miRNA-22 deletion limits white adipose expansion and activates brown fat to attenuate high-fat diet-induced fat mass accumulation.

Szczegóły
Abstrakt

Tytuł:: miRNA-22 deletion limits white adipose expansion and activates brown fat to attenuate high-fat diet-induced fat mass accumulation.
Autorzy:: Lima VM; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Liu J; Department of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Brandão BB; Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Lino CA; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Balbino Silva CS; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Ribeiro MAC; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Oliveira TE; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Real CC; Department of Radiology and Oncology, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, Brazil.
de Paula Faria D; Department of Radiology and Oncology, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, Brazil.
Cederquist C; Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Huang ZP; Center for Translational Medicine, The First Affiliated Hospital, NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, Guangzhou, China.
Hu X; Department of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Barreto-Chaves ML; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Ferreira JCB; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil; Department of Chemical and Systems Biology, Stanford University School of Medicine, California, USA.
Festuccia WT; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Mori MA; Department of Biochemistry and Tissue Biology, Institute of Biology, University of Campinas, Campinas, Brazil.
Kahn CR; Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA.
Wang DZ; Department of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Diniz GP; Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil. Electronic address: .
Źródło:: Metabolism: clinical and experimental [Metabolism] 2021 Apr; Vol. 117, pp. 154723. Date of Electronic Publication: 2021 Feb 05.
Typ publikacji:: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: New York, NY : Elsevier Inc.
Original Publication: New York, Grune & Stratton.
MeSH Terms:: Adipose Tissue, Beige/*metabolism
Adipose Tissue, Brown/*metabolism
Adipose Tissue, White/*metabolism
Diet, High-Fat/*adverse effects
MicroRNAs/*genetics
Adipogenesis/genetics ; Animals ; Cell Differentiation/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism ; Mitochondrial Diseases/genetics ; Mitochondrial Diseases/metabolism ; Obesity/genetics ; Obesity/metabolism
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Grant Information:: P30 DK036836 United States DK NIDDK NIH HHS; R01 DK082659 United States DK NIDDK NIH HHS; R01 HL138757 United States HL NHLBI NIH HHS
Contributed Indexing:: Keywords: Brown adipose tissue; High-fat diet; Obesity; Thermogenesis; miRNA-22
Substance Nomenclature:: 0 (MicroRNAs)
0 (Mirn22 microRNA, mouse)
Entry Date(s):: Date Created: 20210207 Date Completed: 20210405 Latest Revision: 20220402
Update Code:: 20240104
PubMed Central ID:: PMC8935324
DOI:: 10.1016/j.metabol.2021.154723
PMID:: 33549579
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Background: Obesity, characterized by excessive expansion of white adipose tissue (WAT), is associated with numerous metabolic complications. Conversely, brown adipose tissue (BAT) and beige fat are thermogenic tissues that protect mice against obesity and related metabolic disorders. We recently reported that deletion of miR-22 enhances energy expenditure and attenuates WAT expansion in response to a high-fat diet (HFD). However, the molecular mechanisms involved in these effects mediated by miR-22 loss are unclear.
Methods and Results: Here, we show that miR-22 expression is induced during white, beige, and brown adipocyte differentiation in vitro. Deletion of miR-22 reduced white adipocyte differentiation in vitro. Loss of miR-22 prevented HFD-induced expression of adipogenic/lipogenic markers and adipocyte hypertrophy in murine WAT. In addition, deletion of miR-22 protected mice against HFD-induced mitochondrial dysfunction in WAT and BAT. Loss of miR-22 induced WAT browning. Gain- and loss-of-function studies revealed that miR-22 did not affect brown adipogenesis in vitro. Interestingly, miR-22 KO mice fed a HFD displayed increased expression of genes involved in thermogenesis and adrenergic signaling in BAT when compared to WT mice fed the same diet.
Conclusions: Collectively, our findings suggest that loss of miR-22 attenuates fat accumulation in response to a HFD by reducing white adipocyte differentiation and increasing BAT activity, reinforcing miR-22 as a potential therapeutic target for obesity-related disorders.
Competing Interests: Declaration of competing interest The authors declare no conflict of interest.
(Copyright © 2021 Elsevier Inc. All rights reserved.)

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