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Difference between revisions of "Schoenfeld 2023 MiP2023"

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|year=2023
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|abstract=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.
References
[1] Speijer D., Bioessays 2011, 33, 88–94
[2] Yang SY et al., J Biol Chem 1987, 262: 13027–13032
[3] Panov A et al., Biomed Res Int. 2014, :472459
schoenfeld
2023-03-23 06:31
|mipnetlab=DE Magdeburg Schoenfeld P
}}
}}
{{Labeling
{{Labeling
|event=Oral
|event=Oral
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Revision as of 09:19, 24 March 2023

MiPsociety
Brain's difficult relationship to burning fatty acids.

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.

References

[1] Speijer D., Bioessays 2011, 33, 88–94

[2] Yang SY et al., J Biol Chem 1987, 262: 13027–13032

[3] Panov A et al., Biomed Res Int. 2014, :472459 schoenfeld 2023-03-23 06:31


O2k-Network Lab: DE Magdeburg Schoenfeld P


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Event: Oral