TY  - JOUR
AB  - 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.
AU  - Al-Samir, S.*
AU  - Yildirim, A.Ö.
AU  - Sidhaye, V.K.*
AU  - King, L.S.*
AU  - Breves, G.*
AU  - Conlon, T.M.
AU  - Stoeger, C.
AU  - Gailus-Durner, V.
AU  - Fuchs, H.
AU  - Hrabě de Angelis, M.
AU  - Gros, G.*
AU  - Endeward, V.*
C1  - 66805
C2  - 53230
CY  - 6120 Executive Blvd, Suite 600, Rockville, Md, United States
SP  - R109-R119
TI  - Aqp5--/-- mice exhibit reduced maximal O2 consumption under cold exposure, normal pulmonary gas exchange, and impaired formation of brown adipose tissue.
JO  - Am. J. Physiol.-Regul. Integr. Comp. Physiol.
VL  - 324
IS  - 1
PB  - Amer Physiological Soc
PY  - 2022
SN  - 0363-6119
ER  - 

TY  - JOUR
AB  - In humans, numbers of circulating T cells show a circadian rhythm with peak counts during the night and a steep decline in the morning. Sleep per se appears to counter this rhythm by acutely reducing the total number of T cells. The T-cell population, however, is rather heterogeneous, comprising various subpopulations with different features and functions and also different circadian rhythms. Therefore, we examined here whether sleep likewise differentially affects these subsets. We measured eight different T-cell subsets (naive, central memory, effector memory, and effector CD4(+) and CD8(+) T cells) over a 24-h period under conditions of sustained wakefulness compared with a regular sleep-wake cycle in 14 healthy young men. Sleep reduced the number of all T-cell subsets during nighttime with this effect reaching the P < 0.05 level of significance in all but one subpopulation, i.e., effector CD4(+) T cells, where it only approached significance. Furthermore, sleep was associated with an increase in growth hormone, prolactin, and aldosterone levels, whereas concentrations of catecholamines tended to be lower than during nocturnal wakefulness. The effect of sleep uniformly decreasing the different T-cell subsets is surprising considering their differential function and circadian rhythms, and even more so, since the sleep-induced decreases in these subsets are probably conveyed by different hormonal mediators. Although the reductions in cell numbers are rather small, they are comparable to changes seen, for example, after vaccination and are, therefore, likely to be of physiological relevance.
AU  - Besedovsky, L.*
AU  - Dimitrov, S.
AU  - Born, J.
AU  - Lange, T.*
C1  - 50119
C2  - 42064
CY  - Bethesda
SP  - R637-R642
TI  - Nocturnal sleep uniformly reduces numbers of different T-cell subsets in the blood of healthy men.
JO  - Am. J. Physiol.-Regul. Integr. Comp. Physiol.
VL  - 311
IS  - 4
PB  - Amer Physiological Soc
PY  - 2016
SN  - 0363-6119
ER  - 

TY  - JOUR
AB  - Adaptive thermogenesis and thermal conductance in wild-type and UCP1-KO mice. Am J Physiol Regul Integr Comp Physiol 299: R1396-R1406, 2010. First published September 8, 2010; doi:10.1152/ajpregu.00021.2009.-We compared maximal cold-induced heat production (HPmax) and cold limits between warm (WA; 27 degrees C), moderate cold (MCA; 18 degrees C), or cold acclimated (CA; 5 degrees C) wild-type and uncoupling-protein 1 knockout (UCP1-KO) mice. In wild-type mice, HPmax was successively increased after MCA and CA, and the cold limit was lowered to -8.3 degrees C and -18.0 degrees C, respectively. UCP1-KO mice also increased HPmax in response to MCA and CA, although to a lesser extent. Direct comparison revealed a maximal cold-induced recruitment of heat production by +473 mW and +227 mW in wild-type and UCP1-KO mice, respectively. The increase in cold tolerance of UCP1-KO mice from -0.9 degrees C in MCA to -10.1 degrees C in CA could not be directly related to changes in HPmax, indicating that UCP1-KO mice used the dissipated heat more efficiently than wild-type mice. As judged from respiratory quotients, acutely cold-challenged UCP1-KO mice showed a delayed transition toward lipid oxidation, and 5-h cold exposure revealed diminished physical activity and less variability in the control of metabolic rate. We conclude that BAT is required for maximal adaptive thermogenesis but also allows metabolic flexibility and a rapid switch toward sustained lipid-fuelled thermogenesis as an acute response to cold. In both CA groups, expression of contractile proteins (myosin heavy-chain isoforms) showed minor training effects in skeletal muscles, while cardiac muscle of UCP1-KO mice had novel expression of beta cardiac isoform. Neither respiration nor basal proton conductance of skeletal muscle mitochondria were different between genotypes. In subcutaneous white adipose tissue of UCP1-KO mice, cold exposure increased cytochrome-c oxidase activity and expression of the cell death-inducing DFFA-like effector A by 3.6-fold and 15-fold, respectively, indicating the recruitment of mitochondria-rich brown adipocyte-like cells. Absence of functional BAT leads to remodeling of white adipose tissue, which may significantly contribute to adaptive thermogenesis during cold acclimation.
AU  - Meyer, C.W.*
AU  - Willershäuser, M.*
AU  - Jastroch, M.*
AU  - Rourke, B.C.*
AU  - Fromme, T.*
AU  - Oelkrug, R.*
AU  - Heldmaier, G.*
AU  - Klingenspor, M.*
C1  - 4246
C2  - 28188
CY  - Bethesda
SP  - R1396-R1406
TI  - Adaptive thermogenesis and thermal conductance in wild-type and UCP1-KO mice.
JO  - Am. J. Physiol.-Regul. Integr. Comp. Physiol.
VL  - 299
IS  - 5
PB  - Amer. Physiol. Soc.
PY  - 2010
SN  - 0363-6119
ER  - 

TY  - JOUR
AU  - Moellenhoff, E.*
AU  - Blume, A.*
AU  - Culman, J.*
AU  - Chatterjee, B.
AU  - Herdegen, T.*
AU  - Lebrun, C.J.*
AU  - Unger, T.*
C1  - 21742
C2  - 19924
SP  - 1095-1104
TI  - Effect of repetitive icv injections of ANG II on c-Fos and AT1-receptor expression in the rat brain.
JO  - Am. J. Physiol.-Regul. Integr. Comp. Physiol.
VL  - 280
PY  - 2001
SN  - 0363-6119
ER  -