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Clemmensen, C. ; Jall, S. ; Kleinert, M. ; Quarta, C. ; Gruber, T. ; Reber, J. ; Sachs, S. ; Fischer, K. ; Feuchtinger, A. ; Karlas, A. ; Simonds, S.E.* ; Grandl, G. ; Loher, D. ; Sanchez-Quant, E. ; Keipert, S. ; Jastroch, M. ; Hofmann, S.M. ; Nascimento, E.B.M.* ; Schrauwen, P.* ; Ntziachristos, V. ; Cowley, M.A.* ; Finan, B. ; Müller, T.D. ; Tschöp, M.H.

Coordinated targeting of cold and nicotinic receptors synergistically improves obesity and type 2 diabetes.

Nat. Commun. 9:4304 (2018)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Pharmacological stimulation of brown adipose tissue (BAT) thermogenesis to increase energy expenditure is progressively being pursued as a viable anti-obesity strategy. Here, we report that pharmacological activation of the cold receptor transient receptor potential cation channel subfamily M member 8 (TRPM8) with agonist icilin mimics the metabolic benefits of cold exposure. In diet-induced obese (DIO) mice, treatment with icilin enhances energy expenditure, and decreases body weight, without affecting food intake. To further potentiate the thermogenic action profile of icilin and add complementary anorexigenic mechanisms, we set out to identify pharmacological partners next to icilin. To that end, we specifically targeted nicotinic acetylcholine receptor (nAChR) subtype alpha3beta4 (α3β4), which we had recognized as a potential regulator of energy homeostasis and glucose metabolism. Combinatorial targeting of TRPM8 and nAChR α3β4 by icilin and dimethylphenylpiperazinium (DMPP) orchestrates synergistic anorexic and thermogenic pathways to reverse diet-induced obesity, dyslipidemia, and glucose intolerance in DIO mice.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Brown Adipose-tissue; Optimal Housing Temperatures; Central-nervous-system; Thermal Environment; Energy-expenditure; Acetylcholine-receptors; Optoacoustic Tomography; Body-temperature; Healthy-adults; Trp Channels
Sprache englisch
Veröffentlichungsjahr 2018
HGF-Berichtsjahr 2018
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 9, Heft: 1, Seiten: , Artikelnummer: 4304 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Obesity (IDO)
Institute of Biological and Medical Imaging (IBMI)
Research Unit Analytical Pathology (AAP)
Institute of Diabetes and Regeneration Research (IDR)
CF Pathology & Tissue Analytics (CF-PTA)
POF Topic(s) 30201 - Metabolic Health
30502 - Diabetes: Pathophysiology, Prevention and Therapy
30205 - Bioengineering and Digital Health
90000 - German Center for Diabetes Research
30505 - New Technologies for Biomedical Discoveries
Forschungsfeld(er) Helmholtz Diabetes Center
Enabling and Novel Technologies
PSP-Element(e) G-502200-006
G-502200-001
G-508600-007
G-505500-001
G-500390-001
G-501900-221
G-502390-001
A-630600-001
DOI 10.1038/s41467-018-06769-y
WOS ID WOS:000448042500001
Scopus ID 85055463198
PubMed ID 30353008
Erfassungsdatum 2018-10-27
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