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FTO influences adipogenesis by regulating mitotic clonal expansion
Myrte Merkestein1, Samantha Laber1, Fiona McMurray2
11] MRC Harwell, Mammalian Genetics Unit, Harwell Oxford OX11 0RD, UK [2] Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Nature Communications
|April 18, 2015
Summary
The fat mass and obesity-associated (FTO) gene promotes fat cell development. Increased FTO enhances adipogenesis, contributing to obesity, while reduced FTO impairs it, offering new insights into weight regulation.
Area of Science:
- Genetics
- Metabolism
- Obesity Research
Background:
- The fat mass and obesity-associated (FTO) gene is crucial for body weight regulation.
- Mechanisms by which FTO influences obesity are not fully understood.
Purpose of the Study:
- To elucidate the role of FTO in adipogenesis and its contribution to obesity.
Main Methods:
- Investigated adipogenic differentiation in primary adipocytes and mouse embryonic fibroblasts (MEFs) from FTO-overexpressing (FTO-4) and FTO-knockout (FTO-KO) mice.
- Analyzed adipocyte proliferation and expression of RUNX1T1.
Main Results:
- FTO-4 derived cells showed increased adipogenic potential and more adipocytes in high-fat diet fed mice.
- FTO-KO derived cells exhibited reduced adipogenesis.
- FTO's effect on adipogenesis is mediated by the short isoform of RUNX1T1, impacting early adipogenesis and mitotic clonal expansion.
Conclusions:
- Upregulation of FTO enhances adipogenesis and adipocyte proliferation via RUNX1T1, providing mechanistic insight into FTO-driven obesity.
- FTO plays a significant role in regulating fat mass accumulation.
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