Difference between revisions of "Fischer 2022 MitoFit Fe"
(Created page with "{{Publication |title=Fischer C, Valente de Souza L, Komlódi T, Garcia-Souza LF, Volani C, Tymoszuk P, Demetz E, Seifert M, Auer K, Hilbe R, Brigo N, Petzer V, Asshoff M, Gnai...") |
|||
Line 1: | Line 1: | ||
{{MitoFit page name}} | |||
{{Publication | {{Publication | ||
|title=Fischer C, Valente de Souza L, Komlódi T, Garcia-Souza LF, Volani C, Tymoszuk P, Demetz E, Seifert M, Auer K, Hilbe R, Brigo N, Petzer V, Asshoff M, Gnaiger E, Weiss G (2022) Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver. MitoFit | |title=Fischer C, Valente de Souza L, Komlódi T, Garcia-Souza LF, Volani C, Tymoszuk P, Demetz E, Seifert M, Auer K, Hilbe R, Brigo N, Petzer V, Asshoff M, Gnaiger E, Weiss G (2022) Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver. MitoFit Preprints 2022.2. [[doi:10.26124/mitofit:2022-0002]] | ||
|authors=Fischer Christine, Valente de Souza Lara, Komlódi | |info=[[File:MitoFit Preprints pdf.png|left|160px|link= |MitoFit pdf]] [Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver]<br/> | ||
|authors=Fischer Christine, Valente de Souza Lara, Komlódi Timea, Garcia-Souza Luiz F, Volani Chiara, Tymoszuk Piotr, Demetz Egon, Seifert Markus, Auer Kristina, Hilbe Richard, Brigo Natascha, Petzer Verena, Asshoff Malte, Gnaiger Erich, Weiss Guenter | |||
|year=2022-03-03 | |year=2022-03-03 | ||
|journal=MitoFit Prep | |journal=MitoFit Prep | ||
|abstract=Iron is an essential component for metabolic processes including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA) which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mito-chondrial respiration in peripheral blood mononuclear cells (PBMCs) and liver. Furthermore, we evaluated whether mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue. | |abstract=Iron is an essential component for metabolic processes including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA) which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mito-chondrial respiration in peripheral blood mononuclear cells (PBMCs) and liver. Furthermore, we evaluated whether mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue. | ||
<br><br> | |||
|keywords=anemia, iron deficiency, peripheral blood mononuclear cells, liver, mitochondrial function, OXPHOS, mitochondrial respiration, surrogate | |keywords=anemia, iron deficiency, peripheral blood mononuclear cells, liver, mitochondrial function, OXPHOS, mitochondrial respiration, surrogate | ||
|editor=Doerrier C | |editor=Doerrier C | ||
|mipnetlab=AT Innsbruck Oroboros | |mipnetlab=AT Innsbruck Oroboros | ||
}} | }} | ||
ORC'''ID''': [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-5656-5030]] Fischer Christine, [[File:ORCID.png|20px|link=https://orcid.org/0000-0001-9876-1411]] Komlódi Timea, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-1474-5428]] Garcia-Souza Luiz F, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-3600-4735]] Volani Chiara, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-0398-6034]] Tymoszuk Piotr, [[File:ORCID.png|20px|link=https://orcid.org/0000-0002-5723-927X]] Demetz Egon, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-3647-5895]] Gnaiger Erich, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-0709-2158]] Weiss Guenter | |||
__TOC__ | |||
== Data availability == | |||
:::: Original files are not provided by the authors. | |||
== Support == | |||
:::: This research was funded by the Christian Doppler Laboratory for Iron Metabolism and Anemia Research, the FWF funded doctoral program HOROS (W-1253, to GW) and the transnational doctoral program BI-DOC between the Medical University of Innsbruck, Austria and the Institute of Biomedicine, Eurac, in Bolzano, Italy. | |||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration |
Revision as of 14:57, 3 March 2022
Fischer 2022 MitoFit Fe
Fischer C, Valente de Souza L, Komlódi T, Garcia-Souza LF, Volani C, Tymoszuk P, Demetz E, Seifert M, Auer K, Hilbe R, Brigo N, Petzer V, Asshoff M, Gnaiger E, Weiss G (2022) Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver. MitoFit Preprints 2022.2. doi:10.26124/mitofit:2022-0002 |
»
[Mitochondrial respiration in response to iron deficiency anemia. Comparison of peripheral blood mononuclear cells and liver]
Fischer Christine, Valente de Souza Lara, Komlódi Timea, Garcia-Souza Luiz F, Volani Chiara, Tymoszuk Piotr, Demetz Egon, Seifert Markus, Auer Kristina, Hilbe Richard, Brigo Natascha, Petzer Verena, Asshoff Malte, Gnaiger Erich, Weiss Guenter (2022-03-03) MitoFit Prep
Abstract: Iron is an essential component for metabolic processes including oxygen transport within hemoglobin, tricarboxylic acid (TCA) cycle activity and mitochondrial energy transformation. Iron deficiency can thus lead to metabolic dysfunction and eventually result in iron deficiency anemia (IDA) which affects approximately 1.5 billion people worldwide. Using a rat model of IDA induced by phlebotomy, we studied the effects of IDA on mito-chondrial respiration in peripheral blood mononuclear cells (PBMCs) and liver. Furthermore, we evaluated whether mitochondrial function evaluated by high-resolution respirometry in PBMCs reflects corresponding alterations in the liver. Surprisingly, mitochondrial respiratory capacity was increased in PBMCs from rats with IDA compared to controls. In contrast, mitochondrial respiration remained unaffected in livers from IDA rats. Of note, citrate synthase activity indicated an increased mitochondrial density in PBMCs, whereas it remained unchanged in the liver, partly explaining the different responses of mitochondrial respiration in PBMCs and liver. Taken together, these results indicate that mitochondrial function determined in PBMCs cannot serve as a valid surrogate for respiration in the liver. Metabolic adaptions to iron deficiency resulted in different metabolic reprogramming in the blood cells and liver tissue.
• Keywords: anemia, iron deficiency, peripheral blood mononuclear cells, liver, mitochondrial function, OXPHOS, mitochondrial respiration, surrogate
• Bioblast editor: Doerrier C
• O2k-Network Lab: AT Innsbruck Oroboros
ORCID: Fischer Christine, Komlódi Timea, Garcia-Souza Luiz F, Volani Chiara, Tymoszuk Piotr, Demetz Egon, Gnaiger Erich, Weiss Guenter
Data availability
- Original files are not provided by the authors.
Support
- This research was funded by the Christian Doppler Laboratory for Iron Metabolism and Anemia Research, the FWF funded doctoral program HOROS (W-1253, to GW) and the transnational doctoral program BI-DOC between the Medical University of Innsbruck, Austria and the Institute of Biomedicine, Eurac, in Bolzano, Italy.
Labels: MiParea: Respiration
Pathology: Other
Organism: Rat Tissue;cell: Liver, Blood cells Preparation: Permeabilized cells, Homogenate Enzyme: Marker enzyme
Coupling state: LEAK, ROUTINE, OXPHOS, ET Pathway: N, S, NS, Other combinations, ROX HRR: Oxygraph-2k