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Al-Samir, S.* ; Yildirim, A.Ö. ; Sidhaye, V.K.* ; King, L.S.* ; Breves, G.* ; Conlon, T.M. ; Stoeger, C. ; Gailus-Durner, V. ; Fuchs, H. ; Hrabě de Angelis, M. ; Gros, G.* ; Endeward, V.*

Aqp5--/-- mice exhibit reduced maximal O2 consumption under cold exposure, normal pulmonary gas exchange, and impaired formation of brown adipose tissue.

Am. J. Physiol.-Regul. Integr. Comp. Physiol. 324, R109-R119 (2022)
Postprint DOI PMC
Open Access Green
The fundamental body functions that determine maximal O2 uptake (VO2,max) have not been studied in Aqp5 --/-- (aquaporin 5, AQP5) mice. We measured VO2,max to globally assess these functions and then investigated why it was found altered in Aqp5 --/-- mice. VO2,max was measured by the Helox technique, which elicits maximal metabolic rate by intense cold exposure of the animals. We found VO2,max reduced in Aqp5 --/-- mice by 20 - 30% compared to WT. Since AQP5 has been implicated to act as a membrane channel for respiratory gases, we studied whether this is due to the known lack of AQP5 in the alveolar epithelial membranes of Aqp5 --/-- mice. Lung function parameters as well as arterial O2 saturation were normal and identical between Aqp5 --/-- and WT mice, indicating that AQP5 does not contribute to pulmonary O2 exchange. The cause for the decreased VO2,max thus might be found in decreased O2 consumption of an intensely O2-consuming peripheral organ such as activated BAT. We found indeed that absence of AQP5 greatly reduces the amount of interscapular BAT formed in response to 4 weeks' cold exposure, from 63% in WT to 25% in Aqp5 --/-- animals. We conclude that lack of AQP5 does not affect pulmonary O2 exchange, but greatly inhibits transformation of white to brown adipose tissue. Since under cold exposure BAT is a major source of the animals' heat production, reduction of BAT likely causes the decrease in VO2,max under this condition.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Aquaporin 5 ; Alveolar-capillary Barrier ; Gas Channels ; Oxygen Transport Across Membranes ; Pulmonary Diffusion Capacity; Relative Co2/nh3 Selectivities; Oxygen-consumption; Co2 Permeability; Deer Mice; Exercise; Mouse; Aquaporin-1; Peromyscus; Mitochondria; Performance
ISSN (print) / ISBN 0363-6119
e-ISSN 1522-1490
Zeitschrift American Journal of Physiology - Regulatory, Integrative and Comparative Physiology
Quellenangaben Band: 324, Heft: 1, Seiten: R109-R119 Artikelnummer: , Supplement: ,
Verlag American Physiological Society
Verlagsort 6120 Executive Blvd, Suite 600, Rockville, Md, United States
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Biology (LHI)
Institute of Experimental Genetics (IEG)
Förderungen German Federal Ministry of Education and Research
Deutsche Forschungsgemeinschaft for financial