacity of β-oxidation. But, there are ongoing discussions on this question: Do neurons generally burn FA for energy generation?

Respiration and membrane potential of mitochondria of rat brain (RBM) and, for comparison, of liver (RLM) were measured without and with octanoate (l-octanoylcarnitine). In addition, H2O2 generation was measured with Amplex Red.

In line with previous studies, we found no evidence for a noteworthy β-oxidation of FA by RBM. This fits with theoretical considerations (1) and values obtained for capacities of enzymes of β-oxidation (2). But, these results contradict those of a previous study (3), reporting that RBM incubated with mixtures of FA (carnitine derivatives) plus other substrates (e.g. succinate) show substantial β-oxidation.

What could be possible reasons for disregarding FA as energy substrates by neurons? These are mainly: (a) Harmful activities of non-esterified long-chain FA on mitochondria. (b) Burning of FA costs more oxygen than glucose burning with respect to the energy yield. (c) FA oxidation by mitochondria is associated with more sites of superoxide generation. (d) Neurons are equipped with poor antioxidative capacity. In conclusion, burning of FA would expose neurons to intolerably high oxidative stress.

  1. Speijer D (2011] Oxygen radicals shaping evolution: Why fatty acid catabolism leads to peroxisomes while neurons do without it. https://doi.org/10.1002/bies.201000097
  2. Yang SY, He XY, Schultz H (1987) Fatty acid oxidation in rat brain is limited by the low activity of 3-ketoacyl-coenzyme A thiolase. https://doi.org/10.1016/S0021-9258(18)45161-7
  3. Panov A, Orynbayeva Z, Vavilin V, Lyakhovich V (2014) Fatty acids in energy metabolism of the central nervous system. https://doi.org/10.1155/2014/472459


O2k-Network Lab: DE Magdeburg Schoenfeld P


Affiliation

Otto-von-Guericke Universität, 39120 Magdeburg, Germany
Corresponding author: peter.schoenfeld@med.ovgu.de

Labels: MiParea: Respiration 


Organism: Rat  Tissue;cell: Nervous system, Liver 


Regulation: Fatty acid 


Event: Oral