Natural compounds regulate energy metabolism by the modulating the activity of lipid-sensing nuclear receptors

Mol Nutr Food Res. 2013 Jan;57(1):20-33. doi: 10.1002/mnfr.201200522. Epub 2012 Nov 26.

Abstract

Obesity causes excess fat accumulation in various tissues, most notoriously in the adipose tissue, along with other insulin-responsive organs such as skeletal muscle and the liver, which predisposes an individual to the development of metabolic abnormalities. The molecular mechanisms underlying obesity-induced metabolic abnormalities have not been completely elucidated; however, in recent years, the search for therapies to prevent the development of obesity and obesity-associated metabolic disorders has increased. It is known that several nuclear receptors, when activated by specific ligands, regulate carbohydrate and lipid metabolism at the transcriptional level. The expression of lipid metabolism-related enzymes is directly regulated by the activity of various nuclear receptors via their interaction with specific response elements in promoters of those genes. Many natural compounds act as ligands of nuclear receptors and regulate carbohydrate and lipid metabolism by regulating the activities of these nuclear receptors. In this review, we describe our current knowledge of obesity, the role of lipid-sensing nuclear receptors in energy metabolism, and several examples of food factors that act as agonists or antagonists of nuclear receptors, which may be useful for the management of obesity and the accompanying energy metabolism abnormalities.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipocytes / metabolism
  • Adipose Tissue / metabolism
  • Animals
  • Biological Products / pharmacology*
  • Energy Metabolism / physiology*
  • Genetic Predisposition to Disease
  • Humans
  • Insulin / metabolism
  • Lipid Metabolism*
  • Liver X Receptors
  • Metabolic Diseases / metabolism
  • Metabolic Diseases / prevention & control
  • Models, Animal
  • Muscle, Skeletal / metabolism
  • Obesity / genetics
  • Obesity / metabolism*
  • Obesity / prevention & control
  • Orphan Nuclear Receptors / genetics
  • Orphan Nuclear Receptors / metabolism
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • PPAR delta / genetics
  • PPAR delta / metabolism
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Receptors, Cytoplasmic and Nuclear / genetics
  • Receptors, Cytoplasmic and Nuclear / metabolism*

Substances

  • Biological Products
  • Insulin
  • Liver X Receptors
  • Orphan Nuclear Receptors
  • PPAR alpha
  • PPAR delta
  • PPAR gamma
  • Receptors, Cytoplasmic and Nuclear