Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 16, Issue 5, Pages 966-971Publisher
WILEY
DOI: 10.1111/j.1582-4934.2012.01522.x
Keywords
triglycerides; obesity; heart dysfunction; genetic control
Categories
Funding
- NHLBI at NIH
- NHLBI
- NIA at NIH
- Ellison Medical Foundation.
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Introduction High fat diet feeding of Drosophila causes excess fat accumulation Excess fat accumulation is associated with heart dysfunction in Drosophila New players in the fatheart relationship Concluding remarks Obesity and cardiovascular disease are among the world's leading causes of death, especially in Western countries where consumption of high caloric food is commonly accompanied by low physical activity. This lifestyle often leads to energy imbalance, obesity, diabetes and their associated metabolic disorders, including cardiovascular diseases. It has become increasingly recognized that obesity and cardiovascular disease are metabolically linked, and a better understanding of this relationship requires that we uncover the fundamental genetic mechanisms controlling obesity-related heart dysfunction, a goal that has been difficult to achieve in higher organisms with intricate metabolic complexity. However, the high degree of evolutionary conservation of genes and signalling pathways allows researchers to use lower animal models such as Drosophila, which is the simplest genetic model with a heart, to uncover the mechanistic basis of obesity-related heart disease and its likely relevance to humans. Here, we discuss recent advances made by using the power of the Drosophila as a powerful model to investigate the genetic pathways by which a high fat diet may lead to heart dysfunction.
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