PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
Cardiomyocyte Heat Production Measured In Vitro with Temperature Probes and by Means of Differential Isothermal Calorimetry Indicates a Role of the ABA/LANCL1-2 Hormone/Receptors System in Thermogenesis
Version 1
: Received: 18 February 2024 / Approved: 20 February 2024 / Online: 20 February 2024 (11:27:28 CET)
How to cite:
Zocchi, G.; Fontanelli, F.; Spinelli, S.; Sturla, L.; Passalacqua, M.; Urra, J. C. G.; Delsante, S.; Zocchi, E. Cardiomyocyte Heat Production Measured In Vitro with Temperature Probes and by Means of Differential Isothermal Calorimetry Indicates a Role of the ABA/LANCL1-2 Hormone/Receptors System in Thermogenesis. Preprints2024, 2024021087. https://doi.org/10.20944/preprints202402.1087.v1
Zocchi, G.; Fontanelli, F.; Spinelli, S.; Sturla, L.; Passalacqua, M.; Urra, J. C. G.; Delsante, S.; Zocchi, E. Cardiomyocyte Heat Production Measured In Vitro with Temperature Probes and by Means of Differential Isothermal Calorimetry Indicates a Role of the ABA/LANCL1-2 Hormone/Receptors System in Thermogenesis. Preprints 2024, 2024021087. https://doi.org/10.20944/preprints202402.1087.v1
Zocchi, G.; Fontanelli, F.; Spinelli, S.; Sturla, L.; Passalacqua, M.; Urra, J. C. G.; Delsante, S.; Zocchi, E. Cardiomyocyte Heat Production Measured In Vitro with Temperature Probes and by Means of Differential Isothermal Calorimetry Indicates a Role of the ABA/LANCL1-2 Hormone/Receptors System in Thermogenesis. Preprints2024, 2024021087. https://doi.org/10.20944/preprints202402.1087.v1
APA Style
Zocchi, G., Fontanelli, F., Spinelli, S., Sturla, L., Passalacqua, M., Urra, J. C. G., Delsante, S., & Zocchi, E. (2024). Cardiomyocyte Heat Production Measured In Vitro with Temperature Probes and by Means of Differential Isothermal Calorimetry Indicates a Role of the ABA/LANCL1-2 Hormone/Receptors System in Thermogenesis. Preprints. https://doi.org/10.20944/preprints202402.1087.v1
Chicago/Turabian Style
Zocchi, G., Simona Delsante and Elena Zocchi. 2024 "Cardiomyocyte Heat Production Measured In Vitro with Temperature Probes and by Means of Differential Isothermal Calorimetry Indicates a Role of the ABA/LANCL1-2 Hormone/Receptors System in Thermogenesis" Preprints. https://doi.org/10.20944/preprints202402.1087.v1
Abstract
Abscisic acid (ABA) is a conserved “stress hormone” in unicellular organisms, plants and animals. In mammals, ABA and its receptors LANCL1 and LANCL2 stimulate insulin-independent cell glucose uptake and oxidative metabolism: overexpression of LANCL1/2 increases, and their si-lencing conversely reduces, mitochondrial number, respiration and proton gradient dissipation in muscle cells and in brown adipocytes. We hypothesized that the ABA/LANCL hor-mone/receptors system could be involved in thermogenesis.
Heat production by LANCL1/2-overexpressing vs. double-silenced cells was compared in rat H9c2 cardiomyocytes with two different methods: differential temperature measurements using sensitive thermistor probes, and differential isothermal calorimetry.
Results indicate that overexpressing cells generate an approx. double amount of thermal power compared with double-silenced cells, and that addition of ABA further doubles heat production in overexpressing cells. With the temperature probes, we find a time-scale of approx. 4 min for thermogenesis to “turn on” after nutrient addition.
These results identify the ABA/LANCL hormone receptors system as a hitherto unknown regu-lator of cell thermogenesis. Pharmacologic means of increasing metabolic energy dissipation are considered a promising strategy to reduce oxidative stress and lipid accumulation at a cellular and organismic level: from this study, LANCL1-2 proteins emerge as targetable controllers of ther-mogenesis through their natural ligand ABA.
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.