Obesity and nutrient sensing TOR pathway in flies and vertebrates: Functional conservation of genetic mechanisms

Trends Endocrinol Metab. 2011 Feb;22(2):45-52. doi: 10.1016/j.tem.2010.11.002. Epub 2011 Jan 7.


The global prevalence of obesity has grown to epidemic proportions, and 400 million people are now considered to be obese. Excessive accumulation of dietary lipids (obesity) is a known risk factor for the development of deleterious metabolic conditions and has been strongly linked to the progression of heart disease and type 2 diabetes. Investigating the origin and effects of high-fat diet (HFD)-induced obesity and its genetic mediators is an important step in understanding the mechanisms that contribute to obesity. However, the mechanisms that underlie HFD pathophysiology have yet to be elucidated fully. Here we describe recent work in a Drosophila model to investigate the origin and genetic mechanisms that could underlie HFD-induced obesity, type 2 diabetes and cardiac dysfunction.

Publication types

  • Review

MeSH terms

  • Animals
  • Biological Evolution
  • Diabetes Mellitus, Type 2 / etiology
  • Dietary Fats / administration & dosage*
  • Drosophila*
  • Heart Diseases / etiology
  • Humans
  • Insulin / physiology
  • Lipid Metabolism / genetics
  • Longevity
  • Mitochondria / genetics
  • Mitochondria / physiology
  • Models, Biological
  • Obesity / complications
  • Obesity / genetics*
  • Signal Transduction
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / physiology*


  • Dietary Fats
  • Insulin
  • TOR Serine-Threonine Kinases