De-Toring high fat for a healthy heart

Abstract

Evaluation of: Birse RT, Choi J, Reardon K et al. High-fat-diet-induced obesity and heart dysfunction are regulated by the TOR pathway in Drosophila. Cell. Metab. 12, 533–544 (2010).

Excessive intake of nutrients is widely believed to be one of the main contributing factors to the global epidemic of obesity. Despite extensive studies over last few decades, the genetic mechanisms that mediate high-fat diet (HFD)-induced obesity are still not clear. It is also unknown if a similar genetic mechanism underlies the cardiac dysfunction associated with HFD-induced obesity. In a recent study, Birse et al. used a Drosophila model to determine whether the ancient nutrient sensing target of rapamycin (TOR) pathway affects heart function upon challenge with a HFD. As in mammals, this study found that flies fed on HFD became obese, and displayed severe heart dysfunction. Genetic suppression of the TOR signaling pathway prevented fat accumulation and protected flies against HFD-induced cardiac defects. Together with biochemical evidence that HFD affects insulin–TOR signaling, these data suggest that deregulation of TOR activity mediates the deleterious effect of HFD on heart function.

Keywords::

• cardiac disease
• high-fat diet
• lipid metabolism
• obesity
• TOR

Financial & competing interests disclosure

The author has no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.