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Reversine promotes browning of white adipocytes by suppressing miR‐133a
Author(s) -
Kim Saetbyul,
Park Jong Woo,
Lee Min Gyu,
Nam Ki Hong,
Park Jee Hun,
Oh Hwamok,
Lee Jieun,
Han Jihoon,
Yi Sang Ah,
Han JeungWhan
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27148
Subject(s) - prdm16 , browning , white adipose tissue , downregulation and upregulation , thermogenin , thermogenesis , adipose tissue , endocrinology , medicine , chemistry , adipocyte , brown adipose tissue , microbiology and biotechnology , biology , biochemistry , gene
Brown adipocytes are characterized by a high number of uncoupling protein 1 (UCP1)‐positive mitochondrial content and increased thermogenic capacity. As UCP1‐enriched cells can consume lipids by generating heat, browning of white adipocytes is now highlighted as a promising approach for the prevention of obesity and obesity‐associated metabolic diseases. Upon cold exposure or β‐adrenergic stimuli, downregulation of microRNA‐133 ( miR‐133 ) elevates the expression levels of PR domain containing 16 (Prdm16), which has been shown to be a brown adipose determination factor, in brown adipose tissue and subcutaneous white adipose tissues (WAT). Here, we show that treatment of reversine to white adipocytes induces browning via suppression of miR‐133a . Reversine treatment promoted the expression of brown adipocyte marker genes, such as Prdm16 and UCP1 , increasing the mitochondrial content, while decreasing the levels of miR‐133a and white adipocyte marker genes. Ectopic expression of miR‐133a mimic reversed the browning effects of the reversine treatment. Moreover, intraperitoneal administration of reversine in mice upregulated thermogenesis and resulted in resistance to high‐fat diet‐mediated weight gain as well as browning of subcutaneous and epididymal WAT. Taken together, we found a novel way to promote browning of white adipocytes through downregulation of miR‐133a followed by activation of Prdm16, with a synthetic chemical, reversine.