Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor?
Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Hinds, Terry D. [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
|---|
| Schlagwörter: |
|---|
| Umfang: |
4 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors - Fan, Ya-Meng ELSEVIER, 2017transfer abstract, Burlington, Mass |
|---|---|
| Übergeordnetes Werk: |
volume:95 ; year:2016 ; pages:54-57 ; extent:4 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.mehy.2016.08.013 |
|---|
| Katalog-ID: |
ELV035268700 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV035268700 | ||
| 003 | DE-627 | ||
| 005 | 20230625203734.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 180603s2016 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.mehy.2016.08.013 |2 doi | |
| 028 | 5 | 2 | |a GBVA2016009000025.pica |
| 035 | |a (DE-627)ELV035268700 | ||
| 035 | |a (ELSEVIER)S0306-9877(16)30285-7 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | |a 610 | |
| 082 | 0 | 4 | |a 610 |q DE-600 |
| 082 | 0 | 4 | |a 540 |q VZ |
| 082 | 0 | 4 | |a 610 |q VZ |
| 084 | |a 44.00 |2 bkl | ||
| 100 | 1 | |a Hinds, Terry D. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? |
| 264 | 1 | |c 2016transfer abstract | |
| 300 | |a 4 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). | ||
| 520 | |a Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). | ||
| 650 | 7 | |a NAFLD |2 Elsevier | |
| 650 | 7 | |a Biliverdin |2 Elsevier | |
| 650 | 7 | |a PPAR |2 Elsevier | |
| 650 | 7 | |a Heme oxygenase |2 Elsevier | |
| 650 | 7 | |a SPPARM |2 Elsevier | |
| 650 | 7 | |a Bilirubin |2 Elsevier | |
| 650 | 7 | |a NASH |2 Elsevier | |
| 650 | 7 | |a Non-alcoholic fatty liver disease |2 Elsevier | |
| 650 | 7 | |a PPARα |2 Elsevier | |
| 650 | 7 | |a Nuclear receptors |2 Elsevier | |
| 700 | 1 | |a Adeosun, Samuel O. |4 oth | |
| 700 | 1 | |a Alamodi, Abdulhadi A. |4 oth | |
| 700 | 1 | |a Stec, David E. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Harcourt |a Fan, Ya-Meng ELSEVIER |t Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors |d 2017transfer abstract |g Burlington, Mass |w (DE-627)ELV015462293 |
| 773 | 1 | 8 | |g volume:95 |g year:2016 |g pages:54-57 |g extent:4 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.mehy.2016.08.013 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 936 | b | k | |a 44.00 |j Medizin: Allgemeines |q VZ |
| 951 | |a AR | ||
| 952 | |d 95 |j 2016 |h 54-57 |g 4 | ||
| 953 | |2 045F |a 610 | ||
| author_variant |
t d h td tdh |
|---|---|
| matchkey_str |
hindsterrydadeosunsamueloalamodiabdulhad:2016----:osiiuipeeteaisetsshogatvtoot |
| hierarchy_sort_str |
2016transfer abstract |
| bklnumber |
44.00 |
| publishDate |
2016 |
| allfields |
10.1016/j.mehy.2016.08.013 doi GBVA2016009000025.pica (DE-627)ELV035268700 (ELSEVIER)S0306-9877(16)30285-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 VZ 610 VZ 44.00 bkl Hinds, Terry D. verfasserin aut Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? 2016transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors Elsevier Adeosun, Samuel O. oth Alamodi, Abdulhadi A. oth Stec, David E. oth Enthalten in Harcourt Fan, Ya-Meng ELSEVIER Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors 2017transfer abstract Burlington, Mass (DE-627)ELV015462293 volume:95 year:2016 pages:54-57 extent:4 https://doi.org/10.1016/j.mehy.2016.08.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.00 Medizin: Allgemeines VZ AR 95 2016 54-57 4 045F 610 |
| spelling |
10.1016/j.mehy.2016.08.013 doi GBVA2016009000025.pica (DE-627)ELV035268700 (ELSEVIER)S0306-9877(16)30285-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 VZ 610 VZ 44.00 bkl Hinds, Terry D. verfasserin aut Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? 2016transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors Elsevier Adeosun, Samuel O. oth Alamodi, Abdulhadi A. oth Stec, David E. oth Enthalten in Harcourt Fan, Ya-Meng ELSEVIER Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors 2017transfer abstract Burlington, Mass (DE-627)ELV015462293 volume:95 year:2016 pages:54-57 extent:4 https://doi.org/10.1016/j.mehy.2016.08.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.00 Medizin: Allgemeines VZ AR 95 2016 54-57 4 045F 610 |
| allfields_unstemmed |
10.1016/j.mehy.2016.08.013 doi GBVA2016009000025.pica (DE-627)ELV035268700 (ELSEVIER)S0306-9877(16)30285-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 VZ 610 VZ 44.00 bkl Hinds, Terry D. verfasserin aut Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? 2016transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors Elsevier Adeosun, Samuel O. oth Alamodi, Abdulhadi A. oth Stec, David E. oth Enthalten in Harcourt Fan, Ya-Meng ELSEVIER Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors 2017transfer abstract Burlington, Mass (DE-627)ELV015462293 volume:95 year:2016 pages:54-57 extent:4 https://doi.org/10.1016/j.mehy.2016.08.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.00 Medizin: Allgemeines VZ AR 95 2016 54-57 4 045F 610 |
| allfieldsGer |
10.1016/j.mehy.2016.08.013 doi GBVA2016009000025.pica (DE-627)ELV035268700 (ELSEVIER)S0306-9877(16)30285-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 VZ 610 VZ 44.00 bkl Hinds, Terry D. verfasserin aut Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? 2016transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors Elsevier Adeosun, Samuel O. oth Alamodi, Abdulhadi A. oth Stec, David E. oth Enthalten in Harcourt Fan, Ya-Meng ELSEVIER Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors 2017transfer abstract Burlington, Mass (DE-627)ELV015462293 volume:95 year:2016 pages:54-57 extent:4 https://doi.org/10.1016/j.mehy.2016.08.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.00 Medizin: Allgemeines VZ AR 95 2016 54-57 4 045F 610 |
| allfieldsSound |
10.1016/j.mehy.2016.08.013 doi GBVA2016009000025.pica (DE-627)ELV035268700 (ELSEVIER)S0306-9877(16)30285-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 540 VZ 610 VZ 44.00 bkl Hinds, Terry D. verfasserin aut Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? 2016transfer abstract 4 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors Elsevier Adeosun, Samuel O. oth Alamodi, Abdulhadi A. oth Stec, David E. oth Enthalten in Harcourt Fan, Ya-Meng ELSEVIER Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors 2017transfer abstract Burlington, Mass (DE-627)ELV015462293 volume:95 year:2016 pages:54-57 extent:4 https://doi.org/10.1016/j.mehy.2016.08.013 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.00 Medizin: Allgemeines VZ AR 95 2016 54-57 4 045F 610 |
| language |
English |
| source |
Enthalten in Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors Burlington, Mass volume:95 year:2016 pages:54-57 extent:4 |
| sourceStr |
Enthalten in Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors Burlington, Mass volume:95 year:2016 pages:54-57 extent:4 |
| format_phy_str_mv |
Article |
| bklname |
Medizin: Allgemeines |
| institution |
findex.gbv.de |
| topic_facet |
NAFLD Biliverdin PPAR Heme oxygenase SPPARM Bilirubin NASH Non-alcoholic fatty liver disease PPARα Nuclear receptors |
| dewey-raw |
610 |
| isfreeaccess_bool |
false |
| container_title |
Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors |
| authorswithroles_txt_mv |
Hinds, Terry D. @@aut@@ Adeosun, Samuel O. @@oth@@ Alamodi, Abdulhadi A. @@oth@@ Stec, David E. @@oth@@ |
| publishDateDaySort_date |
2016-01-01T00:00:00Z |
| hierarchy_top_id |
ELV015462293 |
| dewey-sort |
3610 |
| id |
ELV035268700 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV035268700</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625203734.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.mehy.2016.08.013</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2016009000025.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV035268700</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0306-9877(16)30285-7</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">540</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Hinds, Terry D.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor?</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">4</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD).</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD).</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NAFLD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Biliverdin</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PPAR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Heme oxygenase</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SPPARM</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Bilirubin</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NASH</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Non-alcoholic fatty liver disease</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PPARα</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Nuclear receptors</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Adeosun, Samuel O.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Alamodi, Abdulhadi A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Stec, David E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Harcourt</subfield><subfield code="a">Fan, Ya-Meng ELSEVIER</subfield><subfield code="t">Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors</subfield><subfield code="d">2017transfer abstract</subfield><subfield code="g">Burlington, Mass</subfield><subfield code="w">(DE-627)ELV015462293</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:95</subfield><subfield code="g">year:2016</subfield><subfield code="g">pages:54-57</subfield><subfield code="g">extent:4</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.mehy.2016.08.013</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.00</subfield><subfield code="j">Medizin: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">95</subfield><subfield code="j">2016</subfield><subfield code="h">54-57</subfield><subfield code="g">4</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| author |
Hinds, Terry D. |
| spellingShingle |
Hinds, Terry D. ddc 610 ddc 540 bkl 44.00 Elsevier NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? |
| authorStr |
Hinds, Terry D. |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV015462293 |
| format |
electronic Article |
| dewey-ones |
610 - Medicine & health 540 - Chemistry & allied sciences |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
610 610 DE-600 540 VZ 610 VZ 44.00 bkl Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors Elsevier |
| topic |
ddc 610 ddc 540 bkl 44.00 Elsevier NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors |
| topic_unstemmed |
ddc 610 ddc 540 bkl 44.00 Elsevier NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors |
| topic_browse |
ddc 610 ddc 540 bkl 44.00 Elsevier NAFLD Elsevier Biliverdin Elsevier PPAR Elsevier Heme oxygenase Elsevier SPPARM Elsevier Bilirubin Elsevier NASH Elsevier Non-alcoholic fatty liver disease Elsevier PPARα Elsevier Nuclear receptors |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
s o a so soa a a a aa aaa d e s de des |
| hierarchy_parent_title |
Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors |
| hierarchy_parent_id |
ELV015462293 |
| dewey-tens |
610 - Medicine & health 540 - Chemistry |
| hierarchy_top_title |
Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV015462293 |
| title |
Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? |
| ctrlnum |
(DE-627)ELV035268700 (ELSEVIER)S0306-9877(16)30285-7 |
| title_full |
Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? |
| author_sort |
Hinds, Terry D. |
| journal |
Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors |
| journalStr |
Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology 500 - Science |
| recordtype |
marc |
| publishDateSort |
2016 |
| contenttype_str_mv |
zzz |
| container_start_page |
54 |
| author_browse |
Hinds, Terry D. |
| container_volume |
95 |
| physical |
4 |
| class |
610 610 DE-600 540 VZ 610 VZ 44.00 bkl |
| format_se |
Elektronische Aufsätze |
| author-letter |
Hinds, Terry D. |
| doi_str_mv |
10.1016/j.mehy.2016.08.013 |
| dewey-full |
610 540 |
| title_sort |
does bilirubin prevent hepatic steatosis through activation of the pparα nuclear receptor? |
| title_auth |
Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? |
| abstract |
Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). |
| abstractGer |
Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). |
| abstract_unstemmed |
Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD). |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
| title_short |
Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor? |
| url |
https://doi.org/10.1016/j.mehy.2016.08.013 |
| remote_bool |
true |
| author2 |
Adeosun, Samuel O. Alamodi, Abdulhadi A. Stec, David E. |
| author2Str |
Adeosun, Samuel O. Alamodi, Abdulhadi A. Stec, David E. |
| ppnlink |
ELV015462293 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth |
| doi_str |
10.1016/j.mehy.2016.08.013 |
| up_date |
2024-07-06T17:08:00.594Z |
| _version_ |
1803850277817679872 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV035268700</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625203734.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2016 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.mehy.2016.08.013</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2016009000025.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV035268700</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0306-9877(16)30285-7</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">540</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Hinds, Terry D.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Does bilirubin prevent hepatic steatosis through activation of the PPARα nuclear receptor?</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">4</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD).</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Several large population studies have demonstrated a negative correlation between serum bilirubin levels and the development of obesity, hepatic steatosis, and cardiovascular disease. Despite the strong correlative data demonstrating the protective role of bilirubin, the mechanism by which bilirubin can protect against these pathologies remains unknown. Bilirubin has long been known as a powerful antioxidant and also has anti-inflammatory actions, each of which may contribute to the protection afforded by increased levels. We have recently described a novel function of bilirubin as a ligand for the peroxisome proliferator-activated receptor-alpha (PPARα), which we show specifically binds to the nuclear receptor. Bilirubin may function as a selective PPAR modulator (SPPARM) to control lipid accumulation and blood glucose. However, it is not known to what degree bilirubin activation of PPARα is responsible for the protection afforded to reduce hepatic steatosis. We hypothesize that bilirubin, acting as a novel SPPARM, increases hepatic fatty acid metabolism through a PPARα-dependent mechanism which reduces hepatic lipid accumulation and protects against hepatic steatosis and non-alcoholic fatty liver disease (NAFLD).</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NAFLD</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Biliverdin</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PPAR</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Heme oxygenase</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SPPARM</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Bilirubin</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">NASH</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Non-alcoholic fatty liver disease</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PPARα</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Nuclear receptors</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Adeosun, Samuel O.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Alamodi, Abdulhadi A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Stec, David E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Harcourt</subfield><subfield code="a">Fan, Ya-Meng ELSEVIER</subfield><subfield code="t">Hierarchical porous NiCo2S4-rGO composites for high-performance supercapacitors</subfield><subfield code="d">2017transfer abstract</subfield><subfield code="g">Burlington, Mass</subfield><subfield code="w">(DE-627)ELV015462293</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:95</subfield><subfield code="g">year:2016</subfield><subfield code="g">pages:54-57</subfield><subfield code="g">extent:4</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.mehy.2016.08.013</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.00</subfield><subfield code="j">Medizin: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">95</subfield><subfield code="j">2016</subfield><subfield code="h">54-57</subfield><subfield code="g">4</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
|
| score |
7.4003525 |