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Beige adipose tissue epigenetics

Jean Z Lin, Stephen R Farmer
In this issue of Genes & Development, Zeng and colleagues (pp. 1822-1836) identify lysine-specific demethylase 1 (LSD1) as a pivotal regulator of whole-body energy expenditure by controlling the oxidative and thermogenic activity of brown adipose tissue (BAT). They show that LSD1 interacts with PRDM16 to repress select white adipose tissue (WAT) genes but also represses hydroxysteroid 11-β-dehydrogenase 1 (HSD11B1) independently of PRDM16 to prevent production of glucocorticoids that impair BAT functions. Their study provides important insight into epigenetic mechanisms regulating the function of BAT...
August 15, 2016: Genes & Development
Dongning Pan, Lei Huang, Lihua J Zhu, Tie Zou, Jianhong Ou, William Zhou, Yong-Xu Wang
Progression from brown preadipocytes to adipocytes engages two transcriptional programs: the expression of adipogenic genes common to both brown fat (BAT) and white fat (WAT), and the expression of BAT-selective genes. However, the dynamics of chromatin states and epigenetic enzymes involved remain poorly understood. Here we show that BAT development is selectively marked and guided by repressive H3K27me3 and is executed by its demethylase Jmjd3. We find that a significant subset of BAT-selective genes, but not common fat genes or WAT-selective genes, are demarcated by H3K27me3 in both brown and white preadipocytes...
December 7, 2015: Developmental Cell
Jun Wu, Heejin Jun, Joseph R McDermott
Thermogenic fat cells that convert chemical energy into heat are present in both mice and humans. Recent years have witnessed great advances in our understanding of the regulation of these adipocytes and an increased appreciation of the potential these cells have to counteract obesity. We summarize recent efforts to understand the formation of these fat cells and critically review genetic models and other experimental tools currently available to further investigate the development and activation of both classical brown and inducible beige fat cells...
May 2015: Trends in Genetics: TIG
Briana Garcia, Heather Francois-Vaughan, Omobola Onikoyi, Stefan Kostadinov, Monique E De Paepe, Philip A Gruppuso, Jennifer A Sanders
Obesity during childhood and beyond may have its origins during fetal or early postnatal life. At present, there are no suitable in vivo experimental models to study factors that modulate or perturb human fetal white adipose tissue (WAT) expansion, remodeling, development, adipogenesis, angiogenesis, or epigenetics. We have developed such a model. It involves the xenotransplantation of midgestation human WAT into the renal subcapsular space of immunocompromised SCID-beige mice. After an initial latency period of approximately 2 weeks, the tissue begins expanding...
December 2014: Journal of Lipid Research
Michael E Symonds, Helen Budge, Alexis C Frazier-Wood
Obesity can have multifactorial causes that may change with development and are not simply attributable to one's genetic constitution. To date, expensive and laborious genome-wide association studies have only ascribed a small contribution of genetic variants to obesity. The emergence of the field of epigenetics now offers a new paradigm with which to study excess fat mass. Currently, however, there are no compelling epigenetic studies to explain the role of epigenetics in obesity, especially from a developmental perspective...
2013: Human Heredity
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