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• W2301352029 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." @default.
• W2301352029 created "2016-06-24" @default.
• W2301352029 creator A5001014125 @default.
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• W2301352029 date "2016-01-28" @default.
• W2301352029 modified "2023-09-27" @default.
• W2301352029 title "A mouse model for a partially inactive obesity-associated human MC3R variant" @default.
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• W2301352029 doi "https://doi.org/10.1038/ncomms10522" @default.
• W2301352029 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4738366" @default.
• W2301352029 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26818770" @default.
• W2301352029 hasPublicationYear "2016" @default.
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