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Article ; Online: Endoplasmic reticulum stress and inflammation in obesity and diabetes.

Hummasti, Sarah / Hotamisligil, Gökhan S

2010 Volume 107, Issue 5, Page(s) 579–591

Abstract: Obesity is a major problem worldwide that increases risk for a wide range of diseases, including diabetes and heart disease. As such, it is increasingly important to understand how excess adiposity can perturb normal metabolic functions. It is now clear ... ...

Abstract	Obesity is a major problem worldwide that increases risk for a wide range of diseases, including diabetes and heart disease. As such, it is increasingly important to understand how excess adiposity can perturb normal metabolic functions. It is now clear that this disruption involves not only pathways controlling lipid and glucose homeostasis but also integration of metabolic and immune response pathways. Under conditions of nutritional excess, this integration can result in a metabolically driven, low-grade, chronic inflammatory state, referred to as "metaflammation," that targets metabolically critical organs and tissues to adversely affect systemic homeostasis. Endoplasmic reticulum dysfunction is another important feature of chronic metabolic disease that is also linked to both metabolic and immune regulation. A thorough understanding of how these pathways intersect to maintain metabolic homeostasis, as well as how this integration is altered under conditions of nutrient excess, is important to fully understand, and subsequently treat, chronic metabolic diseases.
MeSH term(s)	Adipokines/metabolism ; Animals ; Diabetes Complications/etiology ; Diabetes Complications/immunology ; Diabetes Complications/metabolism ; Endoplasmic Reticulum/immunology ; Endoplasmic Reticulum/metabolism ; Energy Metabolism ; Humans ; Inflammation/etiology ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Lipid Metabolism ; Obesity/complications ; Obesity/immunology ; Obesity/metabolism ; Signal Transduction ; Stress, Physiological ; Unfolded Protein Response
Chemical Substances	Adipokines ; Inflammation Mediators
Language	English
Publishing date	2010-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.110.225698
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Article: Adopting new orphans into the family of metabolic regulators.

Hummasti, Sarah / Tontonoz, Peter

Molecular endocrinology (Baltimore, Md.)

2008 Volume 22, Issue 8, Page(s) 1743–1753

Abstract: The importance of the adopted metabolite receptors, such as peroxisome proliferator-activated receptor, liver X receptor, and farnesoid X receptor, in transcriptional control of metabolic pathways has been appreciated for many years. However, it is ... ...

Abstract	The importance of the adopted metabolite receptors, such as peroxisome proliferator-activated receptor, liver X receptor, and farnesoid X receptor, in transcriptional control of metabolic pathways has been appreciated for many years. However, it is becoming increasingly clear that the number of nuclear receptors with roles in metabolism is much larger than initially suspected. Recent years have brought an intense effort to define the biological functions of the most enigmatic group of the nuclear receptor superfamily, the true orphan receptors, including nuclear receptor 4As, estrogen-related receptors, retinoid-related orphan receptors, and Rev-erbs. Unexpectedly, several of these receptors also turn out to have important functions in various aspects of metabolic control.
MeSH term(s)	Animals ; Humans ; Receptors, Estrogen/metabolism ; Receptors, Retinoic Acid/metabolism ; Receptors, Steroid/metabolism
Chemical Substances	Receptors, Estrogen ; Receptors, Retinoic Acid ; Receptors, Steroid
Language	English
Publishing date	2008-02-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639167-9
ISSN	1944-9917 ; 0888-8809
ISSN (online)	1944-9917
ISSN	0888-8809
DOI	10.1210/me.2007-0566
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Article: The peroxisome proliferator-activated receptor N-terminal domain controls isotype-selective gene expression and adipogenesis.

Hummasti, Sarah / Tontonoz, Peter

Molecular endocrinology (Baltimore, Md.)

2006 Volume 20, Issue 6, Page(s) 1261–1275

Abstract: Peroxisome proliferator-activated receptors (PPARgamma, PPARalpha, and PPARdelta) are important regulators of lipid metabolism. Although they share significant structural similarity, the biological effects associated with each PPAR isotype are distinct. ... ...

Abstract	Peroxisome proliferator-activated receptors (PPARgamma, PPARalpha, and PPARdelta) are important regulators of lipid metabolism. Although they share significant structural similarity, the biological effects associated with each PPAR isotype are distinct. For example, PPARalpha and PPARdelta regulate fatty acid catabolism, whereas PPARgamma controls lipid storage and adipogenesis. The different functions of PPARs in vivo can be explained at least in part by the different tissue distributions of the three receptors. The question of whether the receptors have different intrinsic activities and regulate distinct target genes, however, has not been adequately explored. We have engineered cell lines that express comparable amounts of each receptor. Transcriptional profiling of these cells in the presence of selective agonists reveals partially overlapping but distinct patterns of gene regulation by the three PPARs. Moreover, analysis of chimeric receptors points to the N terminus of each receptor as the key determinant of isotype-selective gene expression. For example, the N terminus of PPARgamma confers the ability to promote adipocyte differentiation when fused to the PPARdelta DNA binding domain and ligand binding domain, whereas the N terminus of PPARdelta leads to the inappropriate expression of fatty acid oxidation genes in differentiated adipocytes when fused to PPARgamma. Finally, we demonstrate that the N terminus of each receptor functions in part to limit receptor activity because deletion of the N terminus leads to nonselective activation of target genes. A more detailed understanding of the mechanisms by which the individual PPARs differentially regulate gene expression should aid in the design of more effective drugs, including tissue- and target gene-selective PPAR modulators.
MeSH term(s)	Adipogenesis/genetics ; Adipogenesis/physiology ; Animals ; Base Sequence ; DNA/genetics ; Gene Expression ; Gene Expression Profiling ; Genetic Engineering ; Mice ; NIH 3T3 Cells ; Oligonucleotide Array Sequence Analysis ; PPAR alpha/chemistry ; PPAR alpha/genetics ; PPAR alpha/physiology ; PPAR delta/chemistry ; PPAR delta/genetics ; PPAR delta/physiology ; PPAR gamma/chemistry ; PPAR gamma/genetics ; PPAR gamma/physiology ; Peroxisome Proliferator-Activated Receptors/chemistry ; Peroxisome Proliferator-Activated Receptors/genetics ; Peroxisome Proliferator-Activated Receptors/physiology ; Protein Isoforms/chemistry ; Protein Isoforms/genetics ; Protein Isoforms/physiology ; Protein Structure, Tertiary ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism
Chemical Substances	PPAR alpha ; PPAR delta ; PPAR gamma ; Peroxisome Proliferator-Activated Receptors ; Protein Isoforms ; Recombinant Proteins ; DNA (9007-49-2)
Language	English
Publishing date	2006-06
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	639167-9
ISSN	1944-9917 ; 0888-8809
ISSN (online)	1944-9917
ISSN	0888-8809
DOI	10.1210/me.2006-0025
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Article: HRASLS3 is a PPARgamma-selective target gene that promotes adipocyte differentiation.

Hummasti, Sarah / Hong, Cynthia / Bensinger, Steven J / Tontonoz, Peter

Journal of lipid research

2008 Volume 49, Issue 12, Page(s) 2535–2544

Abstract: The prevalence of obesity and its associated metabolic diseases worldwide has focused attention on understanding the mechanisms underlying adipogenesis. The nuclear receptor PPARgamma has emerged as a central regulator of adipose tissue function and ... ...

Abstract	The prevalence of obesity and its associated metabolic diseases worldwide has focused attention on understanding the mechanisms underlying adipogenesis. The nuclear receptor PPARgamma has emerged as a central regulator of adipose tissue function and formation. Despite the identification of numerous PPARgamma targets involved in a range of processes, from lipid droplet formation to adipokine secretion, information is still lacking on targets downstream of PPARgamma that directly affect fat cell differentiation. Here we identify HRASLS3 as a novel PPARgamma regulated gene with a role in adipogenesis. HRASLS3 expression increases during the differentiation of preadipocyte cell lines and is highly expressed in white and brown adipose tissue in mice. HRASLS3 expression is induced by PPARgamma ligands in preadipocyte cell lines as well in adipose tissue in vivo. We demonstrate that the HRASLS3 promoter contains a functional PPAR response element and is a direct target for regulation by PPARgamma/RXR heterodimers. Finally, we show that overexpression of HRASLS3 augments PPARgamma-driven lipid accumulation and adipogenesis, whereas siRNA-mediated knockdown of HRASLS3 expression decreases differentiation. Together, these results identify HRASLS3 as one of the downstream effectors of PPARgamma action in adipogenesis.
MeSH term(s)	Adipocytes/cytology ; Adipocytes/metabolism ; Adipogenesis ; Animals ; Cell Differentiation ; Mice ; NIH 3T3 Cells ; PPAR gamma/metabolism ; Phospholipases A2, Calcium-Independent ; Proteins/genetics ; Proteins/metabolism ; Transfection
Chemical Substances	PPAR gamma ; Proteins ; Phospholipases A2, Calcium-Independent (EC 3.1.1.4) ; Plaat3 protein, mouse (EC 3.1.1.4)
Language	English
Publishing date	2008-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.M800269-JLR200
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Article ; Online: The role of adipocyte XBP1 in metabolic regulation during lactation.

Gregor, Margaret F / Misch, Emily S / Yang, Ling / Hummasti, Sarah / Inouye, Karen E / Lee, Ann-Hwee / Bierie, Brian / Hotamisligil, Gökhan S

Cell reports

2013 Volume 3, Issue 5, Page(s) 1430–1439

Abstract: The adipocyte is central to organismal metabolism and exhibits significant functional and morphological plasticity during its formation and lifespan. Remarkable transformations of this cell occur during obesity and lactation, and thus it is essential to ... ...

Abstract	The adipocyte is central to organismal metabolism and exhibits significant functional and morphological plasticity during its formation and lifespan. Remarkable transformations of this cell occur during obesity and lactation, and thus it is essential to gain a better understanding of adipocyte function in these two metabolic processes. Considering the critical importance of the cellular organelle endoplasmic reticulum (ER) in adapting to fluctuations in synthetic processes, we explored the role of XBP1, a central regulator of ER adaptive responses, in adipocyte formation and function. Unexpectedly, deletion of adipocyte-XBP1 in vivo in mice (XBP1ΔAd) had no effect on adipocyte formation or on systemic homeostatic metabolism in mice fed a a regular or high-fat diet. However, during lactation, XBP1ΔAd dams displayed increased adiposity, decreased milk production, and decreased litter growth as compared with control dams. Moreover, we demonstrate that XBP1 is regulated during lactation and responds to prolactin to alter lipogenic gene expression. These results demonstrate a role for adipocyte-XBP1 in the regulation of lactational metabolism.
MeSH term(s)	3T3-L1 Cells ; Adipocytes/metabolism ; Adiposity ; Animals ; Cells, Cultured ; DNA-Binding Proteins/deficiency ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Diet, High-Fat ; Endoplasmic Reticulum/metabolism ; Female ; Lactation/metabolism ; Mammary Glands, Animal/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Prolactin/metabolism ; RNA, Messenger/metabolism ; RNA, Ribosomal, 18S/metabolism ; Regulatory Factor X Transcription Factors ; Transcription Factors/deficiency ; Transcription Factors/genetics ; Transcription Factors/metabolism ; X-Box Binding Protein 1
Chemical Substances	DNA-Binding Proteins ; RNA, Messenger ; RNA, Ribosomal, 18S ; Regulatory Factor X Transcription Factors ; Transcription Factors ; X-Box Binding Protein 1 ; Xbp1 protein, mouse ; Prolactin (9002-62-4)
Language	English
Publishing date	2013-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2013.03.042
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Article ; Online: Restoration of the unfolded protein response in pancreatic β cells protects mice against type 1 diabetes.

Engin, Feyza / Yermalovich, Alena / Nguyen, Truc / Ngyuen, Truc / Hummasti, Sarah / Fu, Wenxian / Eizirik, Decio L / Mathis, Diane / Hotamisligil, Gökhan S

Science translational medicine

2013 Volume 5, Issue 211, Page(s) 211ra156

Abstract: Perturbations in endoplasmic reticulum (ER) homeostasis can evoke stress responses leading to aberrant glucose and lipid metabolism. ER dysfunction is linked to inflammatory disorders, but its role in the pathogenesis of autoimmune type 1 diabetes (T1D) ... ...

Abstract	Perturbations in endoplasmic reticulum (ER) homeostasis can evoke stress responses leading to aberrant glucose and lipid metabolism. ER dysfunction is linked to inflammatory disorders, but its role in the pathogenesis of autoimmune type 1 diabetes (T1D) remains unknown. We identified defects in the expression of unfolded protein response (UPR) mediators ATF6 (activating transcription factor 6) and XBP1 (X-box binding protein 1) in β cells from two different T1D mouse models and then demonstrated similar defects in pancreatic β cells from T1D patients. Administration of a chemical ER stress mitigator, tauroursodeoxycholic acid (TUDCA), at the prediabetic stage resulted in a marked reduction of diabetes incidence in the T1D mouse models. This reduction was accompanied by (i) a significant decrease in aggressive lymphocytic infiltration in the pancreas, (ii) improved survival and morphology of β cells, (iii) reduced β cell apoptosis, (iv) preserved insulin secretion, and (v) restored expression of UPR mediators. TUDCA's actions were dependent on ATF6 and were lost in mice with β cell-specific deletion of ATF6. These data indicate that proper maintenance of the UPR is essential for the preservation of β cells and that defects in this process can be chemically restored for preventive or therapeutic interventions in T1D.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/prevention & control ; Female ; Humans ; Islets of Langerhans/metabolism ; Male ; Mice ; Mice, Inbred NOD ; Unfolded Protein Response
Language	English
Publishing date	2013-11-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.3006534
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Article: HRASLS3 is a PPARγ-selective target gene that promotes adipocyte differentiation

Hummasti, Sarah / Hong, Cynthia / Bensinger, Steven J / Tontonoz, Peter

Journal of lipid research JLR. 2008 Dec., v. 49, no. 12

2008

Abstract: The prevalence of obesity and its associated metabolic diseases worldwide has focused attention on understanding the mechanisms underlying adipogenesis. The nuclear receptor PPARγ has emerged as a central regulator of adipose tissue function and ... ...

Abstract	The prevalence of obesity and its associated metabolic diseases worldwide has focused attention on understanding the mechanisms underlying adipogenesis. The nuclear receptor PPARγ has emerged as a central regulator of adipose tissue function and formation. Despite the identification of numerous PPARγ targets involved in a range of processes, from lipid droplet formation to adipokine secretion, information is still lacking on targets downstream of PPARγ that directly affect fat cell differentiation. Here we identify HRASLS3 as a novel PPARγ regulated gene with a role in adipogenesis. HRASLS3 expression increases during the differentiation of preadipocyte cell lines and is highly expressed in white and brown adipose tissue in mice. HRASLS3 expression is induced by PPARγ ligands in preadipocyte cell lines as well in adipose tissue in vivo. We demonstrate that the HRASLS3 promoter contains a functional PPAR response element and is a direct target for regulation by PPARγ/RXR heterodimers. Finally, we show that overexpression of HRASLS3 augments PPARγ-driven lipid accumulation and adipogenesis, whereas siRNA-mediated knockdown of HRASLS3 expression decreases differentiation. Together, these results identify HRASLS3 as one of the downstream effectors of PPARγ action in adipogenesis.
Language	English
Dates of publication	2008-12
Size	p. 2535-2544.
Publishing place	American Society for Biochemistry and Molecular Biology
Document type	Article
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The Role of Adipocyte XBP1 in Metabolic Regulation during Lactation

Margaret F. Gregor / Emily S. Misch / Ling Yang / Sarah Hummasti / Karen E. Inouye / Ann-Hwee Lee / Brian Bierie / Gökhan S. Hotamisligil

Cell Reports, Vol 3, Iss 5, Pp 1430-

2013 Volume 1439

Abstract	The adipocyte is central to organismal metabolism and exhibits significant functional and morphological plasticity during its formation and lifespan. Remarkable transformations of this cell occur during obesity and lactation, and thus it is essential to gain a better understanding of adipocyte function in these two metabolic processes. Considering the critical importance of the cellular organelle endoplasmic reticulum (ER) in adapting to fluctuations in synthetic processes, we explored the role of XBP1, a central regulator of ER adaptive responses, in adipocyte formation and function. Unexpectedly, deletion of adipocyte-XBP1 in vivo in mice (XBP1ΔAd) had no effect on adipocyte formation or on systemic homeostatic metabolism in mice fed a a regular or high-fat diet. However, during lactation, XBP1ΔAd dams displayed increased adiposity, decreased milk production, and decreased litter growth as compared with control dams. Moreover, we demonstrate that XBP1 is regulated during lactation and responds to prolactin to alter lipogenic gene expression. These results demonstrate a role for adipocyte-XBP1 in the regulation of lactational metabolism.
Keywords	Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2013-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article: Liver X receptors are regulators of adipocyte gene expression but not differentiation: identification of apoD as a direct target.

Hummasti, Sarah / Laffitte, Bryan A / Watson, Michael A / Galardi, Cristin / Chao, Lily C / Ramamurthy, Lakshman / Moore, John T / Tontonoz, Peter

Journal of lipid research

2004 Volume 45, Issue 4, Page(s) 616–625

Abstract: The liver X receptors alpha and beta (LXRalpha and LXRbeta) have been shown to play important roles in lipid homeostasis in liver and macrophages, however, their function in adipose tissue is not well defined. Both LXRs are highly expressed in fat, and ... ...

Abstract	The liver X receptors alpha and beta (LXRalpha and LXRbeta) have been shown to play important roles in lipid homeostasis in liver and macrophages, however, their function in adipose tissue is not well defined. Both LXRs are highly expressed in fat, and the expression of LXRalpha increases during adipogenesis. Furthermore, LXRalpha expression is induced by peroxisome proliferator-activated receptor gamma (PPARgamma), the master regulator of fat cell differentiation. Here we investigate the role of LXRs in adipocyte differentiation and gene expression and their potential crosstalk with the PPARgamma pathway. We demonstrate that LXR agonists have no significant effect on the differentiation of 3T3-F442A or 3T3-L1 preadipocytes in vitro and do not alter the expression of differentiation-linked PPARgamma target genes in vivo. Moreover, retroviral expression of LXRalpha in NIH-3T3 cells does not alter the adipogenic potential of these cells and neither augments nor inhibits the action of PPARgamma. However, transcriptional profiling studies reveal that LXRs are important regulators of adipocyte gene expression. We identify the multifunction lipid carrier protein apolipoprotein D and the lipogenic protein Spot 14 as LXR responsive genes both in vitro and in vivo. Thus, although LXRs do not influence adipocyte differentiation per se, these receptors are likely to play an important role in the modulation of lipid metabolism in adipocytes.
MeSH term(s)	3T3 Cells ; Adipocytes/cytology ; Adipocytes/metabolism ; Animals ; Apolipoproteins/biosynthesis ; Apolipoproteins/genetics ; Apolipoproteins D ; Cell Differentiation ; DNA-Binding Proteins ; Gene Expression Profiling ; Gene Expression Regulation ; Glycoproteins/biosynthesis ; Glycoproteins/genetics ; Liver X Receptors ; Membrane Transport Proteins/biosynthesis ; Membrane Transport Proteins/genetics ; Mice ; Nuclear Proteins ; Orphan Nuclear Receptors ; PPAR gamma/metabolism ; Proteins/genetics ; Receptor Cross-Talk ; Receptors, Cytoplasmic and Nuclear/physiology ; Transcription Factors
Chemical Substances	APOD protein, human ; Apolipoproteins ; Apolipoproteins D ; DNA-Binding Proteins ; Glycoproteins ; Liver X Receptors ; Membrane Transport Proteins ; NR1H3 protein, human ; Nr1h3 protein, mouse ; Nuclear Proteins ; Orphan Nuclear Receptors ; PPAR gamma ; Proteins ; Receptors, Cytoplasmic and Nuclear ; THRSP protein, human ; Thrsp protein, mouse ; Transcription Factors
Language	English
Publishing date	2004-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.M300312-JLR200
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Article: Activation of liver X receptor improves glucose tolerance through coordinate regulation of glucose metabolism in liver and adipose tissue.

Laffitte, Bryan A / Chao, Lily C / Li, Jing / Walczak, Robert / Hummasti, Sarah / Joseph, Sean B / Castrillo, Antonio / Wilpitz, Damien C / Mangelsdorf, David J / Collins, Jon L / Saez, Enrique / Tontonoz, Peter

Proceedings of the National Academy of Sciences of the United States of America

2003 Volume 100, Issue 9, Page(s) 5419–5424

Abstract: The control of lipid and glucose metabolism is closely linked. The nuclear receptors liver X receptor (LXR)alpha and LXR beta have been implicated in gene expression linked to lipid homeostasis; however, their role in glucose metabolism is not clear. We ... ...

Abstract	The control of lipid and glucose metabolism is closely linked. The nuclear receptors liver X receptor (LXR)alpha and LXR beta have been implicated in gene expression linked to lipid homeostasis; however, their role in glucose metabolism is not clear. We demonstrate here that the synthetic LXR agonist GW3965 improves glucose tolerance in a murine model of diet-induced obesity and insulin resistance. Analysis of gene expression in LXR agonist-treated mice reveals coordinate regulation of genes involved in glucose metabolism in liver and adipose tissue. In the liver, activation of LXR led to the suppression of the gluconeogenic program including down-regulation of peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1), phosphoenolpyruvate carboxykinase (PEPCK), and glucose-6-phosphatase expression. Inhibition of gluconeogenic genes was accompanied by an induction in expression of glucokinase, which promotes hepatic glucose utilization. In adipose tissue, activation of LXR led to the transcriptional induction of the insulin-sensitive glucose transporter, GLUT4. We show that the GLUT4 promoter is a direct transcriptional target for the LXR/retinoid X receptor heterodimer and that the ability of LXR ligands to induce GLUT4 expression is abolished in LXR null cells and animals. Consistent with their effects on GLUT4 expression, LXR agonists promote glucose uptake in 3T3-L1 adipocytes in vitro. Thus, activation of LXR alters the expression of genes in liver and adipose tissue that collectively would be expected to limit hepatic glucose output and improve peripheral glucose uptake. These results outline a role for LXRs in the coordination of lipid and glucose metabolism.
MeSH term(s)	3T3 Cells ; Adipose Tissue/metabolism ; Animals ; Base Sequence ; DNA Primers ; DNA-Binding Proteins ; Female ; Glucose/metabolism ; Glucose Transporter Type 4 ; Glucose-6-Phosphatase/metabolism ; Liver/enzymology ; Liver/metabolism ; Liver X Receptors ; Mice ; Mice, Inbred C57BL ; Monosaccharide Transport Proteins/metabolism ; Muscle Proteins ; Orphan Nuclear Receptors ; Phosphoenolpyruvate Carboxykinase (ATP)/metabolism ; Promoter Regions, Genetic ; Receptors, Cytoplasmic and Nuclear/metabolism ; Transcription Factors/metabolism
Chemical Substances	DNA Primers ; DNA-Binding Proteins ; Glucose Transporter Type 4 ; Liver X Receptors ; Monosaccharide Transport Proteins ; Muscle Proteins ; Nr1h3 protein, mouse ; Orphan Nuclear Receptors ; Receptors, Cytoplasmic and Nuclear ; Slc2a4 protein, mouse ; Transcription Factors ; peroxisome-proliferator-activated receptor-gamma coactivator-1 ; Glucose-6-Phosphatase (EC 3.1.3.9) ; Phosphoenolpyruvate Carboxykinase (ATP) (EC 4.1.1.49) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2003-04-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0830671100
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