1
40
3
-
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/10.1194/jlr.M016048" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M016048</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2234-2244
Issue
12
Volume
52
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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
A name given to the resource
Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner
Publisher
An entity responsible for making the resource available
Journal of Lipid Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-12
Subject
The topic of the resource
beta-oxidation; Biochemistry & Molecular Biology; birth-weight; diet-induced obesity; fatty-acid oxidation; hepatic steatosis; induced; insulin sensitivity; insulin-resistance; lipid-metabolism; liver; negative feedback-regulation; oxygen consumption; quotient; respiratory; retinoic acid; signaling pathways; skeletal-muscle
Creator
An entity primarily responsible for making the resource
Park Y J; Kim S C; Kim J; Anakk S; Lee J M; Tseng H T; Yechoor V; Park J; Choi J S; Jang H C; Lee K U; Novak C M; Moore D D; Lee Y K
Description
An account of the resource
Mixed background SHP(-/-) mice are resistant to diet-induced obesity due to increased energy expenditure caused by enhanced PGC-1 alpha expression in brown adipocytes. However, congenic SHP(-/-) mice on the C57BL/6 background showed normal expression of PGC-1 alpha and other genes involved in brown adipose tissue thermogenesis. Thus, we reinvestigated the impact of small heterodimer partner (SHP) deletion on diet-induced obesity and insulin resistance using congenic SHP(-/-) mice. Compared with their C57BL/6 wild-type counterparts, SHP(-/-) mice subjected to a 6 month challenge with a Western diet (WestD) were leaner but more glucose intolerant, showed hepatic insulin resistance despite decreased triglyceride accumulation and increased beta-oxidation, exhibited alterations in peripheral tissue uptake of dietary lipids, maintained a higher respiratory quotient, which did not decrease even after WestD feeding, and displayed islet dysfunction. Hepatic mRNA expression analysis revealed that many genes expressed higher in SHP(-/-) mice fed WestD were direct peroxisome proliferator-activated receptor alpha (PPAR alpha) targets. Indeed, transient transfection and chromatin immunoprecipitation verified that SHP strongly repressed PPAR alpha-mediated transactivation. SHP is a pivotal metabolic sensor controlling lipid homeostasis in response to an energy-laden diet through regulating PPAR alpha-mediated transactivation. The resultant hepatic fatty acid oxidation enhancement and dietary fat redistribution protect the mice from diet-induced obesity and hepatic steatosis but accelerate development of type 2 diabetes.-Park, Y. J., S. C. Kim, J. Kim, S. Anakk, J. M. Lee, H-T. Tseng, V. Yechoor, J. Park, J-S. Choi, H. C. Jang, K-U. Lee, C. M. Novak, D. D. Moore, and Y. K. Lee. Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner. J. Lipid Res. 2011. 52: 2234-2244.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M016048" target="_blank" rel="noreferrer noopener">10.1194/jlr.M016048</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2011
Anakk S
beta-oxidation
Biochemistry & Molecular Biology
birth-weight
Choi J S
diet-induced obesity
fatty-acid oxidation
hepatic steatosis
Induced
insulin sensitivity
insulin-resistance
Jang H C
Journal Article
Journal of lipid research
Kim J
Kim S C
Lee J M
Lee K U
Lee Y K
lipid-metabolism
Liver
Moore D D
negative feedback-regulation
Novak C M
Oxygen Consumption
Park J
Park Y J
quotient
respiratory
retinoic acid
signaling pathways
skeletal-muscle
Tseng H T
Yechoor V
-
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/10.1359/jbmr.2002.17.4.652" target="_blank" rel="noreferrer noopener">http://doi.org/10.1359/jbmr.2002.17.4.652</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
652-660
Issue
4
Volume
17
Search for Full-text
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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
A name given to the resource
Cartilage calcification studied by proton nuclear magnetic resonance microscopy
Publisher
An entity responsible for making the resource available
Journal of Bone and Mineral Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
2002-04
Subject
The topic of the resource
bioreactor; bone; calcification; calcium; cartilage; chondrocyte; Endocrinology & Metabolism; expression; growth-plate; mineral phase; nuclear magnetic resonance microscopy; retinoic acid; tissue
Creator
An entity primarily responsible for making the resource
Potter K; Leapman R D; Basser P J; Landis W J
Description
An account of the resource
A three-dimensional (3D) mineralizing culture system using hollow fiber bioreactors has been developed to study the early stages of endochondral ossification by proton nuclear magnetic resonance (NMR) microscopy. Chondrocytes harvested from the cephalic half of the sterna from 17-day-old chick embryos were terminally differentiated with 33 nM of retinoic acid for I week and mineralization was initiated by the addition of 1% beta-glycerophosphate to the culture medium. Histological sections taken after 6 weeks of development in culture confirmed calcification of the cartilage matrix formed in bioreactors. Calcium to phosphorus ratios (1.62-1.68) from X-ray microanalysis supported electron diffraction of thin tissue sections showing the presence of a poorly crystalline hydroxyapatite mineral phase in the cultures. After 4 weeks of culture, quantitative proton NMR images showed water proton magnetization transfer rate constants (km) were higher in premineralized cartilage compared with uncalcified cartilage, a result suggesting collagen enrichment of the matrix. Notably after 5 weeks mineral deposits formed in bioreactors principally in the collagen-enriched zones of the cartilage with increased km values. This caused marked reductions in water proton longitudinal (T-1) and transverse (T-2) relaxation times and water diffusion coefficients (D). These results support the hypothesis that mineralization proceeds in association with a collagen template. After 6 weeks of culture development, the water proton T2 values decreased by 13% and D increased by 7% in uncalcified areas, compared with the same regions of tissue examined 1 week earlier. These changes could be attributed to the formation of small mineral inclusions in the cartilage, possibly mediated by matrix vesicles, which may play an important role in cartilage calcification. In summary, NMR images acquired before and after the onset of mineralization of the same tissue provide unique insights into the matrix events leading to endochondral mineral formation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1359/jbmr.2002.17.4.652" target="_blank" rel="noreferrer noopener">10.1359/jbmr.2002.17.4.652</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2002
Basser P J
bioreactor
Bone
Calcification
calcium
Cartilage
chondrocyte
Endocrinology & Metabolism
expression
growth-plate
Journal Article
Journal of Bone and Mineral Research
Landis W J
Leapman R D
mineral phase
nuclear magnetic resonance microscopy
Potter K
retinoic acid
tissue
-
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
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1-11
Issue
1
Volume
41
Search for Full-text
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<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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
A name given to the resource
HNF4 and COUP-TFII interact to modulate transcription of the cholesterol 7 alpha-hydroxylase gene (CYP7A1)
Publisher
An entity responsible for making the resource available
Journal of Lipid Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
2000-01
Subject
The topic of the resource
bile-acid synthesis; bile acids; Biochemistry & Molecular Biology; chicken ovalbumin; cholesterol metabolism; dna-binding; hepatocyte nuclear factor 4; hepatocyte nuclear factor 4; hormone-receptor superfamily; messenger-rna; orphan receptors; promoter; receptors; response elements; retinoic acid; thyroid-hormone; transcriptional regulation; upstream promoter transcription factor II
Creator
An entity primarily responsible for making the resource
Stroup D; Chiang J Y L
Description
An account of the resource
The gene for cholesterol 7 alpha-hydroxylase (CYP7A1) contains a sequence at nt -149 to -118 that was found to play a large role in determining the overall transcriptional activity and regulation of the promoter. Hepatocyte nuclear factor 4 (HNF4) and chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) synergistically activate transcription of the CYP7A1 promoter, Transactivation of CYP7A1 by HNF4 in the human hepatoma cell line, HepG2, was enhanced by cotransfection with COUP-TFII or the basal transcription element binding protein (BTEB), HNF4 prepared from rat liver nuclear extracts bound to oligomers homologous to the nt -146 to -134 sequences in electrophoretic mobility shift assays (EMSA), which corresponded to a conserved region containing a direct repeat of hormone response elements spaced by one nucleotide (DR1), The sequences surrounding this DR1 were found to be essential for the HNF4 transactivation. In vitro-translated COUP-TFII was found to bind the adjacent sequences from nt -139 to -128 (DRO), but COUP-TFII interacted with this region at a much lower affinity than to the COUP-TFII-site at nt -72 to -57 (DR4), Mutations at nt -139 to -128 or nt -72 to -57 reduced the COUP-TFII and HNF4 synergy; however, these COUP-TFII-binding sequences were not absolutely required for the cooperative effect of HNF4 and COUP-TFII on transactivation. These results indicated that the observed transactivation was the result of protein/protein interactions facilitated by the juxtaposition of the binding elements.
Identifier
An unambiguous reference to the resource within a given context
n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2000
BILE acids
bile-acid synthesis
Biochemistry & Molecular Biology
Chiang J Y L
chicken ovalbumin
cholesterol metabolism
dna-binding
Hepatocyte Nuclear Factor 4
hormone-receptor superfamily
Journal Article
Journal of lipid research
messenger-rna
orphan receptors
promoter
Receptors
Response Elements
retinoic acid
Stroup D
thyroid-hormone
transcriptional regulation
upstream promoter transcription factor II