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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
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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
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2012
2012-01
Subject
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*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
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Li Tiangang; Francl Jessica M; Boehme Shannon; Ochoa Adrian; Zhang Youcai; Klaassen Curtis D; Erickson Sandra K; Chiang John Y L
Description
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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
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<a href="http://doi.org/10.1074/jbc.M111.305789" target="_blank" rel="noreferrer noopener">10.1074/jbc.M111.305789</a>
Rights
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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).
*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