BCL11B gene heterozygosity causes weight loss accompanied by increased energy consumption, but not defective adipogenesis, in mice

• Published in: Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2017-05, Vol.81 (5), p.922-930
• Main Authors: Inoue, Jun, Ihara, Yusuke, Tsukamoto, Daisuke, Yasumoto, Keisuke, Hashidume, Tsutomu, Kamimura, Kenya, Hirano, Shigeki, Shimizu, Makoto, Kominami, Ryo, Sato, Ryuichiro
• Format: Article
• Language: English
• Subjects: adipocytes; Adipogenesis - genetics; Adipose Tissue, White - cytology; Adipose Tissue, White - metabolism; Animals; Body Weight - genetics; Cell Differentiation - genetics; Diet, High-Fat - adverse effects; energy metabolism; Energy Metabolism - genetics; fatty liver; Heterozygote; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease - chemically induced; Non-alcoholic Fatty Liver Disease - genetics; Non-alcoholic Fatty Liver Disease - metabolism; Non-alcoholic Fatty Liver Disease - pathology; Obesity - chemically induced; Obesity - genetics; Obesity - metabolism; Obesity - pathology; Repressor Proteins - deficiency; Repressor Proteins - genetics; Tumor Suppressor Proteins - deficiency; Tumor Suppressor Proteins - genetics
• ISSN: 0916-8451; 1347-6947
• DOI: 10.1080/09168451.2016.1274642

BCL11B is a zinc finger-type transcription factor that regulates the development of the white adipose tissue (WAT), skin, central nervous system, and immune system. BCL11B is required for proper adipocyte differentiation, and BCL11B−/− embryos at E19.5 have very low amounts of the subcutaneous WAT. Here, we demonstrated that BCL11B+/− mice have lower body weight than BCL11B+/+ mice, whereas the expression of adipogenic marker genes in the WAT was comparable between BCL11B+/+ and BCL11B+/− mice. Histological analysis indicated that BCL11B+/− mice fed a high-fat diet have much smaller white adipocytes and lipid droplets in the WAT and liver, respectively. In addition, BCL11B+/− mice had increased energy consumption under both standard and high-fat diets. Thus, this study identifies BCL11B as a regulator of energy metabolism, and it is unlikely that BCL11B functions in the WAT contribute to energy metabolism in BCL11B+/− mice. BCL11B+/− mice have much smaller white adipocytes in the WAT and much smaller lipid droplets in the liver under a high-fat diet.