Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions
To investigate the effects of fimasartan on nonalcoholic fatty liver disease in hyperlipidemic and hypertensive conditions, the levels of biomarkers related to fatty acid metabolism were determined in HepG2 and differentiated 3T3-L1 cells treated by high fatty acid and liver and visceral fat tissue...
Saved in:
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2017-01-01
|
| Series: | PPAR Research |
| Online Access: | http://dx.doi.org/10.1155/2017/8048720 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832552341173174272 |
|---|---|
| author | Yong-Jik Lee Yoo-Na Jang Yoon-Mi Han Hyun-Min Kim Jong-Min Jeong Hong Seog Seo |
| author_facet | Yong-Jik Lee Yoo-Na Jang Yoon-Mi Han Hyun-Min Kim Jong-Min Jeong Hong Seog Seo |
| author_sort | Yong-Jik Lee |
| collection | DOAJ |
| description | To investigate the effects of fimasartan on nonalcoholic fatty liver disease in hyperlipidemic and hypertensive conditions, the levels of biomarkers related to fatty acid metabolism were determined in HepG2 and differentiated 3T3-L1 cells treated by high fatty acid and liver and visceral fat tissue samples of spontaneously hypertensive rats (SHRs) given high-fat diet. In HepG2 cells and liver tissues, fimasartan was shown to increase the protein levels of peroxisome proliferator-activated receptor delta (PPARδ), phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK), phosphorylated acetyl-CoA carboxylase (p-ACC), malonyl-CoA decarboxylase (MCD), medium chain acyl-CoA dehydrogenase (MCAD), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and it led to a decrease in the protein levels of 11 beta-hydroxysteroid dehydrogenase 1 (11β-HSDH1), fatty acid synthase (FAS), and tumor necrosis factor-alpha (TNF-α). Fimasartan decreased lipid contents in HepG2 and differentiated 3T3-L1 cells and liver tissues. In addition, fimasartan increased the adiponectin level in visceral fat tissues. The antiadipogenic effects of fimasartan were offset by PPARδ antagonist (GSK0660). Consequently, fimasartan ameliorates nonalcoholic fatty liver disease mainly through the activation of oxidative metabolism represented by PPARδ-AMPK-PGC-1α pathway. |
| format | Article |
| id | doaj-art-133dbd17a78a46a499676c3a3f641e69 |
| institution | Kabale University |
| issn | 1687-4757 1687-4765 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | PPAR Research |
| spelling | doaj-art-133dbd17a78a46a499676c3a3f641e692025-02-03T05:58:51ZengWileyPPAR Research1687-47571687-47652017-01-01201710.1155/2017/80487208048720Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive ConditionsYong-Jik Lee0Yoo-Na Jang1Yoon-Mi Han2Hyun-Min Kim3Jong-Min Jeong4Hong Seog Seo5Cardiovascular Center, Guro Hospital, Korea University, 80 Guro-dong, Guro-gu, Seoul 152-703, Republic of KoreaCardiovascular Center, Guro Hospital, Korea University, 80 Guro-dong, Guro-gu, Seoul 152-703, Republic of KoreaCardiovascular Center, Guro Hospital, Korea University, 80 Guro-dong, Guro-gu, Seoul 152-703, Republic of KoreaCardiovascular Center, Guro Hospital, Korea University, 80 Guro-dong, Guro-gu, Seoul 152-703, Republic of KoreaCardiovascular Center, Guro Hospital, Korea University, 80 Guro-dong, Guro-gu, Seoul 152-703, Republic of KoreaCardiovascular Center, Guro Hospital, Korea University, 80 Guro-dong, Guro-gu, Seoul 152-703, Republic of KoreaTo investigate the effects of fimasartan on nonalcoholic fatty liver disease in hyperlipidemic and hypertensive conditions, the levels of biomarkers related to fatty acid metabolism were determined in HepG2 and differentiated 3T3-L1 cells treated by high fatty acid and liver and visceral fat tissue samples of spontaneously hypertensive rats (SHRs) given high-fat diet. In HepG2 cells and liver tissues, fimasartan was shown to increase the protein levels of peroxisome proliferator-activated receptor delta (PPARδ), phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK), phosphorylated acetyl-CoA carboxylase (p-ACC), malonyl-CoA decarboxylase (MCD), medium chain acyl-CoA dehydrogenase (MCAD), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and it led to a decrease in the protein levels of 11 beta-hydroxysteroid dehydrogenase 1 (11β-HSDH1), fatty acid synthase (FAS), and tumor necrosis factor-alpha (TNF-α). Fimasartan decreased lipid contents in HepG2 and differentiated 3T3-L1 cells and liver tissues. In addition, fimasartan increased the adiponectin level in visceral fat tissues. The antiadipogenic effects of fimasartan were offset by PPARδ antagonist (GSK0660). Consequently, fimasartan ameliorates nonalcoholic fatty liver disease mainly through the activation of oxidative metabolism represented by PPARδ-AMPK-PGC-1α pathway.http://dx.doi.org/10.1155/2017/8048720 |
| spellingShingle | Yong-Jik Lee Yoo-Na Jang Yoon-Mi Han Hyun-Min Kim Jong-Min Jeong Hong Seog Seo Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions PPAR Research |
| title | Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions |
| title_full | Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions |
| title_fullStr | Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions |
| title_full_unstemmed | Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions |
| title_short | Fimasartan Ameliorates Nonalcoholic Fatty Liver Disease through PPARδ Regulation in Hyperlipidemic and Hypertensive Conditions |
| title_sort | fimasartan ameliorates nonalcoholic fatty liver disease through pparδ regulation in hyperlipidemic and hypertensive conditions |
| url | http://dx.doi.org/10.1155/2017/8048720 |
| work_keys_str_mv | AT yongjiklee fimasartanamelioratesnonalcoholicfattyliverdiseasethroughppardregulationinhyperlipidemicandhypertensiveconditions AT yoonajang fimasartanamelioratesnonalcoholicfattyliverdiseasethroughppardregulationinhyperlipidemicandhypertensiveconditions AT yoonmihan fimasartanamelioratesnonalcoholicfattyliverdiseasethroughppardregulationinhyperlipidemicandhypertensiveconditions AT hyunminkim fimasartanamelioratesnonalcoholicfattyliverdiseasethroughppardregulationinhyperlipidemicandhypertensiveconditions AT jongminjeong fimasartanamelioratesnonalcoholicfattyliverdiseasethroughppardregulationinhyperlipidemicandhypertensiveconditions AT hongseogseo fimasartanamelioratesnonalcoholicfattyliverdiseasethroughppardregulationinhyperlipidemicandhypertensiveconditions |