Chemoprevention of obesity by dietary natural compounds targeting mitochondrial regulation

Mol Nutr Food Res. 2017 Jun;61(6). doi: 10.1002/mnfr.201600721. Epub 2016 Dec 30.

Abstract

Mitochondria are at the center stage in the control of energy homeostasis in many organs and tissues including adipose tissue. Recently, abundant evidence from experimental studies has clearly supported the strong correlation between mitochondrial dysfunction in adipocytes and obesity. Various physiological conditions such as excessive nutrition, genetic factors, hypoxia, and toxins disrupt mitochondrial function by impairing mitochondrial biogenesis, dynamics, and oxidative capacity. Mitochondrial dysfunction in adipocytes could have an impact on differentiation, adipogenesis, insulin sensitivity, and the significant alteration in their metabolic function, which ultimately results in obesity and type 2 diabetes. Numerous dietary natural compounds are the subject of research for the prevention and treatment of obesity through reprogramming multiple metabolic pathways. Some of them have the potential against obesity by modulating insulin signaling, decreasing oxidative damage, downregulating adipokines secretion, and increasing mitochondrial DNA that improves mitochondrial function and thus maintain metabolic homeostasis. Here, we focus on and summarize and briefly discuss the currently known targets and the mitochondria-targeting effects of dietary natural compounds in the intervention of obesity.

Keywords: Adipocytes; Chemoprevention; Mitochondrial; Obesity.

Publication types

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

MeSH terms

  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Adipogenesis / drug effects
  • Animals
  • Biological Products / pharmacology*
  • Chemoprevention*
  • DNA, Mitochondrial / genetics*
  • DNA, Mitochondrial / metabolism
  • Disease Models, Animal
  • Homeostasis / drug effects
  • Humans
  • Insulin Resistance
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Obesity / drug therapy*
  • Obesity / prevention & control*

Substances

  • Biological Products
  • DNA, Mitochondrial