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Article: Corrigendum: Signaling Pathways Regulating Thermogenesis.

Tabuchi, Chihiro / Sul, Hei Sook

2021 Volume 12, Page(s) 698619

Abstract: This corrects the article DOI: 10.3389/fendo.2021.595020.]. ...

Abstract	[This corrects the article DOI: 10.3389/fendo.2021.595020.].
Language	English
Publishing date	2021-06-22
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2021.698619
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Signaling Pathways Regulating Thermogenesis.

Tabuchi, Chihiro / Sul, Hei Sook

Frontiers in endocrinology

2021 Volume 12, Page(s) 595020

Abstract: Obesity, an excess accumulation of white adipose tissue (WAT), has become a global epidemic and is associated with complex diseases, such as type 2 diabetes and cardiovascular diseases. Presently, there are no safe and effective therapeutic agents to ... ...

Abstract	Obesity, an excess accumulation of white adipose tissue (WAT), has become a global epidemic and is associated with complex diseases, such as type 2 diabetes and cardiovascular diseases. Presently, there are no safe and effective therapeutic agents to treat obesity. In contrast to white adipocytes that store energy as triglycerides in unilocular lipid droplet, brown and brown-like or beige adipocytes utilize fatty acids (FAs) and glucose at a high rate mainly by uncoupling protein 1 (UCP1) action to uncouple mitochondrial proton gradient from ATP synthesis, dissipating energy as heat. Recent studies on the presence of brown or brown-like adipocytes in adult humans have revealed their potential as therapeutic targets in combating obesity. Classically, the main signaling pathway known to activate thermogenesis in adipocytes is β
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/metabolism ; Animals ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Humans ; Signal Transduction ; Thermogenesis ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism
Chemical Substances	Uncoupling Protein 1
Language	English
Publishing date	2021-03-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2021.595020
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Article ; Online: Targeting lipogenesis in the treatment of metabolic diseases and cancer.

Viscarra, Jose A / Sul, Hei Sook

Oncotarget

2018 Volume 9, Issue 3, Page(s) 2969–2970

Language	English
Publishing date	2018-01-09
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.23004
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Article ; Online: Epigenetic Regulation of Hepatic Lipogenesis: Role in Hepatosteatosis and Diabetes.

Viscarra, Jose / Sul, Hei Sook

Diabetes

2020 Volume 69, Issue 4, Page(s) 525–531

Abstract: Hepatosteatosis, which is frequently associated with development of metabolic syndrome and insulin resistance, manifests when triglyceride (TG) input in the liver is greater than TG output, resulting in the excess accumulation of TG. Dysregulation of ... ...

Abstract	Hepatosteatosis, which is frequently associated with development of metabolic syndrome and insulin resistance, manifests when triglyceride (TG) input in the liver is greater than TG output, resulting in the excess accumulation of TG. Dysregulation of lipogenesis therefore has the potential to increase lipid accumulation in the liver, leading to insulin resistance and type 2 diabetes. Recently, efforts have been made to examine the epigenetic regulation of metabolism by histone-modifying enzymes that alter chromatin accessibility for activation or repression of transcription. For regulation of lipogenic gene transcription, various known lipogenic transcription factors, such as USF1, ChREBP, and LXR, interact with and recruit specific histone modifiers, directing specificity toward lipogenesis. Alteration or impairment of the functions of these histone modifiers can lead to dysregulation of lipogenesis and thus hepatosteatosis leading to insulin resistance and type 2 diabetes.
MeSH term(s)	Animals ; Diabetes Mellitus/metabolism ; Epigenesis, Genetic ; Fatty Liver/metabolism ; Humans ; Insulin Resistance ; Lipogenesis/physiology ; Liver/metabolism ; Metabolic Syndrome/metabolism
Language	English
Publishing date	2020-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/dbi18-0032
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Article ; Online: Epigenetic dynamics of the thermogenic gene program of adipocytes.

Yi, Danielle / Nguyen, Hai P / Sul, Hei Sook

The Biochemical journal

2020 Volume 477, Issue 6, Page(s) 1137–1148

Abstract: Brown adipose tissue (BAT) is a metabolically beneficial organ capable of burning fat by dissipating chemical energy into heat, thereby increasing energy expenditure. Moreover, subcutaneous white adipose tissue can undergo so-called browning/beiging. The ...

Abstract	Brown adipose tissue (BAT) is a metabolically beneficial organ capable of burning fat by dissipating chemical energy into heat, thereby increasing energy expenditure. Moreover, subcutaneous white adipose tissue can undergo so-called browning/beiging. The recent recognition of the presence of brown or beige adipocytes in human adults has attracted much attention to elucidate the molecular mechanism underlying the thermogenic adipose program. Many key transcriptional regulators critical for the thermogenic gene program centering on activating the UCP1 promoter, have been discovered. Thermogenic gene expression in brown adipocytes rely on co-ordinated actions of a multitude of transcription factors, including EBF2, PPARγ, Zfp516 and Zc3h10. These transcription factors probably integrate into a cohesive network for BAT gene program. Moreover, these transcription factors recruit epigenetic factors, such as LSD1 and MLL3/4, for specific histone signatures to establish the favorable chromatin landscape. In this review, we discuss advances made in understanding the molecular mechanism underlying the thermogenic gene program, particularly epigenetic regulation.
MeSH term(s)	Adipocytes/metabolism ; Adipocytes, Brown/metabolism ; Adipose Tissue, Brown/metabolism ; Animals ; Epigenesis, Genetic/physiology ; Histones/genetics ; Histones/metabolism ; Humans ; Thermogenesis/physiology ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Histones ; Transcription Factors
Language	English
Publishing date	2020-03-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20190599
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Article ; Online: Histone demethylase JMJD1C is phosphorylated by mTOR to activate de novo lipogenesis

Jose A. Viscarra / Yuhui Wang / Hai P. Nguyen / Yoon Gi Choi / Hei Sook Sul

Nature Communications, Vol 11, Iss 1, Pp 1-

2020 Volume 16

Abstract: In response to insulin, liver cells increase de novo lipogenesis via the transcription factors USF-1 and SREBP. Here the authors show that USF-1 recruits JMJD1C, after its phosphorylation by mTOR, to lipogenic promoters where JMJD1C demethylates histone ... ...

Abstract	In response to insulin, liver cells increase de novo lipogenesis via the transcription factors USF-1 and SREBP. Here the authors show that USF-1 recruits JMJD1C, after its phosphorylation by mTOR, to lipogenic promoters where JMJD1C demethylates histone H3, contributing to lipogenesis by an epigenetic mechanism.
Keywords	Science ; Q
Language	English
Publishing date	2020-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Genetic and epigenetic control of adipose development.

Gulyaeva, Olga / Dempersmier, Jon / Sul, Hei Sook

Biochimica et biophysica acta. Molecular and cell biology of lipids

2018 Volume 1864, Issue 1, Page(s) 3–12

Abstract: White adipose tissue (WAT) is the primary energy storage organ and its excess contributes to obesity, while brown adipose tissue (BAT) and inducible thermogenic (beige/brite) adipocytes in WAT dissipate energy via Ucp1 to maintain body temperature. BAT ... ...

Abstract	White adipose tissue (WAT) is the primary energy storage organ and its excess contributes to obesity, while brown adipose tissue (BAT) and inducible thermogenic (beige/brite) adipocytes in WAT dissipate energy via Ucp1 to maintain body temperature. BAT and subcutaneous WAT develop perinatally while visceral WAT forms after birth from precursors expressing distinct markers, such as Myf5, Pref-1, Wt1, and Prx1, depending on the anatomical location. In addition to the embryonic adipose precursors, a pool of endothelial cells or mural cells expressing Pparγ, Pdgfrβ, Sma and Zfp423 may become adipocytes during WAT expansion in adults. Several markers, such as Cd29, Cd34, Sca1, Cd24, Pdgfrα and Pref-1 are detected in adult WAT SVF cells that can be differentiated into adipocytes. However, potential heterogeneity and differences in developmental stage of these cells are not clear. Beige cells form in a depot- and condition-specific manner by de novo differentiation of precursors or by transdifferentiation. Thermogenic gene activation in brown and beige adipocytes relies on common transcriptional machinery that includes Prdm16, Zfp516, Pgc1α and Ebf2. Moreover, through changing the chromatin landscape, histone methyltransferases, such as Mll3/4 and Ehmt1, as well as demethylases, such as Lsd1, play an important role in regulating the thermogenic gene program. With the presence of BAT and beige/brite cells in human adults, increasing thermogenic activity of BAT and BAT-like tissues may help promote energy expenditure to combat obesity.
MeSH term(s)	Adipose Tissue, Brown/growth & development ; Adipose Tissue, White/growth & development ; Animals ; Epigenesis, Genetic ; Humans
Language	English
Publishing date	2018-04-25
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	60-7
ISSN	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbalip.2018.04.016
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Article: Shades of brown: a model for thermogenic fat.

Dempersmier, Jon / Sul, Hei Sook

Frontiers in endocrinology

2015 Volume 6, Page(s) 71

Abstract: Brown adipose tissue (BAT) is specialized to burn fuels to perform thermogenesis in defense of body temperature against cold. Recent discovery of metabolically active and relevant amounts of BAT in adult humans have made it a potentially attractive ... ...

Abstract	Brown adipose tissue (BAT) is specialized to burn fuels to perform thermogenesis in defense of body temperature against cold. Recent discovery of metabolically active and relevant amounts of BAT in adult humans have made it a potentially attractive target for development of anti-obesity therapeutics. There are two types of brown adipocytes: classical brown adipocytes and brown adipocyte-like cells, so-called beige/brite cells, which arise in white adipose tissue in response to cold and hormonal stimuli. These cells may derive from distinct origins, and while functionally similar, have different gene signatures. Here, we highlight recent advances in the understanding of brown and beige/brite adipocytes as well as transcriptional regulation for development and function of murine brown and beige/brite adipocytes focusing on EBF2, IRF4, and ZFP516, in addition to PRDM16 as a coregulator. We also discuss hormonal regulation of brown and beige/brite adipocytes including several factors secreted from various tissues, including BMP7, FGF21, and irisin, as well as those from BAT itself, such as Nrg4 and adenosine.
Language	English
Publishing date	2015
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2015.00071
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Article: Genetic and epigenetic control of adipose development

Gulyaeva, Olga / Dempersmier, Jon / Sul, Hei Sook

Biochimica et biophysica acta. 2019 Jan., v. 1864, no. 1

2019

Abstract	White adipose tissue (WAT) is the primary energy storage organ and its excess contributes to obesity, while brown adipose tissue (BAT) and inducible thermogenic (beige/brite) adipocytes in WAT dissipate energy via Ucp1 to maintain body temperature. BAT and subcutaneous WAT develop perinatally while visceral WAT forms after birth from precursors expressing distinct markers, such as Myf5, Pref-1, Wt1, and Prx1, depending on the anatomical location. In addition to the embryonic adipose precursors, a pool of endothelial cells or mural cells expressing Pparγ, Pdgfrβ, Sma and Zfp423 may become adipocytes during WAT expansion in adults. Several markers, such as Cd29, Cd34, Sca1, Cd24, Pdgfrα and Pref-1 are detected in adult WAT SVF cells that can be differentiated into adipocytes. However, potential heterogeneity and differences in developmental stage of these cells are not clear. Beige cells form in a depot- and condition-specific manner by de novo differentiation of precursors or by transdifferentiation. Thermogenic gene activation in brown and beige adipocytes relies on common transcriptional machinery that includes Prdm16, Zfp516, Pgc1α and Ebf2. Moreover, through changing the chromatin landscape, histone methyltransferases, such as Mll3/4 and Ehmt1, as well as demethylases, such as Lsd1, play an important role in regulating the thermogenic gene program. With the presence of BAT and beige/brite cells in human adults, increasing thermogenic activity of BAT and BAT-like tissues may help promote energy expenditure to combat obesity.
Keywords	adipocytes ; adults ; body temperature ; brown adipose tissue ; chromatin ; endothelial cells ; energy expenditure ; epigenetics ; gene activation ; genes ; histones ; methyltransferases ; obesity ; peroxisome proliferator-activated receptor gamma ; platelet-derived growth factor receptor alpha ; platelet-derived growth factor receptor beta ; primary energy ; transcription (genetics) ; white adipose tissue
Language	English
Dates of publication	2019-01
Size	p. 3-12.
Publishing place	Elsevier B.V.
Document type	Article
ISSN	1388-1981
DOI	10.1016/j.bbalip.2018.04.016
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Histone demethylase JMJD1C is phosphorylated by mTOR to activate de novo lipogenesis.

Viscarra, Jose A / Wang, Yuhui / Nguyen, Hai P / Choi, Yoon Gi / Sul, Hei Sook

Nature communications

2020 Volume 11, Issue 1, Page(s) 796

Abstract: Fatty acid and triglyceride synthesis increases greatly in response to feeding and insulin. This lipogenic induction involves coordinate transcriptional activation of various enzymes in lipogenic pathway, including fatty acid synthase and glycerol-3- ... ...

Abstract	Fatty acid and triglyceride synthesis increases greatly in response to feeding and insulin. This lipogenic induction involves coordinate transcriptional activation of various enzymes in lipogenic pathway, including fatty acid synthase and glycerol-3-phosphate acyltransferase. Here, we show that JMJD1C is a specific histone demethylase for lipogenic gene transcription in liver. In response to feeding/insulin, JMJD1C is phosphorylated at T505 by mTOR complex to allow direct interaction with USF-1 for recruitment to lipogenic promoter regions. Thus, by demethylating H3K9me2, JMJD1C alters chromatin accessibility to allow transcription. Consequently, JMJD1C promotes lipogenesis in vivo to increase hepatic and plasma triglyceride levels, showing its role in metabolic adaption for activation of the lipogenic program in response to feeding/insulin, and its contribution to development of hepatosteatosis resulting in insulin resistance.
MeSH term(s)	Animals ; Diet, High-Fat/adverse effects ; Eating/genetics ; Eating/physiology ; Female ; Gene Expression Regulation ; Genome-Wide Association Study ; Hep G2 Cells ; Histones/metabolism ; Humans ; Insulin/metabolism ; Insulin/pharmacology ; Insulin Resistance ; Jumonji Domain-Containing Histone Demethylases/genetics ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Lipogenesis/drug effects ; Lipogenesis/genetics ; Lipogenesis/physiology ; Lysine/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Oxidoreductases, N-Demethylating/genetics ; Oxidoreductases, N-Demethylating/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; TOR Serine-Threonine Kinases/metabolism ; Triglycerides/blood ; Triglycerides/metabolism ; Upstream Stimulatory Factors/metabolism
Chemical Substances	Histones ; Insulin ; Triglycerides ; USF1 protein, human ; Upstream Stimulatory Factors ; JMJD1C protein, human (EC 1.14.11.-) ; JMJD1c protein, mouse (EC 1.14.11.-) ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; Oxidoreductases, N-Demethylating (EC 1.5.-) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2020-02-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-14617-1
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