1
40
2
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Text
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URL Address
<a href="http://doi.org/10.1186/s12929-015-0133-3" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12929-015-0133-3</a>
Pages
30–30
Volume
22
Dublin Core
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Title
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The orphan nuclear receptor small heterodimer partner is required for thiazolidinedione effects in leptin-deficient mice.
Publisher
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Journal of biomedical science
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-05
Subject
The topic of the resource
Animals; Bile Acids and Salts/metabolism; Cytoplasmic and Nuclear/biosynthesis/*genetics/metabolism; Diabetes Mellitus/*drug therapy/genetics/metabolism; Gene Expression Regulation/drug effects; Glucose/metabolism; Hepatocytes/drug effects; Humans; Insulin Resistance/genetics; Insulin/*metabolism; Leptin/deficiency/genetics; Lipid Metabolism/drug effects; Messenger/genetics; Mice; Obese; PPAR gamma/*biosynthesis/genetics; Receptors; RNA; Thiazolidinediones/*administration & dosage
Creator
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Tseng Hsiu-Ting; Park Young Joo; Lee Yoon-Kwang; Moore David D
Description
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BACKGROUND: Small heterodimer partner (SHP, NR0B2) is involved in diverse metabolic pathways, including hepatic bile acid, lipid and glucose homeostasis, and has been implicated in effects on the peroxisome proliferator-activated receptor gamma (PPARgamma), a master regulator of adipogenesis and the receptor for antidiabetic drugs thiazolidinediones (TZDs). In this study, we aim to investigate the role of SHP in TZD response by comparing TZD-treated leptin-deficient (ob/ob) and leptin-, SHP-deficient (ob/ob;Shp(-/-)) double mutant mice. RESULTS: Both ob/ob and double mutant ob/ob;Shp(-/-) mice developed hyperglycemia, insulin resistance, and hyperlipidemia, but hepatic fat accumulation was decreased in the double mutant ob/ob;Shp(-/-) mice. PPARgamma2 mRNA levels were markedly lower in ob/ob;Shp(-/-) liver and decreased to a lesser extent in adipose tissue. The TZD troglitazone did not reduce glucose or circulating triglyceride levels in ob/ob;Shp(-/-) mice. Expression of the adipocytokines, such as adiponectin and resistin, was not stimulated by troglitazone treatment. Expression of hepatic lipogenic genes was also reduced in ob/ob;Shp(-/-) mice. Moreover, overexpression of SHP by adenovirus infection increased PPARgamma2 mRNA levels in mouse primary hepatocytes. CONCLUSIONS: Our results suggest that SHP is required for both antidiabetic and hypolipidemic effects of TZDs in ob/ob mice through regulation of PPARgamma expression.
Identifier
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<a href="http://doi.org/10.1186/s12929-015-0133-3" target="_blank" rel="noreferrer noopener">10.1186/s12929-015-0133-3</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Animals
Bile Acids and Salts/metabolism
Cytoplasmic and Nuclear/biosynthesis/*genetics/metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus/*drug therapy/genetics/metabolism
Gene Expression Regulation/drug effects
Glucose/metabolism
Hepatocytes/drug effects
Humans
Insulin Resistance/genetics
Insulin/*metabolism
Journal of biomedical science
Lee Yoon-Kwang
Leptin/deficiency/genetics
Lipid Metabolism/drug effects
Messenger/genetics
Mice
Moore David D
NEOMED College of Medicine
Obese
Park Young Joo
PPAR gamma/*biosynthesis/genetics
Receptors
RNA
Thiazolidinediones/*administration & dosage
Tseng Hsiu-Ting
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M111.305789" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M111.305789</a>
Pages
1861–1873
Issue
3
Volume
287
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Glucose and insulin induction of bile acid synthesis: mechanisms and implication in diabetes and obesity.
Publisher
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The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
*Gene Expression Regulation; Animals; Bile Acids and Salts/*biosynthesis; Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism; Cytoplasmic and Nuclear/genetics/metabolism; Diabetes Mellitus; Dietary Fats/administration & dosage/adverse effects; Enzymologic; Epigenesis; Experimental/genetics/*metabolism; Fasting/metabolism; Genetic/genetics; Glucose/*metabolism/pharmacology; Insulin/*metabolism; Mice; Obesity/etiology/genetics/*metabolism; Postprandial Period/genetics; Receptors; Sweetening Agents/pharmacology; Transgenic
Creator
An entity primarily responsible for making the resource
Li Tiangang; Francl Jessica M; Boehme Shannon; Ochoa Adrian; Zhang Youcai; Klaassen Curtis D; Erickson Sandra K; Chiang John Y L
Description
An account of the resource
Bile acids facilitate postprandial absorption of nutrients. Bile acids also activate the farnesoid X receptor (FXR) and the G protein-coupled receptor TGR5 and play a major role in regulating lipid, glucose, and energy metabolism. Transgenic expression of cholesterol 7alpha-hydroxylase (CYP7A1) prevented high fat diet-induced diabetes and obesity in mice. In this study, we investigated the nutrient effects on bile acid synthesis. Refeeding of a chow diet to fasted mice increased CYP7A1 expression, bile acid pool size, and serum bile acids in wild type and humanized CYP7A1-transgenic mice. Chromatin immunoprecipitation assays showed that glucose increased histone acetylation and decreased histone methylation on the CYP7A1 gene promoter. Refeeding also induced CYP7A1 in fxr-deficient mice, indicating that FXR signaling did not play a role in postprandial regulation of bile acid synthesis. In streptozocin-induced type I diabetic mice and genetically obese type II diabetic ob/ob mice, hyperglycemia increased histone acetylation status on the CYP7A1 gene promoter, leading to elevated basal Cyp7a1 expression and an enlarged bile acid pool with altered bile acid composition. However, refeeding did not further increase CYP7A1 expression in diabetic mice. In summary, this study demonstrates that glucose and insulin are major postprandial factors that induce CYP7A1 gene expression and bile acid synthesis. Glucose induces CYP7A1 gene expression mainly by epigenetic mechanisms. In diabetic mice, CYP7A1 chromatin is hyperacetylated, and fasting to refeeding response is impaired and may exacerbate metabolic disorders in diabetes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M111.305789" target="_blank" rel="noreferrer noopener">10.1074/jbc.M111.305789</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
2012
Animals
Bile Acids and Salts/*biosynthesis
Boehme Shannon
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism
Cytoplasmic and Nuclear/genetics/metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus
Dietary Fats/administration & dosage/adverse effects
Enzymologic
Epigenesis
Erickson Sandra K
Experimental/genetics/*metabolism
Fasting/metabolism
Francl Jessica M
Genetic/genetics
Glucose/*metabolism/pharmacology
Insulin/*metabolism
Klaassen Curtis D
Li Tiangang
Mice
NEOMED College of Medicine
Obesity/etiology/genetics/*metabolism
Ochoa Adrian
Postprandial Period/genetics
Receptors
Sweetening Agents/pharmacology
The Journal of biological chemistry
Transgenic
Zhang Youcai