Egr1 plays a major role in the transcriptional response of white adipocytes to insulin and environmental cues

被引:9
作者
Meriin, A. B. [1 ]
Zaarur, N. [1 ]
Roy, D. [2 ]
Kandror, K. V. [1 ]
机构
[1] Boston Univ, Dept Biochem, Sch Med, Boston, MA 02118 USA
[2] Ohio State Univ, Dept Neurosci, Columbus, OH USA
关键词
Egr1; insulin; adipocytes; ATGL; leptin; circadian rhythms; ADIPOSE TRIGLYCERIDE LIPASE; HORMONE-SENSITIVE LIPASE; CIRCADIAN CLOCK; FATTY-ACID; TRIACYLGLYCEROL LIPASE; GLUCOSE-HOMEOSTASIS; INHIBITS LIPOLYSIS; LIPID MOBILIZATION; MESSENGER-RNA; EXPRESSION;
D O I
10.3389/fcell.2022.1003030
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
It is believed that insulin regulates metabolic functions of white adipose tissue primarily at the post-translational level via the PI3K-Akt-mediated pathway. Still, changes in transcription also play an important role in the response of white adipocytes to insulin and environmental signals. One transcription factor that is dramatically and rapidly induced in adipocytes by insulin and nutrients is called Early Growth Response 1, or Egr1. Among other functions, it directly binds to promoters of leptin and ATGL stimulating the former and inhibiting the latter. Furthermore, expression of Egr1 in adipocytes demonstrates cell autonomous circadian pattern suggesting that Egr1 not only mediates the effect of insulin and nutrients on lipolysis and leptin production but also, coordinates insulin action with endogenous circadian rhythms of adipose tissue.
引用
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页数:8
相关论文
共 82 条
[1]   Leptin [J].
Ahima, RS ;
Flier, JS .
ANNUAL REVIEW OF PHYSIOLOGY, 2000, 62 :413-437
[2]  
ALEXANDERBRIDGES M, 1992, MOL CELL BIOCHEM, V109, P99
[3]   Adipose triglyceride lipase in human skeletal muscle is upregulated by exercise training [J].
Alsted, Thomas J. ;
Nybo, Lars ;
Schweiger, Martina ;
Fledelius, Christian ;
Jacobsen, Poul ;
Zimmermann, Robert ;
Zechner, Rudolf ;
Kiens, Bente .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2009, 296 (03) :E445-E453
[4]   Time for Food: The Intimate Interplay between Nutrition, Metabolism, and the Circadian Clock [J].
Asher, Gad ;
Sassone-Corsi, Paolo .
CELL, 2015, 161 (01) :84-92
[5]   Contribution of Adipose Triglyceride Lipase and Hormone-sensitive Lipase to Lipolysis in hMADS Adipocytes [J].
Bezaire, Veronic ;
Mairal, Aline ;
Ribet, Carole ;
Lefort, Corinne ;
Girousse, Amandine ;
Jocken, Johan ;
Laurencikiene, Jurga ;
Anesia, Rodica ;
Rodriguez, Anne-Marie ;
Ryden, Mikael ;
Stenson, Britta M. ;
Dani, Christian ;
Ailhaud, Gerard ;
Arner, Peter ;
Langin, Dominique .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (27) :18282-18291
[6]   The transcription factors Egr1 and Egr2 have opposing influences on adipocyte differentiation [J].
Boyle, K. B. ;
Hadaschik, D. ;
Virtue, S. ;
Cawthorn, W. P. ;
Ridley, S. H. ;
O'Rahilly, S. ;
Siddle, K. .
CELL DEATH AND DIFFERENTIATION, 2009, 16 (05) :782-789
[7]   Identification of two polymorphisms in the early growth response protein-1 gene: possible association with lipid variables [J].
Brand, E ;
Herrmann, SM ;
Nicaud, V ;
Evans, A ;
Ruidavets, JB ;
Arveiler, D ;
Luc, G ;
Cambien, F ;
Soubrier, F .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2000, 78 (02) :81-86
[8]   Integrating adipocyte insulin signaling and metabolism in the multi-omics era [J].
Calejman, C. Martinez ;
Doxsey, W. G. ;
Fazakerley, D. J. ;
Guertin, D. A. .
TRENDS IN BIOCHEMICAL SCIENCES, 2022, 47 (06) :531-546
[9]   Medicine in the Fourth Dimension [J].
Cederroth, Christopher R. ;
Albrecht, Urs ;
Bass, Joseph ;
Brown, Steven A. ;
Dyhrfjeld-Johnsen, Jonas ;
Gachon, Frederic ;
Green, Carla B. ;
Hastings, Michael H. ;
Helfrich-Forster, Charlotte ;
Hogenesch, John B. ;
Levi, Francis ;
Loudon, Andrew ;
Lundkvist, Gabriella B. ;
Meijer, Johanna H. ;
Rosbash, Michael ;
Takahashi, Joseph S. ;
Young, Michael ;
Canlon, Barbara .
CELL METABOLISM, 2019, 30 (02) :238-250
[10]   Time-Restricted Feeding Is a Preventative and Therapeutic Intervention against Diverse Nutritional Challenges [J].
Chaix, Amandine ;
Zarrinpar, Amir ;
Phuong Miu ;
Panda, Satchidananda .
CELL METABOLISM, 2014, 20 (06) :991-1005