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3 results on '"endocrine cross talk"'

1. Long-term cold adaptation does not require FGF21 or UCP1

Author

Martin Jastroch, Isabel Hamp, Elisabeth Graf, Sithandiwe E. Mazibuko, Maria Kutschke, Evert M. van Schothorst, Daniel Lamp, Stefan Lehr, Frauke Neff, Oliver Plettenburg, Mario Ost, Thomas Schwarzmayr, Susanne Keipert, Sonja Hartwig, Matthias H. Tschöp, and Laura Brachthäuser

Subjects
0301 basic medicine, medicine.medical_specialty, FGF21, Pm20d1, beige adipose tissue, Physiology, Acclimatization, Adipose Tissue, White, adaptive thermogenesis, cold exposure, Adaptive Thermogenesis, Beige Adipose Tissue, Browning, Cold Exposure, Endocrine Cross Talk, Energy Metabolism, Mitochondrial Respiration, Uncoupling Protein, White adipose tissue, Biology, Mice, 03 medical and health sciences, 0302 clinical medicine, Adipose Tissue, Brown, mitochondrial respiration, Internal medicine, energy metabolism, Brown adipose tissue, medicine, Cold acclimation, Animals, Uncoupling protein, Molecular Biology, Uncoupling Protein 1, VLAG, Mice, Knockout, browning, Thermogenesis, Cell Biology, Thermogenin, Cold Temperature, Fibroblast Growth Factors, 030104 developmental biology, medicine.anatomical_structure, Endocrinology, uncoupling protein, Human and Animal Physiology, Knockout mouse, WIAS, Fysiologie van Mens en Dier, endocrine cross talk, 030217 neurology & neurosurgery
Abstract

Brown adipose tissue (BAT)-dependent thermogenesis and its suggested augmenting hormone, FGF21, are potential therapeutic targets in current obesity and diabetes research. Here, we studied the role of UCP1 and FGF21 for metabolic homeostasis in the cold and dissected underlying molecular mechanisms using UCP1-FGF21 double-knockout mice. We report that neither UCP1 nor FGF21, nor even compensatory increases of FGF21 serum levels in UCP1 knockout mice, are required for defense of body temperature or for maintenance of energy metabolism and body weight. Remarkably, cold-induced browning of inguinal white adipose tissue (iWAT) is FGF21 independent. Global RNA sequencing reveals major changes in response to UCP1- but not FGF21-ablation in BAT, iWAT, and muscle. Markers of mitochondrial failure and inflammation are observed in BAT, but in particular the enhanced metabolic reprogramming in iWAT supports the thermogenic role of UCP1 and excludes an important thermogenic role of endogenous FGF21 in normal cold acclimation.

Published
2017

2. Long-Term Cold Adaptation Does Not Require FGF21 or UCP1

Author

Keipert, Susanne, Kutschke, Maria, Ost, Mario, Schwarzmayr, Thomas, van Schothorst, Evert M., Lamp, Daniel, Brachthäuser, Laura, Hamp, Isabel, Mazibuko, Sithandiwe E., Hartwig, Sonja, Lehr, Stefan, Graf, Elisabeth, Plettenburg, Oliver, Neff, Frauke, Tschöp, Matthias H., Jastroch, Martin, Keipert, Susanne, Kutschke, Maria, Ost, Mario, Schwarzmayr, Thomas, van Schothorst, Evert M., Lamp, Daniel, Brachthäuser, Laura, Hamp, Isabel, Mazibuko, Sithandiwe E., Hartwig, Sonja, Lehr, Stefan, Graf, Elisabeth, Plettenburg, Oliver, Neff, Frauke, Tschöp, Matthias H., and Jastroch, Martin

Abstract

Brown adipose tissue (BAT)-dependent thermogenesis and its suggested augmenting hormone, FGF21, are potential therapeutic targets in current obesity and diabetes research. Here, we studied the role of UCP1 and FGF21 for metabolic homeostasis in the cold and dissected underlying molecular mechanisms using UCP1-FGF21 double-knockout mice. We report that neither UCP1 nor FGF21, nor even compensatory increases of FGF21 serum levels in UCP1 knockout mice, are required for defense of body temperature or for maintenance of energy metabolism and body weight. Remarkably, cold-induced browning of inguinal white adipose tissue (iWAT) is FGF21 independent. Global RNA sequencing reveals major changes in response to UCP1- but not FGF21-ablation in BAT, iWAT, and muscle. Markers of mitochondrial failure and inflammation are observed in BAT, but in particular the enhanced metabolic reprogramming in iWAT supports the thermogenic role of UCP1 and excludes an important thermogenic role of endogenous FGF21 in normal cold acclimation.

Published
2017

3. Long-Term Cold Adaptation Does Not Require FGF21 or UCP1.

Author

Keipert S, Kutschke M, Ost M, Schwarzmayr T, van Schothorst EM, Lamp D, Brachthäuser L, Hamp I, Mazibuko SE, Hartwig S, Lehr S, Graf E, Plettenburg O, Neff F, Tschöp MH, and Jastroch M

Subjects
Adipose Tissue, Brown cytology, Adipose Tissue, White cytology, Animals, Fibroblast Growth Factors genetics, Mice, Mice, Knockout, Uncoupling Protein 1 genetics, Acclimatization physiology, Adipose Tissue, Brown metabolism, Adipose Tissue, White metabolism, Cold Temperature, Fibroblast Growth Factors metabolism, Thermogenesis physiology, Uncoupling Protein 1 metabolism
Abstract

Brown adipose tissue (BAT)-dependent thermogenesis and its suggested augmenting hormone, FGF21, are potential therapeutic targets in current obesity and diabetes research. Here, we studied the role of UCP1 and FGF21 for metabolic homeostasis in the cold and dissected underlying molecular mechanisms using UCP1-FGF21 double-knockout mice. We report that neither UCP1 nor FGF21, nor even compensatory increases of FGF21 serum levels in UCP1 knockout mice, are required for defense of body temperature or for maintenance of energy metabolism and body weight. Remarkably, cold-induced browning of inguinal white adipose tissue (iWAT) is FGF21 independent. Global RNA sequencing reveals major changes in response to UCP1- but not FGF21-ablation in BAT, iWAT, and muscle. Markers of mitochondrial failure and inflammation are observed in BAT, but in particular the enhanced metabolic reprogramming in iWAT supports the thermogenic role of UCP1 and excludes an important thermogenic role of endogenous FGF21 in normal cold acclimation., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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