High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › fagfællebedømt

Standard

High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells. / Hansen, Camilla; Olsen, Karina; Pilegaard, Henriette; Bangsbo, Jens; Gliemann, Lasse; Hellsten, Ylva.

I: Physiological Reports, Bind 9, Nr. 14, e14855, 2021.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › fagfællebedømt

Harvard

Hansen, C, Olsen, K, Pilegaard, H, Bangsbo, J, Gliemann, L & Hellsten, Y 2021, 'High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells', Physiological Reports, bind 9, nr. 14, e14855. https://doi.org/10.14814/phy2.14855

APA

Hansen, C., Olsen, K., Pilegaard, H., Bangsbo, J., Gliemann, L., & Hellsten, Y. (2021). High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells. Physiological Reports, 9(14), [e14855]. https://doi.org/10.14814/phy2.14855

Vancouver

Hansen C, Olsen K, Pilegaard H, Bangsbo J, Gliemann L, Hellsten Y. High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells. Physiological Reports. 2021;9(14). e14855. https://doi.org/10.14814/phy2.14855

Author

Hansen, Camilla ; Olsen, Karina ; Pilegaard, Henriette ; Bangsbo, Jens ; Gliemann, Lasse ; Hellsten, Ylva. / High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells. I: Physiological Reports. 2021 ; Bind 9, Nr. 14.

Bibtex

@article{c72125e42912498da6d9c76aa5222bd1,
title = "High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells",
abstract = "The influence of glucose and palmitic acid (PA) on mitochondrial respiration and emission of hydrogen peroxide (H2O2) was determined in skeletal muscle-derived microvascular endothelial cells. Measurements were assessed in intact and permeabilized (cells treated with 0.025% saponin) low passage endothelial cells with acute-or prolonged (3 days) incubation with regular (1.7 mM) or elevated (2.2 mM) PA concentrations and regular (5 mM) or elevated (11 mM) glucose concentrations. In intact cells, acute incubation with 1.7 mM PA alone or with 1.7 mM PA + 5 mM glucose (p < .001) led to a lower mitochondrial respiration (p < 0.01) and markedly higher H2O2/O2 emission (p < 0.05) than with 5 mM glucose alone. Prolonged incubation of intact cells with 1.7 mM PA +5 mM glucose led to 34% (p < 0.05) lower respiration and 2.5-fold higher H2O2/O2 emission (p < 0.01) than incubation with 5 mM glucose alone. Prolonged incubation of intact cells with elevated glucose led to 60% lower (p < 0.05) mitochondrial respiration and 4.6-fold higher H2O2/O2 production than incubation with 5 mM glucose in intact cells (p < 0.001). All effects observed in intact cells were present also in permeabilized cells (State 2). In conclusion, our results show that acute and prolonged lipid availability, as well as prolonged hyperglycemia, induces mitochondrial dysfunction as evidenced by lower mitochondrial respiration and enhanced H2O2/O2 emission. Elevated plasma substrate availability may lead to microvascular dysfunction in skeletal muscle by impairing endothelial mitochondrial function.",
keywords = "Faculty of Science, Glucose, Mitochondria, Palmitic acid, Reactive oxygen species, Respirometry, Vascular",
author = "Camilla Hansen and Karina Olsen and Henriette Pilegaard and Jens Bangsbo and Lasse Gliemann and Ylva Hellsten",
note = "{\textcopyright} 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.",
year = "2021",
doi = "10.14814/phy2.14855",
language = "English",
volume = "9",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "Wiley Periodicals, Inc.",
number = "14",

}

RIS

TY - JOUR

T1 - High metabolic substrate load induces mitochondrial dysfunction in rat skeletal muscle microvascular endothelial cells

AU - Hansen, Camilla

AU - Olsen, Karina

AU - Pilegaard, Henriette

AU - Bangsbo, Jens

AU - Gliemann, Lasse

AU - Hellsten, Ylva

N1 - © 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.

PY - 2021

Y1 - 2021

N2 - The influence of glucose and palmitic acid (PA) on mitochondrial respiration and emission of hydrogen peroxide (H2O2) was determined in skeletal muscle-derived microvascular endothelial cells. Measurements were assessed in intact and permeabilized (cells treated with 0.025% saponin) low passage endothelial cells with acute-or prolonged (3 days) incubation with regular (1.7 mM) or elevated (2.2 mM) PA concentrations and regular (5 mM) or elevated (11 mM) glucose concentrations. In intact cells, acute incubation with 1.7 mM PA alone or with 1.7 mM PA + 5 mM glucose (p < .001) led to a lower mitochondrial respiration (p < 0.01) and markedly higher H2O2/O2 emission (p < 0.05) than with 5 mM glucose alone. Prolonged incubation of intact cells with 1.7 mM PA +5 mM glucose led to 34% (p < 0.05) lower respiration and 2.5-fold higher H2O2/O2 emission (p < 0.01) than incubation with 5 mM glucose alone. Prolonged incubation of intact cells with elevated glucose led to 60% lower (p < 0.05) mitochondrial respiration and 4.6-fold higher H2O2/O2 production than incubation with 5 mM glucose in intact cells (p < 0.001). All effects observed in intact cells were present also in permeabilized cells (State 2). In conclusion, our results show that acute and prolonged lipid availability, as well as prolonged hyperglycemia, induces mitochondrial dysfunction as evidenced by lower mitochondrial respiration and enhanced H2O2/O2 emission. Elevated plasma substrate availability may lead to microvascular dysfunction in skeletal muscle by impairing endothelial mitochondrial function.

AB - The influence of glucose and palmitic acid (PA) on mitochondrial respiration and emission of hydrogen peroxide (H2O2) was determined in skeletal muscle-derived microvascular endothelial cells. Measurements were assessed in intact and permeabilized (cells treated with 0.025% saponin) low passage endothelial cells with acute-or prolonged (3 days) incubation with regular (1.7 mM) or elevated (2.2 mM) PA concentrations and regular (5 mM) or elevated (11 mM) glucose concentrations. In intact cells, acute incubation with 1.7 mM PA alone or with 1.7 mM PA + 5 mM glucose (p < .001) led to a lower mitochondrial respiration (p < 0.01) and markedly higher H2O2/O2 emission (p < 0.05) than with 5 mM glucose alone. Prolonged incubation of intact cells with 1.7 mM PA +5 mM glucose led to 34% (p < 0.05) lower respiration and 2.5-fold higher H2O2/O2 emission (p < 0.01) than incubation with 5 mM glucose alone. Prolonged incubation of intact cells with elevated glucose led to 60% lower (p < 0.05) mitochondrial respiration and 4.6-fold higher H2O2/O2 production than incubation with 5 mM glucose in intact cells (p < 0.001). All effects observed in intact cells were present also in permeabilized cells (State 2). In conclusion, our results show that acute and prolonged lipid availability, as well as prolonged hyperglycemia, induces mitochondrial dysfunction as evidenced by lower mitochondrial respiration and enhanced H2O2/O2 emission. Elevated plasma substrate availability may lead to microvascular dysfunction in skeletal muscle by impairing endothelial mitochondrial function.

KW - Faculty of Science

KW - Glucose

KW - Mitochondria

KW - Palmitic acid

KW - Reactive oxygen species

KW - Respirometry

KW - Vascular

U2 - 10.14814/phy2.14855

DO - 10.14814/phy2.14855

M3 - Journal article

C2 - 34288561

VL - 9

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 14

M1 - e14855

ER -

ID: 275374323