Adipose tissue–specific dysregulation of angiotensinogen by oxidative stress in obesity
Abstract Adipose tissue expresses all components of the renin-angiotensin system including angiotensinogen (AGT). Recent studies have highlighted a potential role of AGT in adipose tissue function and homeostasis. However, some controversies surround the regulatory mechanisms of AGT in obese adipose...
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| Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 2010-09, Vol.59 (9), p.1241-1251 |
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| creator | Okada, Sadanori Kozuka, Chisayo Masuzaki, Hiroaki Yasue, Shintaro Ishii-Yonemoto, Takako Tanaka, Tomohiro Yamamoto, Yuji Noguchi, Michio Kusakabe, Toru Tomita, Tsutomu Fujikura, Junji Ebihara, Ken Hosoda, Kiminori Sakaue, Hiroshi Kobori, Hiroyuki Ham, Mira Lee, Yun Sok Kim, Jae Bum Saito, Yoshihiko Nakao, Kazuwa |
| description | Abstract Adipose tissue expresses all components of the renin-angiotensin system including angiotensinogen (AGT). Recent studies have highlighted a potential role of AGT in adipose tissue function and homeostasis. However, some controversies surround the regulatory mechanisms of AGT in obese adipose tissue. In this context, we here demonstrated that the AGT messenger RNA (mRNA) level in human subcutaneous adipose tissue was significantly reduced in obese subjects as compared with nonobese subjects. Adipose tissue AGT mRNA level in obese mice was also lower as compared with their lean littermates; however, the hepatic AGT mRNA level remained unchanged. When 3T3-L1 adipocytes were cultured for a long period, the adipocytes became hypertrophic with a marked increase in the production of reactive oxygen species. Expression and secretion of AGT continued to decrease during the course of adipocyte hypertrophy. Treatment of the 3T3-L1 and primary adipocytes with reactive oxygen species (hydrogen peroxide) or tumor necrosis factor α caused a significant decrease in the expression and secretion of AGT. On the other hand, treatment with the antioxidant N -acetyl cysteine suppressed the decrease in the expression and secretion of AGT in the hypertrophied 3T3-L1 adipocytes. Finally, treatment of obese db/db mice with N -acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver. The present study demonstrates for the first time that oxidative stress dysregulates AGT in obese adipose tissue, providing a novel insight into the adipose tissue–specific interaction between the regulation of AGT and oxidative stress in the pathophysiology of obesity. |
| doi_str_mv | 10.1016/j.metabol.2009.11.016 |
| format | Article |
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Recent studies have highlighted a potential role of AGT in adipose tissue function and homeostasis. However, some controversies surround the regulatory mechanisms of AGT in obese adipose tissue. In this context, we here demonstrated that the AGT messenger RNA (mRNA) level in human subcutaneous adipose tissue was significantly reduced in obese subjects as compared with nonobese subjects. Adipose tissue AGT mRNA level in obese mice was also lower as compared with their lean littermates; however, the hepatic AGT mRNA level remained unchanged. When 3T3-L1 adipocytes were cultured for a long period, the adipocytes became hypertrophic with a marked increase in the production of reactive oxygen species. Expression and secretion of AGT continued to decrease during the course of adipocyte hypertrophy. Treatment of the 3T3-L1 and primary adipocytes with reactive oxygen species (hydrogen peroxide) or tumor necrosis factor α caused a significant decrease in the expression and secretion of AGT. On the other hand, treatment with the antioxidant N -acetyl cysteine suppressed the decrease in the expression and secretion of AGT in the hypertrophied 3T3-L1 adipocytes. Finally, treatment of obese db/db mice with N -acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver. The present study demonstrates for the first time that oxidative stress dysregulates AGT in obese adipose tissue, providing a novel insight into the adipose tissue–specific interaction between the regulation of AGT and oxidative stress in the pathophysiology of obesity.</description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/j.metabol.2009.11.016</identifier><identifier>PMID: 20045538</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adipocytes - cytology ; Adipocytes - metabolism ; Adult ; Angiotensinogen - genetics ; Angiotensinogen - metabolism ; Animals ; Cell Size ; Cells, Cultured ; Endocrinology & Metabolism ; Female ; Humans ; Male ; Mice ; Mice, Obese ; Middle Aged ; Obesity - genetics ; Obesity - metabolism ; Obesity - physiopathology ; Oxidative Stress ; Reactive Oxygen Species - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Subcutaneous Fat - metabolism ; Subcutaneous Fat - physiopathology ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Metabolism, clinical and experimental, 2010-09, Vol.59 (9), p.1241-1251</ispartof><rights>Elsevier Inc.</rights><rights>2010 Elsevier Inc.</rights><rights>Copyright 2010 Elsevier Inc. All rights reserved.</rights><rights>2010 Elsevier Inc. All rights reserved. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c521t-b2775e8229ea249ab8b3ff6b8d7d16ae0b134346eb2ea59b7a68affcea50b70a3</citedby><cites>FETCH-LOGICAL-c521t-b2775e8229ea249ab8b3ff6b8d7d16ae0b134346eb2ea59b7a68affcea50b70a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.metabol.2009.11.016$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20045538$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okada, Sadanori</creatorcontrib><creatorcontrib>Kozuka, Chisayo</creatorcontrib><creatorcontrib>Masuzaki, Hiroaki</creatorcontrib><creatorcontrib>Yasue, Shintaro</creatorcontrib><creatorcontrib>Ishii-Yonemoto, Takako</creatorcontrib><creatorcontrib>Tanaka, Tomohiro</creatorcontrib><creatorcontrib>Yamamoto, Yuji</creatorcontrib><creatorcontrib>Noguchi, Michio</creatorcontrib><creatorcontrib>Kusakabe, Toru</creatorcontrib><creatorcontrib>Tomita, Tsutomu</creatorcontrib><creatorcontrib>Fujikura, Junji</creatorcontrib><creatorcontrib>Ebihara, Ken</creatorcontrib><creatorcontrib>Hosoda, Kiminori</creatorcontrib><creatorcontrib>Sakaue, Hiroshi</creatorcontrib><creatorcontrib>Kobori, Hiroyuki</creatorcontrib><creatorcontrib>Ham, Mira</creatorcontrib><creatorcontrib>Lee, Yun Sok</creatorcontrib><creatorcontrib>Kim, Jae Bum</creatorcontrib><creatorcontrib>Saito, Yoshihiko</creatorcontrib><creatorcontrib>Nakao, Kazuwa</creatorcontrib><title>Adipose tissue–specific dysregulation of angiotensinogen by oxidative stress in obesity</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description>Abstract Adipose tissue expresses all components of the renin-angiotensin system including angiotensinogen (AGT). Recent studies have highlighted a potential role of AGT in adipose tissue function and homeostasis. However, some controversies surround the regulatory mechanisms of AGT in obese adipose tissue. In this context, we here demonstrated that the AGT messenger RNA (mRNA) level in human subcutaneous adipose tissue was significantly reduced in obese subjects as compared with nonobese subjects. Adipose tissue AGT mRNA level in obese mice was also lower as compared with their lean littermates; however, the hepatic AGT mRNA level remained unchanged. When 3T3-L1 adipocytes were cultured for a long period, the adipocytes became hypertrophic with a marked increase in the production of reactive oxygen species. Expression and secretion of AGT continued to decrease during the course of adipocyte hypertrophy. Treatment of the 3T3-L1 and primary adipocytes with reactive oxygen species (hydrogen peroxide) or tumor necrosis factor α caused a significant decrease in the expression and secretion of AGT. On the other hand, treatment with the antioxidant N -acetyl cysteine suppressed the decrease in the expression and secretion of AGT in the hypertrophied 3T3-L1 adipocytes. Finally, treatment of obese db/db mice with N -acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver. The present study demonstrates for the first time that oxidative stress dysregulates AGT in obese adipose tissue, providing a novel insight into the adipose tissue–specific interaction between the regulation of AGT and oxidative stress in the pathophysiology of obesity.</description><subject>Adipocytes - cytology</subject><subject>Adipocytes - metabolism</subject><subject>Adult</subject><subject>Angiotensinogen - genetics</subject><subject>Angiotensinogen - metabolism</subject><subject>Animals</subject><subject>Cell Size</subject><subject>Cells, Cultured</subject><subject>Endocrinology & Metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Obese</subject><subject>Middle Aged</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Obesity - physiopathology</subject><subject>Oxidative Stress</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Subcutaneous Fat - metabolism</subject><subject>Subcutaneous Fat - physiopathology</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUstuFDEQtBCIbAKfAJobpxnanvclKIqAIEXiABw4WbanZ-ll1l5szypz4x_4Q74Er3aJgAsny91V1XZVM_aMQ8GBNy83xRaj0m4qBEBfcF6k6gO24nUp8q4BeMhWAKLJoerrM3YewgYA2rZrHrOzRKnquuxW7PPVQDsXMIsUwow_v_8IOzQ0ksmGJXhcz5OK5GzmxkzZNbmINpB1a7SZXjJ3R0Pq7zEL0WMIGSWkxkBxecIejWoK-PR0XrBPb15_vL7Jb9-_fXd9dZubWvCYa9G2NXZC9KhE1Svd6XIcG90N7cAbhaB5WZVVg1qgqnvdqqZT42jSBXQLqrxgl0fd3ay3OBi00atJ7jxtlV-kUyT_7lj6ItduL0XXc1GWSeDFScC7bzOGKLcUDE6TsujmINuqB2iSjQlZH5HGu5DMGe-ncJCHVORGnlKRh1Qk5zJVE-_5n0-8Z_2OIQFeHQGYjNoTehkMoTU4kEcT5eDovyMu_1EwE1kyavqKC4aNm71NKUgug5AgPxxW47AZkP5W9RzKXz2Wuo4</recordid><startdate>20100901</startdate><enddate>20100901</enddate><creator>Okada, Sadanori</creator><creator>Kozuka, Chisayo</creator><creator>Masuzaki, Hiroaki</creator><creator>Yasue, Shintaro</creator><creator>Ishii-Yonemoto, Takako</creator><creator>Tanaka, Tomohiro</creator><creator>Yamamoto, Yuji</creator><creator>Noguchi, Michio</creator><creator>Kusakabe, Toru</creator><creator>Tomita, Tsutomu</creator><creator>Fujikura, Junji</creator><creator>Ebihara, Ken</creator><creator>Hosoda, Kiminori</creator><creator>Sakaue, Hiroshi</creator><creator>Kobori, Hiroyuki</creator><creator>Ham, Mira</creator><creator>Lee, Yun Sok</creator><creator>Kim, Jae Bum</creator><creator>Saito, Yoshihiko</creator><creator>Nakao, Kazuwa</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100901</creationdate><title>Adipose tissue–specific dysregulation of angiotensinogen by oxidative stress in obesity</title><author>Okada, Sadanori ; 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Recent studies have highlighted a potential role of AGT in adipose tissue function and homeostasis. However, some controversies surround the regulatory mechanisms of AGT in obese adipose tissue. In this context, we here demonstrated that the AGT messenger RNA (mRNA) level in human subcutaneous adipose tissue was significantly reduced in obese subjects as compared with nonobese subjects. Adipose tissue AGT mRNA level in obese mice was also lower as compared with their lean littermates; however, the hepatic AGT mRNA level remained unchanged. When 3T3-L1 adipocytes were cultured for a long period, the adipocytes became hypertrophic with a marked increase in the production of reactive oxygen species. Expression and secretion of AGT continued to decrease during the course of adipocyte hypertrophy. Treatment of the 3T3-L1 and primary adipocytes with reactive oxygen species (hydrogen peroxide) or tumor necrosis factor α caused a significant decrease in the expression and secretion of AGT. On the other hand, treatment with the antioxidant N -acetyl cysteine suppressed the decrease in the expression and secretion of AGT in the hypertrophied 3T3-L1 adipocytes. Finally, treatment of obese db/db mice with N -acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver. The present study demonstrates for the first time that oxidative stress dysregulates AGT in obese adipose tissue, providing a novel insight into the adipose tissue–specific interaction between the regulation of AGT and oxidative stress in the pathophysiology of obesity.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>20045538</pmid><doi>10.1016/j.metabol.2009.11.016</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes - cytology Adipocytes - metabolism Adult Angiotensinogen - genetics Angiotensinogen - metabolism Animals Cell Size Cells, Cultured Endocrinology & Metabolism Female Humans Male Mice Mice, Obese Middle Aged Obesity - genetics Obesity - metabolism Obesity - physiopathology Oxidative Stress Reactive Oxygen Species - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism Subcutaneous Fat - metabolism Subcutaneous Fat - physiopathology Tumor Necrosis Factor-alpha - metabolism |
| title | Adipose tissue–specific dysregulation of angiotensinogen by oxidative stress in obesity |
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