Imperial College London
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ProfessorAylinHanyaloglu

Faculty of Medicine, Department of Metabolism, Digestion and Reproduction

Professor in Molecular Medicine
 
 
 
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Contact

 

+44 (0)20 7594 2128a.hanyaloglu Website

 
 
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Assistant

 

Miss Kiran Dosanjh +44 (0)20 7594 2176

 
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Location

 

2009Institute of Reproductive and Developmental BiologyHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Schilperoort:2018:10.15252/emmm.201708047,
author = {Schilperoort, M and van, Dam AD and Hoeke, G and Shabalina, IG and Okolo, A and Hanyaloglu, AC and Dib, LH and Mol, IM and Caengprasath, N and Chan, Y-W and Damak, S and Miller, AR and Coskun, T and Shimpukade, B and Ulven, T and Kooijman, S and Rensen, PC and Christian, M},
doi = {10.15252/emmm.201708047},
journal = {EMBO Molecular Medicine},
title = {The GPR120 agonist TUG-891 promotes metabolic health by stimulating mitochondrial respiration in brown fat},
url = {http://dx.doi.org/10.15252/emmm.201708047},
volume = {10},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Brown adipose tissue (BAT) activation stimulates energy expenditure in human adults, which makes it an attractive target to combat obesity and related disorders. Recent studies demonstrated a role for G protein-coupled receptor 120 (GPR120) in BAT thermogenesis. Here, we investigated the therapeutic potential of GPR120 agonism and addressed GPR120-mediated signaling in BAT We found that activation of GPR120 by the selective agonist TUG-891 acutely increases fat oxidation and reduces body weight and fat mass in C57Bl/6J mice. These effects coincided with decreased brown adipocyte lipid content and increased nutrient uptake by BAT, confirming increased BAT activity. Consistent with these observations, GPR120 deficiency reduced expression of genes involved in nutrient handling in BAT Stimulation of brown adipocytes in vitro with TUG-891 acutely induced O2 consumption, through GPR120-dependent and GPR120-independent mechanisms. TUG-891 not only stimulated GPR120 signaling resulting in intracellular calcium release, mitochondrial depolarization, and mitochondrial fission, but also activated UCP1. Collectively, these data suggest that activation of brown adipocytes with the GPR120 agonist TUG-891 is a promising strategy to increase lipid combustion and reduce obesity.
AU  - Schilperoort,M
AU  - van,Dam AD
AU  - Hoeke,G
AU  - Shabalina,IG
AU  - Okolo,A
AU  - Hanyaloglu,AC
AU  - Dib,LH
AU  - Mol,IM
AU  - Caengprasath,N
AU  - Chan,Y-W
AU  - Damak,S
AU  - Miller,AR
AU  - Coskun,T
AU  - Shimpukade,B
AU  - Ulven,T
AU  - Kooijman,S
AU  - Rensen,PC
AU  - Christian,M
DO  - 10.15252/emmm.201708047
PY  - 2018///
SN  - 1757-4676
TI  - The GPR120 agonist TUG-891 promotes metabolic health by stimulating mitochondrial respiration in brown fat
T2  - EMBO Molecular Medicine
UR  - http://dx.doi.org/10.15252/emmm.201708047
UR  - http://hdl.handle.net/10044/1/56775
VL  - 10
ER  -
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