title: Adipose tissue browning and metabolic health.
abstract: Accumulation of excess white adipose tissue (WAT) has deleterious consequences for metabolic health. The activation of brown adipose tissue (BAT), the primary organ for heat production, confers beneficial effects on adiposity, insulin resistance and hyperlipidaemia, at least in mice. As the amount of metabolically active BAT seems to be particularly low in patients with obesity or diabetes mellitus who require immediate therapy, new avenues are needed to increase the capacity for adaptive thermogenesis. In this light, we review the findings that BAT in human adults might consist of not only classic brown adipocytes but also inducible brown adipocytes (also called beige, brown-in-white, or brite adipocytes), which are phenotypically distinct from both white and brown adipocytes. Stimulating the development of beige adipocytes in WAT (so called 'browning') might reduce adverse effects of WAT and could help to improve metabolic health. This article focuses on the development and regulatory control of beige adipocytes at the transcriptional and hormonal levels. Emerging insights into the metabolic role of beige adipocytes are also discussed, along with the developments that can be expected from these promising targets for therapy of metabolic disease in the future.
authors.affiliation: Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
authors.forename: Alexander
authors.initials: A
authors.lastname: Bartelt
authors.affiliation: Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246 Hamburg, Germany.
authors.forename: Joerg
authors.initials: J
authors.lastname: Heeren
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D052437:Adipocytes, Brown / Q000473:pathology; D052438:Adipocytes, White / Q000473:pathology; D002001:Adipose Tissue, Brown / Q000502:physiology*; D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D008659:Metabolic Diseases / Q000473:pathology / Q000503:physiopathology; D008660:Metabolism / Q000502:physiology*; D051379:Mice; D022722:Thermogenesis / Q000502:physiology*