Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human

Mice deficient in the lipid sensor GPR120 develop obesity, glucose intolerance and fatty liver when fed a high-fat diet, and a loss-of-function variant in the GPR120 gene strongly contributes to increased obesity in human. A signal for obesity The G-protein-coupled receptor GPR120 is a receptor for...

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Published inNature (London) Vol. 483; no. 7389; pp. 350 - 354
Main Authors Ichimura, Atsuhiko, Hirasawa, Akira, Poulain-Godefroy, Odile, Bonnefond, Amélie, Hara, Takafumi, Yengo, Loïc, Kimura, Ikuo, Leloire, Audrey, Liu, Ning, Iida, Keiko, Choquet, Hélène, Besnard, Philippe, Lecoeur, Cécile, Vivequin, Sidonie, Ayukawa, Kumiko, Takeuchi, Masato, Ozawa, Kentaro, Tauber, Maithé, Maffeis, Claudio, Morandi, Anita, Buzzetti, Raffaella, Elliott, Paul, Pouta, Anneli, Jarvelin, Marjo-Riitta, Körner, Antje, Kiess, Wieland, Pigeyre, Marie, Caiazzo, Roberto, Van Hul, Wim, Van Gaal, Luc, Horber, Fritz, Balkau, Beverley, Lévy-Marchal, Claire, Rouskas, Konstantinos, Kouvatsi, Anastasia, Hebebrand, Johannes, Hinney, Anke, Scherag, Andre, Pattou, François, Meyre, David, Koshimizu, Taka-aki, Wolowczuk, Isabelle, Tsujimoto, Gozoh, Froguel, Philippe
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 15.03.2012
Nature Publishing Group
Subjects
631/208/2489/144
631/443/319
631/443/319/1642/393
Adipocytes - metabolism
Adipocytes - pathology
Adipogenesis
Adipose Tissue - metabolism
Adipose Tissue - pathology
Animals
Biological and medical sciences
Calcium Signaling
Causes of
Cell Differentiation
Diet, High-Fat
DNA Mutational Analysis
Energy Metabolism
Europe - ethnology
Exons - genetics
Fatty Liver - complications
Fatty Liver - genetics
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Glucagon-Like Peptide 1 - metabolism
Glucose - metabolism
Glucose Intolerance - complications
Humanities and Social Sciences
Humans
Insulin - metabolism
Insulin Resistance
letter
Lipogenesis
Liver - metabolism
Macrophages - metabolism
Medical sciences
Metabolic diseases
Mice
multidisciplinary
Mutation - genetics
Obesity
Obesity - complications
Obesity - genetics
Obesity - metabolism
Obesity - pathology
Physiological aspects
Receptors, G-Protein-Coupled - deficiency
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
Science
Science (multidisciplinary)
Signal Transduction - genetics
Vertebrates: nervous system and sense organs
White People - genetics
Europe
France
Finland
Appetite
Human
Obesity
Pancreatic hormone
Digestive system
Rodentia
Nutrition disorder
Homeostasis
Lipids
Free fatty acid
Feeding
Vertebrata
Mammalia
Mouse
Animal
Fat
Unsaturated fatty acid
Nutrient
Nutritional status
Food
G protein
Biological receptor
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Abstract Mice deficient in the lipid sensor GPR120 develop obesity, glucose intolerance and fatty liver when fed a high-fat diet, and a loss-of-function variant in the GPR120 gene strongly contributes to increased obesity in human. A signal for obesity The G-protein-coupled receptor GPR120 is a receptor for free fatty acids, and is involved in homeostasis mechanisms such as fat-cell generation and the regulation of appetite. Here it is shown that without GPR120, mice on a high-fat diet develop obesity, glucose intolerance and fatty liver. In humans, GPR120 expression in adipose tissue is shown to be significantly elevated in obesity. The authors also identify a mutation that inhibits GPR120 signalling activity and is associated with an increased risk for obesity in Europeans. Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes 1 , 2 , 3 , 4 . Several G-protein-coupled receptors have been identified as free-fatty-acid receptors important in physiology as well as in several diseases 3 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 . GPR120 (also known as O3FAR1) functions as a receptor for unsaturated long-chain free fatty acids and has a critical role in various physiological homeostasis mechanisms such as adipogenesis, regulation of appetite and food preference 5 , 6 , 14 , 15 , 16 . Here we show that GPR120-deficient mice fed a high-fat diet develop obesity, glucose intolerance and fatty liver with decreased adipocyte differentiation and lipogenesis and enhanced hepatic lipogenesis. Insulin resistance in such mice is associated with reduced insulin signalling and enhanced inflammation in adipose tissue. In human, we show that GPR120 expression in adipose tissue is significantly higher in obese individuals than in lean controls. GPR120 exon sequencing in obese subjects reveals a deleterious non-synonymous mutation (p.R270H) that inhibits GPR120 signalling activity. Furthermore, the p.R270H variant increases the risk of obesity in European populations. Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.
AbstractList Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes (1-4). Several G-protein-coupled receptors have been identified as freefatty-acid receptors important in physiology as well as in several diseases (3,5-13). GPR120 (also known as O3FAR1) functions as a receptor for unsaturated long-chain free fatty acids and has a critical role in various physiological homeostasis mechanisms such as adipogenesis, regulation of appetite and food preference (5,6,14-16). Here we show that GPR120-deficient mice fed a high-fat diet develop obesity, glucose intolerance and fatty liver with decreased adipocyte differentiation and lipogenesis and enhanced hepatic lipogenesis. Insulin resistance in such mice is associated with reduced insulin signalling and enhanced inflammation in adipose tissue. In human, we show that GPR120 expression in adipose tissue is significantly higher in obese individuals than in lean controls. GPR120 exon sequencing in obese subjects reveals a deleterious non-synonymous mutation (p.R270H) that inhibits GPR120 signalling activity. Furthermore, the p.R270H variant increases the risk of obesity in European populations. Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.
Mice deficient in the lipid sensor GPR120 develop obesity, glucose intolerance and fatty liver when fed a high-fat diet, and a loss-of-function variant in the GPR120 gene strongly contributes to increased obesity in human. A signal for obesity The G-protein-coupled receptor GPR120 is a receptor for free fatty acids, and is involved in homeostasis mechanisms such as fat-cell generation and the regulation of appetite. Here it is shown that without GPR120, mice on a high-fat diet develop obesity, glucose intolerance and fatty liver. In humans, GPR120 expression in adipose tissue is shown to be significantly elevated in obesity. The authors also identify a mutation that inhibits GPR120 signalling activity and is associated with an increased risk for obesity in Europeans. Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes 1 , 2 , 3 , 4 . Several G-protein-coupled receptors have been identified as free-fatty-acid receptors important in physiology as well as in several diseases 3 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 . GPR120 (also known as O3FAR1) functions as a receptor for unsaturated long-chain free fatty acids and has a critical role in various physiological homeostasis mechanisms such as adipogenesis, regulation of appetite and food preference 5 , 6 , 14 , 15 , 16 . Here we show that GPR120-deficient mice fed a high-fat diet develop obesity, glucose intolerance and fatty liver with decreased adipocyte differentiation and lipogenesis and enhanced hepatic lipogenesis. Insulin resistance in such mice is associated with reduced insulin signalling and enhanced inflammation in adipose tissue. In human, we show that GPR120 expression in adipose tissue is significantly higher in obese individuals than in lean controls. GPR120 exon sequencing in obese subjects reveals a deleterious non-synonymous mutation (p.R270H) that inhibits GPR120 signalling activity. Furthermore, the p.R270H variant increases the risk of obesity in European populations. Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.
Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes. Several G-protein-coupled receptors have been identified as free-fatty-acid receptors important in physiology as well as in several diseases. GPR120 (also known as O3FAR1) functions as a receptor for unsaturated long-chain free fatty acids and has a critical role in various physiological homeostasis mechanisms such as adipogenesis, regulation of appetite and food preference. Here we show that GPR120-deficient mice fed a high-fat diet develop obesity, glucose intolerance and fatty liver with decreased adipocyte differentiation and lipogenesis and enhanced hepatic lipogenesis. Insulin resistance in such mice is associated with reduced insulin signalling and enhanced inflammation in adipose tissue. In human, we show that GPR120 expression in adipose tissue is significantly higher in obese individuals than in lean controls. GPR120 exon sequencing in obese subjects reveals a deleterious non-synonymous mutation (p.R270H) that inhibits GPR120 signalling activity. Furthermore, the p.R270H variant increases the risk of obesity in European populations. Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.
Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes. Several G-protein-coupled receptors have been identified as free-fatty-acid receptors important in physiology as well as in several diseases. GPR120 (also known as O3FAR1) functions as a receptor for unsaturated long-chain free fatty acids and has a critical role in various physiological homeostasis mechanisms such as adipogenesis, regulation of appetite and food preference. Here we show that GPR120-deficient mice fed a high-fat diet develop obesity, glucose intolerance and fatty liver with decreased adipocyte differentiation and lipogenesis and enhanced hepatic lipogenesis. Insulin resistance in such mice is associated with reduced insulin signalling and enhanced inflammation in adipose tissue. In human, we show that GPR120 expression in adipose tissue is significantly higher in obese individuals than in lean controls. GPR120 exon sequencing in obese subjects reveals a deleterious non-synonymous mutation (p.R270H) that inhibits GPR120 signalling activity. Furthermore, the p.R270H variant increases the risk of obesity in European populations. Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes. Several G-protein-coupled receptors have been identified as free-fatty-acid receptors important in physiology as well as in several diseases. GPR120 (also known as O3FAR1) functions as a receptor for unsaturated long-chain free fatty acids and has a critical role in various physiological homeostasis mechanisms such as adipogenesis, regulation of appetite and food preference. Here we show that GPR120-deficient mice fed a high-fat diet develop obesity, glucose intolerance and fatty liver with decreased adipocyte differentiation and lipogenesis and enhanced hepatic lipogenesis. Insulin resistance in such mice is associated with reduced insulin signalling and enhanced inflammation in adipose tissue. In human, we show that GPR120 expression in adipose tissue is significantly higher in obese individuals than in lean controls. GPR120 exon sequencing in obese subjects reveals a deleterious non-synonymous mutation (p.R270H) that inhibits GPR120 signalling activity. Furthermore, the p.R270H variant increases the risk of obesity in European populations. Overall, this study demonstrates that the lipid sensor GPR120 has a key role in sensing dietary fat and, therefore, in the control of energy balance in both humans and rodents.
Audience Academic
Author Pouta, Anneli
Van Hul, Wim
Maffeis, Claudio
Buzzetti, Raffaella
Kimura, Ikuo
Choquet, Hélène
Hirasawa, Akira
Ichimura, Atsuhiko
Tsujimoto, Gozoh
Bonnefond, Amélie
Rouskas, Konstantinos
Besnard, Philippe
Vivequin, Sidonie
Lévy-Marchal, Claire
Van Gaal, Luc
Horber, Fritz
Yengo, Loïc
Lecoeur, Cécile
Hebebrand, Johannes
Kiess, Wieland
Tauber, Maithé
Balkau, Beverley
Wolowczuk, Isabelle
Poulain-Godefroy, Odile
Liu, Ning
Körner, Antje
Scherag, Andre
Iida, Keiko
Ozawa, Kentaro
Elliott, Paul
Meyre, David
Hinney, Anke
Pigeyre, Marie
Morandi, Anita
Caiazzo, Roberto
Leloire, Audrey
Kouvatsi, Anastasia
Koshimizu, Taka-aki
Jarvelin, Marjo-Riitta
Hara, Takafumi
Ayukawa, Kumiko
Takeuchi, Masato
Pattou, François
Froguel, Philippe
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  organization: Centre National de la Recherche Scientifique (CNRS)-Unité mixte de recherche (UMR) 8199, Lille Pasteur Institute, Lille 59000, France, Lille Nord de France University, Lille 59000, France, Department of Genomics of Common Disease, School of Public Health, Imperial College London, Hammersmith Hospital, London W12 0NN, UK
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Issue 7389
Keywords Appetite
Human
Obesity
Pancreatic hormone
Digestive system
Rodentia
Nutrition disorder
Homeostasis
Lipids
Free fatty acid
Feeding
Vertebrata
Mammalia
Mouse
Animal
Fat
Unsaturated fatty acid
Nutrient
Nutritional status
Food
G protein
Biological receptor
Language English
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CC BY 4.0
2012 Macmillan Publishers Limited. All rights reserved
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Snippet Mice deficient in the lipid sensor GPR120 develop obesity, glucose intolerance and fatty liver when fed a high-fat diet, and a loss-of-function variant in the...
Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes. Several G-protein-coupled...
Free fatty acids provide an important energy source as nutrients, and act as signalling molecules in various cellular processes (1-4). Several...
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pubmed
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crossref
springer
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Enrichment Source
Publisher
StartPage 350
SubjectTerms 631/208/2489/144
631/443/319
631/443/319/1642/393
Adipocytes - metabolism
Adipocytes - pathology
Adipogenesis
Adipose Tissue - metabolism
Adipose Tissue - pathology
Animals
Biological and medical sciences
Calcium Signaling
Causes of
Cell Differentiation
Diet, High-Fat
DNA Mutational Analysis
Energy Metabolism
Europe - ethnology
Exons - genetics
Fatty Liver - complications
Fatty Liver - genetics
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Glucagon-Like Peptide 1 - metabolism
Glucose - metabolism
Glucose Intolerance - complications
Humanities and Social Sciences
Humans
Insulin - metabolism
Insulin Resistance
letter
Lipogenesis
Liver - metabolism
Macrophages - metabolism
Medical sciences
Metabolic diseases
Mice
multidisciplinary
Mutation - genetics
Obesity
Obesity - complications
Obesity - genetics
Obesity - metabolism
Obesity - pathology
Physiological aspects
Receptors, G-Protein-Coupled - deficiency
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - metabolism
Science
Science (multidisciplinary)
Signal Transduction - genetics
Vertebrates: nervous system and sense organs
White People - genetics
Title Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human
URI https://link.springer.com/article/10.1038/nature10798
https://www.ncbi.nlm.nih.gov/pubmed/22343897
https://www.proquest.com/docview/928910242
Volume 483
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