The role of autophagy in brown and beige adipose tissue plasticity

J Physiol Biochem. 2020 May;76(2):213-226. doi: 10.1007/s13105-019-00708-1. Epub 2019 Dec 6.

Abstract

Since the rediscovery of active brown and beige adipose tissues in humans a decade ago, great efforts have been made to identify the mechanisms underlying the activation and inactivation of these tissues, with the hope of designing potential strategies to fight against obesity and associated metabolic disorders such as type 2 diabetes. Active brown/beige fat increases the energy expenditure and is associated with reduced hyperglycemia and hyperlipidemia, whereas its atrophy and inactivation have been associated with obesity and aging. Autophagy, which is the process by which intracellular components are degraded within the lysosomes, has recently emerged as an important regulatory mechanism of brown/beige fat plasticity. Studies have shown that autophagy participates in the intracellular remodeling events that occur during brown/beige adipogenesis, thermogenic activation, and inactivation. The autophagic degradation of mitochondria appears to be important for the inactivation of brown fat and the transition from beige-to-white adipose tissue. Moreover, autophagic dysregulation in adipose tissues has been associated with obesity. Thus, understanding the regulatory mechanisms that control autophagy in the physiology and pathophysiology of adipose tissues might suggest novel treatments against obesity and its associated metabolic diseases.

Keywords: Autophagy; Beige adipose tissue; Brown adipose tissue; Metabolism; Mitophagy; White adipose tissue.

Publication types

  • Review

MeSH terms

  • Adipogenesis
  • Adipose Tissue, Beige / cytology
  • Adipose Tissue, Beige / metabolism*
  • Adipose Tissue, Beige / pathology
  • Adipose Tissue, Brown / cytology
  • Adipose Tissue, Brown / metabolism*
  • Adipose Tissue, Brown / pathology
  • Animals
  • Autophagy*
  • Humans
  • Metabolic Diseases / metabolism*
  • Mitochondria / metabolism
  • Obesity / metabolism*
  • Thermogenesis