A mouse model for a partially inactive obesity-associated human MC3R variant

We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous knock-in mouse models in which we replace murine Mc3r with wild-type human ( MC3R hWT/hWT ) and double-mutant (C17A+G241A) human ( MC3R hDM/hDM )...

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Published inNature communications Vol. 7; no. 1; p. 10522
Main Authors Lee, Bonggi, Koo, Jashin, Yun Jun, Joo, Gavrilova, Oksana, Lee, Yongjun, Seo, Arnold Y., Taylor-Douglas, Dezmond C., Adler-Wailes, Diane C., Chen, Faye, Gardner, Ryan, Koutzoumis, Dimitri, Sherafat Kazemzadeh, Roya, Roberson, Robin B., Yanovski, Jack A.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 28.01.2016
Nature Publishing Group
Nature Portfolio
Subjects
13/100
13/51
14
42/109
59/57
631/1647/334/1874/345
631/443/319/1642/393
631/80/86
64/60
692/308
82/80
Adipocytes - metabolism
Adiponectin - metabolism
Adipose tissue
Adipose Tissue - metabolism
Animals
Body composition
Body fat
Disease Models, Animal
Eating
Energy Metabolism
Fats - metabolism
Gene Knock-In Techniques
Humanities and Social Sciences
Humans
Leptin - metabolism
Metabolism
Mice
multidisciplinary
Obesity
Obesity - genetics
Obesity - metabolism
Obesity - physiopathology
Proteins
Receptor, Melanocortin, Type 3 - genetics
Receptor, Melanocortin, Type 3 - metabolism
Science
Science (multidisciplinary)
Signal transduction
Stem cells
United States > US
Maryland
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Abstract We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous knock-in mouse models in which we replace murine Mc3r with wild-type human ( MC3R hWT/hWT ) and double-mutant (C17A+G241A) human ( MC3R hDM/hDM ) MC3R , that MC3R hDM/hDM have greater weight and fat mass, increased energy intake and feeding efficiency, but reduced length and fat-free mass compared with MC3R hWT/hWT . MC3R hDM/hDM mice do not have increased adipose tissue inflammatory cell infiltration or greater expression of inflammatory markers despite their greater fat mass. Serum adiponectin levels are increased in MC3R hDM/hDM mice and MC3R hDM/hDM human subjects. MC3R hDM/hDM bone- and adipose tissue-derived mesenchymal stem cells (MSCs) differentiate into adipocytes that accumulate more triglyceride than MC3R hWT/hWT MSCs. MC3R hDM/hDM impacts nutrient partitioning to generate increased adipose tissue that appears metabolically healthy. These data confirm the importance of MC3R signalling in human metabolism and suggest a previously-unrecognized role for the MC3R in adipose tissue development. The melanocortin receptor, MC3R, regulates organismal energy homeostasis. Here, Lee et al . create knock-in mice with the a mutated version of the human MC3R receptor found in obese children, and show these mice have more fat and smaller bone, yet are by and large metabolically healthy.
AbstractList We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous knock-in mouse models in which we replace murine Mc3r with wild-type human (MC3RhWT/hWT ) and double-mutant (C17A+G241A) human (MC3RhDM/hDM ) MC3R, that MC3RhDM/hDM have greater weight and fat mass, increased energy intake and feeding efficiency, but reduced length and fat-free mass compared with MC3RhWT/hWT . MC3RhDM/hDM mice do not have increased adipose tissue inflammatory cell infiltration or greater expression of inflammatory markers despite their greater fat mass. Serum adiponectin levels are increased in MC3RhDM/hDM mice and MC3RhDM/hDM human subjects. MC3RhDM/hDM bone- and adipose tissue-derived mesenchymal stem cells (MSCs) differentiate into adipocytes that accumulate more triglyceride than MC3RhWT/hWT MSCs. MC3RhDM/hDM impacts nutrient partitioning to generate increased adipose tissue that appears metabolically healthy. These data confirm the importance of MC3R signalling in human metabolism and suggest a previously-unrecognized role for the MC3R in adipose tissue development.
We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous knock-in mouse models in which we replace murine Mc3r with wild-type human ( MC3R hWT/hWT ) and double-mutant (C17A+G241A) human ( MC3R hDM/hDM ) MC3R , that MC3R hDM/hDM have greater weight and fat mass, increased energy intake and feeding efficiency, but reduced length and fat-free mass compared with MC3R hWT/hWT . MC3R hDM/hDM mice do not have increased adipose tissue inflammatory cell infiltration or greater expression of inflammatory markers despite their greater fat mass. Serum adiponectin levels are increased in MC3R hDM/hDM mice and MC3R hDM/hDM human subjects. MC3R hDM/hDM bone- and adipose tissue-derived mesenchymal stem cells (MSCs) differentiate into adipocytes that accumulate more triglyceride than MC3R hWT/hWT MSCs. MC3R hDM/hDM impacts nutrient partitioning to generate increased adipose tissue that appears metabolically healthy. These data confirm the importance of MC3R signalling in human metabolism and suggest a previously-unrecognized role for the MC3R in adipose tissue development.
We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous knock-in mouse models in which we replace murine Mc3r with wild-type human ( MC3R hWT/hWT ) and double-mutant (C17A+G241A) human ( MC3R hDM/hDM ) MC3R , that MC3R hDM/hDM have greater weight and fat mass, increased energy intake and feeding efficiency, but reduced length and fat-free mass compared with MC3R hWT/hWT . MC3R hDM/hDM mice do not have increased adipose tissue inflammatory cell infiltration or greater expression of inflammatory markers despite their greater fat mass. Serum adiponectin levels are increased in MC3R hDM/hDM mice and MC3R hDM/hDM human subjects. MC3R hDM/hDM bone- and adipose tissue-derived mesenchymal stem cells (MSCs) differentiate into adipocytes that accumulate more triglyceride than MC3R hWT/hWT MSCs. MC3R hDM/hDM impacts nutrient partitioning to generate increased adipose tissue that appears metabolically healthy. These data confirm the importance of MC3R signalling in human metabolism and suggest a previously-unrecognized role for the MC3R in adipose tissue development. The melanocortin receptor, MC3R, regulates organismal energy homeostasis. Here, Lee et al . create knock-in mice with the a mutated version of the human MC3R receptor found in obese children, and show these mice have more fat and smaller bone, yet are by and large metabolically healthy.
We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous knock-in mouse models in which we replace murine Mc3r with wild-type human (MC3R(hWT/hWT)) and double-mutant (C17A+G241A) human (MC3R(hDM/hDM)) MC3R, that MC3R(hDM/hDM) have greater weight and fat mass, increased energy intake and feeding efficiency, but reduced length and fat-free mass compared with MC3R(hWT/hWT). MC3R(hDM/hDM) mice do not have increased adipose tissue inflammatory cell infiltration or greater expression of inflammatory markers despite their greater fat mass. Serum adiponectin levels are increased in MC3R(hDM/hDM) mice and MC3R(hDM/hDM) human subjects. MC3R(hDM/hDM) bone- and adipose tissue-derived mesenchymal stem cells (MSCs) differentiate into adipocytes that accumulate more triglyceride than MC3R(hWT/hWT) MSCs. MC3R(hDM/hDM) impacts nutrient partitioning to generate increased adipose tissue that appears metabolically healthy. These data confirm the importance of MC3R signalling in human metabolism and suggest a previously-unrecognized role for the MC3R in adipose tissue development.
The melanocortin receptor, MC3R, regulates organismal energy homeostasis. Here, Lee et al. create knock-in mice with the a mutated version of the human MC3R receptor found in obese children, and show these mice have more fat and smaller bone, yet are by and large metabolically healthy.
ArticleNumber 10522
Author Seo, Arnold Y.
Lee, Bonggi
Koo, Jashin
Yun Jun, Joo
Adler-Wailes, Diane C.
Gardner, Ryan
Chen, Faye
Lee, Yongjun
Yanovski, Jack A.
Sherafat Kazemzadeh, Roya
Koutzoumis, Dimitri
Roberson, Robin B.
Gavrilova, Oksana
Taylor-Douglas, Dezmond C.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26818770$$D View this record in MEDLINE/PubMed
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Present address: KBIO, 123, Osongsaengmyeong-ro, Osong-eup, Heungdeok-gu, Cheongju-si, Chungbuk 28160, Korea
Present address: Section on Eukaryotic DNA Replication and Gene Regulation, Program in Genomics of Differentiation, NICHD, National Institutes of Health, 6 Center Drive, Bethesda, Maryland 20892, USA
Present address: College of Pharmacy, Pusan National University, Gumjung-Gu, Busan, South Korea
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Snippet We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous...
We previously reported children homozygous for two MC3R sequence variants (C17A+G241A) have greater fat mass than controls. Here we show, using homozygous...
The melanocortin receptor, MC3R, regulates organismal energy homeostasis. Here, Lee et al. create knock-in mice with the a mutated version of the human MC3R...
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Adipocytes - metabolism
Adiponectin - metabolism
Adipose tissue
Adipose Tissue - metabolism
Animals
Body composition
Body fat
Disease Models, Animal
Eating
Energy Metabolism
Fats - metabolism
Gene Knock-In Techniques
Humanities and Social Sciences
Humans
Leptin - metabolism
Metabolism
Mice
multidisciplinary
Obesity
Obesity - genetics
Obesity - metabolism
Obesity - physiopathology
Proteins
Receptor, Melanocortin, Type 3 - genetics
Receptor, Melanocortin, Type 3 - metabolism
Science
Science (multidisciplinary)
Signal transduction
Stem cells
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Title A mouse model for a partially inactive obesity-associated human MC3R variant
URI https://link.springer.com/article/10.1038/ncomms10522
https://www.ncbi.nlm.nih.gov/pubmed/26818770
https://www.proquest.com/docview/1760843306
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https://pubmed.ncbi.nlm.nih.gov/PMC4738366
https://doaj.org/article/221cc26ea0964e6589ae36eae44b565c
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