Genetic backgrounds determine brown remodeling of white fat in rodents

Abstract Objective Genetic background largely contributes to the complexity of metabolic responses and dysfunctions. Induction of brown adipose features in white fat, known as brown remodeling, has been appreciated as a promising strategy to offset the positive energy balance in obesity and further...

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Published inMolecular metabolism (Germany) Vol. 5; no. 10; pp. 948 - 958
Main Authors Ferrannini, Giulia, Namwanje, Maria, Fang, Bin, Damle, Manashree, Li, Dylan, Liu, Qiongming, Lazar, Mitchell A, Qiang, Li
Format Journal Article
LanguageEnglish
Published Germany Elsevier 01.10.2016
Subjects
Endocrinology & Metabolism
Original
Hoxc10
Genetic background
Browning brake
Brown remodeling
White adipose tissue
Cold exposure
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Summary:Abstract Objective Genetic background largely contributes to the complexity of metabolic responses and dysfunctions. Induction of brown adipose features in white fat, known as brown remodeling, has been appreciated as a promising strategy to offset the positive energy balance in obesity and further to improve metabolism. Here we address the effects of genetic background on this process. Methods We investigated browning remodeling in a depot-specific manner by comparing the response of C57BL/6J, 129/Sv and FVB/NJ mouse strains to cold. Results Surprisingly, 129/Sv and FVB/NJ mice showed distinct brown remodeling features despite their similar resistance to metabolic disorders in comparison to the obesity-prone C57BL/6J mice. FVB/NJ mice demonstrated a preference of brown remodeling in inguinal subcutaneous white adipose tissue (iWAT), whereas 129/Sv mice displayed robust brown remodeling in visceral epididymal fat (eWAT). We further compared gene expression in different depots by RNA-sequencing and identified Hoxc10 as a novel “brake” of brown remodeling in iWAT. Conclusion Rodent genetic background determines the brown remodeling of different white fat depots. This study provides new insights into the role of genetic variation in fat remodeling in susceptibility to metabolic diseases.
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Giulia Ferrannini and Maria Namwanje contributed equally to this work.
ISSN:2212-8778
2212-8778
DOI:10.1016/j.molmet.2016.08.013