A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice
Obesity is a chronic peripheral inflammation condition that is strongly correlated with neurodegenerative diseases and associated with exposure to environmental chemicals. The aryl hydrocarbon receptor (AhR) is a ligand-activated nuclear receptor activated by environmental chemical, such as dioxins,...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2022-11, Vol.23 (23), p.14871 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 23 |
| container_start_page | 14871 |
| container_title | International journal of molecular sciences |
| container_volume | 23 |
| creator | Kang, Sora Lee, Aden Geonhee Im, Suyeol Oh, Seung Jun Yoon, Hye Ji Park, Jeong Ho Pak, Youngmi Kim |
| description | Obesity is a chronic peripheral inflammation condition that is strongly correlated with neurodegenerative diseases and associated with exposure to environmental chemicals. The aryl hydrocarbon receptor (AhR) is a ligand-activated nuclear receptor activated by environmental chemical, such as dioxins, and also is a regulator of inflammation through interacting with nuclear factor (NF)-κB. In this study, we evaluated the anti-obesity and anti-inflammatory activity of HBU651, a novel AhR antagonist. In BV2 microglia cells, HBU651 successfully inhibited lipopolysaccharide (LPS)-mediated nuclear localization of NF-κB and production of NF-κB-dependent proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. It also restored LPS-induced mitochondrial dysfunction. While mice being fed a high-fat diet (HFD) induced peripheral and central inflammation and obesity, HBU651 alleviated HFD-induced obesity, insulin resistance, glucose intolerance, dyslipidemia, and liver enzyme activity, without hepatic and renal damage. HBU651 ameliorated the production of inflammatory cytokines and chemokines, proinflammatory Ly6c
monocytes, and macrophage infiltration in the blood, liver, and adipose tissue. HBU651 also decreased microglial activation in the arcuate nucleus in the hypothalamus. These findings suggest that HBU651 may be a potential candidate for the treatment of obesity-related metabolic diseases. |
| doi_str_mv | 10.3390/ijms232314871 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9736602</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2753309600</sourcerecordid><originalsourceid>FETCH-LOGICAL-c415t-4e94d05b753ef59ce4ec9c811f83cef2a16e77bd264c77a21d48bc6285867a363</originalsourceid><addsrcrecordid>eNpdkUFv1DAQhS1ERcvCkSuyxIVLqB07dnxBCoWyKxWKED1HjjPZ9SqxU9uptP-BH42rlqrtaZ40n57ezEPoHSWfGFPk1O6nWLKSUV5L-gKdUF6WBSFCvnykj9HrGPeEZLBSr9AxE1wpquoT9LfBP_0NjLgJhxGvD33wRofOO_wbDMzJB9y4pLfe2Zjw-suVqChuJhitDzpBxL8g2HkHQY9Yuz47zD7t9Kgna_DGDVlMOtnsZx1e2-2uONcJf7WQio3rFwM9vuwgAv5hDbxBR4MeI7y9nyt0df7tz9m6uLj8vjlrLgrDaZUKDor3pOpkxWColAEORpma0qFmBoZSUwFSdn0puJFSl7TndWdEWVe1kJoJtkKf73znpZugN-BSzt_OwU46HFqvbft04-yu3fqbVkkmRP7iCn28Nwj-eoGY2slGA-OoHfgltmWOxogShGT0wzN075fg8nmZ4nXFa8J4poo7ygQfY4DhIQwl7W3P7ZOeM__-8QUP9P9i2T9riqUA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2748548034</pqid></control><display><type>article</type><title>A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Kang, Sora ; Lee, Aden Geonhee ; Im, Suyeol ; Oh, Seung Jun ; Yoon, Hye Ji ; Park, Jeong Ho ; Pak, Youngmi Kim</creator><creatorcontrib>Kang, Sora ; Lee, Aden Geonhee ; Im, Suyeol ; Oh, Seung Jun ; Yoon, Hye Ji ; Park, Jeong Ho ; Pak, Youngmi Kim</creatorcontrib><description>Obesity is a chronic peripheral inflammation condition that is strongly correlated with neurodegenerative diseases and associated with exposure to environmental chemicals. The aryl hydrocarbon receptor (AhR) is a ligand-activated nuclear receptor activated by environmental chemical, such as dioxins, and also is a regulator of inflammation through interacting with nuclear factor (NF)-κB. In this study, we evaluated the anti-obesity and anti-inflammatory activity of HBU651, a novel AhR antagonist. In BV2 microglia cells, HBU651 successfully inhibited lipopolysaccharide (LPS)-mediated nuclear localization of NF-κB and production of NF-κB-dependent proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. It also restored LPS-induced mitochondrial dysfunction. While mice being fed a high-fat diet (HFD) induced peripheral and central inflammation and obesity, HBU651 alleviated HFD-induced obesity, insulin resistance, glucose intolerance, dyslipidemia, and liver enzyme activity, without hepatic and renal damage. HBU651 ameliorated the production of inflammatory cytokines and chemokines, proinflammatory Ly6c
monocytes, and macrophage infiltration in the blood, liver, and adipose tissue. HBU651 also decreased microglial activation in the arcuate nucleus in the hypothalamus. These findings suggest that HBU651 may be a potential candidate for the treatment of obesity-related metabolic diseases.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms232314871</identifier><identifier>PMID: 36499198</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adipose tissue ; Alzheimer's disease ; Animals ; Arcuate nucleus ; Aromatic compounds ; Body fat ; Chemokines ; Cytokines ; Diet, High-Fat ; Dioxins ; Dyslipidemia ; Enzymatic activity ; Enzyme activity ; Glucose ; Glucose tolerance ; High fat diet ; Hydrocarbons ; Hypothalamus ; Inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Insulin ; Insulin resistance ; Interleukin 6 ; Intolerance ; Ligands ; Lipids ; Lipopolysaccharides ; Liver ; Localization ; Macrophages ; Metabolic disorders ; Metabolism ; Metastases ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Microglia ; Mitochondria ; Monocytes ; NF-kappa B - metabolism ; NF-κB protein ; Obesity ; Obesity - drug therapy ; Obesity - etiology ; Obesity - metabolism ; Receptors, Aryl Hydrocarbon - metabolism ; Transcription factors ; Tumor Necrosis Factor-alpha ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>International journal of molecular sciences, 2022-11, Vol.23 (23), p.14871</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-4e94d05b753ef59ce4ec9c811f83cef2a16e77bd264c77a21d48bc6285867a363</citedby><cites>FETCH-LOGICAL-c415t-4e94d05b753ef59ce4ec9c811f83cef2a16e77bd264c77a21d48bc6285867a363</cites><orcidid>0000-0003-4466-8224 ; 0000-0001-7424-3484 ; 0000-0001-5244-4648</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9736602/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9736602/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36499198$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kang, Sora</creatorcontrib><creatorcontrib>Lee, Aden Geonhee</creatorcontrib><creatorcontrib>Im, Suyeol</creatorcontrib><creatorcontrib>Oh, Seung Jun</creatorcontrib><creatorcontrib>Yoon, Hye Ji</creatorcontrib><creatorcontrib>Park, Jeong Ho</creatorcontrib><creatorcontrib>Pak, Youngmi Kim</creatorcontrib><title>A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Obesity is a chronic peripheral inflammation condition that is strongly correlated with neurodegenerative diseases and associated with exposure to environmental chemicals. The aryl hydrocarbon receptor (AhR) is a ligand-activated nuclear receptor activated by environmental chemical, such as dioxins, and also is a regulator of inflammation through interacting with nuclear factor (NF)-κB. In this study, we evaluated the anti-obesity and anti-inflammatory activity of HBU651, a novel AhR antagonist. In BV2 microglia cells, HBU651 successfully inhibited lipopolysaccharide (LPS)-mediated nuclear localization of NF-κB and production of NF-κB-dependent proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. It also restored LPS-induced mitochondrial dysfunction. While mice being fed a high-fat diet (HFD) induced peripheral and central inflammation and obesity, HBU651 alleviated HFD-induced obesity, insulin resistance, glucose intolerance, dyslipidemia, and liver enzyme activity, without hepatic and renal damage. HBU651 ameliorated the production of inflammatory cytokines and chemokines, proinflammatory Ly6c
monocytes, and macrophage infiltration in the blood, liver, and adipose tissue. HBU651 also decreased microglial activation in the arcuate nucleus in the hypothalamus. These findings suggest that HBU651 may be a potential candidate for the treatment of obesity-related metabolic diseases.</description><subject>Adipose tissue</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Arcuate nucleus</subject><subject>Aromatic compounds</subject><subject>Body fat</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Diet, High-Fat</subject><subject>Dioxins</subject><subject>Dyslipidemia</subject><subject>Enzymatic activity</subject><subject>Enzyme activity</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>High fat diet</subject><subject>Hydrocarbons</subject><subject>Hypothalamus</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Interleukin 6</subject><subject>Intolerance</subject><subject>Ligands</subject><subject>Lipids</subject><subject>Lipopolysaccharides</subject><subject>Liver</subject><subject>Localization</subject><subject>Macrophages</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Obese</subject><subject>Microglia</subject><subject>Mitochondria</subject><subject>Monocytes</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Obesity</subject><subject>Obesity - drug therapy</subject><subject>Obesity - etiology</subject><subject>Obesity - metabolism</subject><subject>Receptors, Aryl Hydrocarbon - metabolism</subject><subject>Transcription factors</subject><subject>Tumor Necrosis Factor-alpha</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUFv1DAQhS1ERcvCkSuyxIVLqB07dnxBCoWyKxWKED1HjjPZ9SqxU9uptP-BH42rlqrtaZ40n57ezEPoHSWfGFPk1O6nWLKSUV5L-gKdUF6WBSFCvnykj9HrGPeEZLBSr9AxE1wpquoT9LfBP_0NjLgJhxGvD33wRofOO_wbDMzJB9y4pLfe2Zjw-suVqChuJhitDzpBxL8g2HkHQY9Yuz47zD7t9Kgna_DGDVlMOtnsZx1e2-2uONcJf7WQio3rFwM9vuwgAv5hDbxBR4MeI7y9nyt0df7tz9m6uLj8vjlrLgrDaZUKDor3pOpkxWColAEORpma0qFmBoZSUwFSdn0puJFSl7TndWdEWVe1kJoJtkKf73znpZugN-BSzt_OwU46HFqvbft04-yu3fqbVkkmRP7iCn28Nwj-eoGY2slGA-OoHfgltmWOxogShGT0wzN075fg8nmZ4nXFa8J4poo7ygQfY4DhIQwl7W3P7ZOeM__-8QUP9P9i2T9riqUA</recordid><startdate>20221128</startdate><enddate>20221128</enddate><creator>Kang, Sora</creator><creator>Lee, Aden Geonhee</creator><creator>Im, Suyeol</creator><creator>Oh, Seung Jun</creator><creator>Yoon, Hye Ji</creator><creator>Park, Jeong Ho</creator><creator>Pak, Youngmi Kim</creator><general>MDPI AG</general><general>MDPI</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4466-8224</orcidid><orcidid>https://orcid.org/0000-0001-7424-3484</orcidid><orcidid>https://orcid.org/0000-0001-5244-4648</orcidid></search><sort><creationdate>20221128</creationdate><title>A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice</title><author>Kang, Sora ; Lee, Aden Geonhee ; Im, Suyeol ; Oh, Seung Jun ; Yoon, Hye Ji ; Park, Jeong Ho ; Pak, Youngmi Kim</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-4e94d05b753ef59ce4ec9c811f83cef2a16e77bd264c77a21d48bc6285867a363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adipose tissue</topic><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>Arcuate nucleus</topic><topic>Aromatic compounds</topic><topic>Body fat</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Diet, High-Fat</topic><topic>Dioxins</topic><topic>Dyslipidemia</topic><topic>Enzymatic activity</topic><topic>Enzyme activity</topic><topic>Glucose</topic><topic>Glucose tolerance</topic><topic>High fat diet</topic><topic>Hydrocarbons</topic><topic>Hypothalamus</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>Insulin</topic><topic>Insulin resistance</topic><topic>Interleukin 6</topic><topic>Intolerance</topic><topic>Ligands</topic><topic>Lipids</topic><topic>Lipopolysaccharides</topic><topic>Liver</topic><topic>Localization</topic><topic>Macrophages</topic><topic>Metabolic disorders</topic><topic>Metabolism</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Obese</topic><topic>Microglia</topic><topic>Mitochondria</topic><topic>Monocytes</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Obesity</topic><topic>Obesity - drug therapy</topic><topic>Obesity - etiology</topic><topic>Obesity - metabolism</topic><topic>Receptors, Aryl Hydrocarbon - metabolism</topic><topic>Transcription factors</topic><topic>Tumor Necrosis Factor-alpha</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kang, Sora</creatorcontrib><creatorcontrib>Lee, Aden Geonhee</creatorcontrib><creatorcontrib>Im, Suyeol</creatorcontrib><creatorcontrib>Oh, Seung Jun</creatorcontrib><creatorcontrib>Yoon, Hye Ji</creatorcontrib><creatorcontrib>Park, Jeong Ho</creatorcontrib><creatorcontrib>Pak, Youngmi Kim</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kang, Sora</au><au>Lee, Aden Geonhee</au><au>Im, Suyeol</au><au>Oh, Seung Jun</au><au>Yoon, Hye Ji</au><au>Park, Jeong Ho</au><au>Pak, Youngmi Kim</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-11-28</date><risdate>2022</risdate><volume>23</volume><issue>23</issue><spage>14871</spage><pages>14871-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Obesity is a chronic peripheral inflammation condition that is strongly correlated with neurodegenerative diseases and associated with exposure to environmental chemicals. The aryl hydrocarbon receptor (AhR) is a ligand-activated nuclear receptor activated by environmental chemical, such as dioxins, and also is a regulator of inflammation through interacting with nuclear factor (NF)-κB. In this study, we evaluated the anti-obesity and anti-inflammatory activity of HBU651, a novel AhR antagonist. In BV2 microglia cells, HBU651 successfully inhibited lipopolysaccharide (LPS)-mediated nuclear localization of NF-κB and production of NF-κB-dependent proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. It also restored LPS-induced mitochondrial dysfunction. While mice being fed a high-fat diet (HFD) induced peripheral and central inflammation and obesity, HBU651 alleviated HFD-induced obesity, insulin resistance, glucose intolerance, dyslipidemia, and liver enzyme activity, without hepatic and renal damage. HBU651 ameliorated the production of inflammatory cytokines and chemokines, proinflammatory Ly6c
monocytes, and macrophage infiltration in the blood, liver, and adipose tissue. HBU651 also decreased microglial activation in the arcuate nucleus in the hypothalamus. These findings suggest that HBU651 may be a potential candidate for the treatment of obesity-related metabolic diseases.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36499198</pmid><doi>10.3390/ijms232314871</doi><orcidid>https://orcid.org/0000-0003-4466-8224</orcidid><orcidid>https://orcid.org/0000-0001-7424-3484</orcidid><orcidid>https://orcid.org/0000-0001-5244-4648</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2022-11, Vol.23 (23), p.14871 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9736602 |
| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Adipose tissue Alzheimer's disease Animals Arcuate nucleus Aromatic compounds Body fat Chemokines Cytokines Diet, High-Fat Dioxins Dyslipidemia Enzymatic activity Enzyme activity Glucose Glucose tolerance High fat diet Hydrocarbons Hypothalamus Inflammation Inflammation - drug therapy Inflammation - metabolism Insulin Insulin resistance Interleukin 6 Intolerance Ligands Lipids Lipopolysaccharides Liver Localization Macrophages Metabolic disorders Metabolism Metastases Mice Mice, Inbred C57BL Mice, Obese Microglia Mitochondria Monocytes NF-kappa B - metabolism NF-κB protein Obesity Obesity - drug therapy Obesity - etiology Obesity - metabolism Receptors, Aryl Hydrocarbon - metabolism Transcription factors Tumor Necrosis Factor-alpha Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | A Novel Aryl Hydrocarbon Receptor Antagonist HBU651 Ameliorates Peripheral and Hypothalamic Inflammation in High-Fat Diet-Induced Obese Mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-31T19%3A42%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20Novel%20Aryl%20Hydrocarbon%20Receptor%20Antagonist%20HBU651%20Ameliorates%20Peripheral%20and%20Hypothalamic%20Inflammation%20in%20High-Fat%20Diet-Induced%20Obese%20Mice&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Kang,%20Sora&rft.date=2022-11-28&rft.volume=23&rft.issue=23&rft.spage=14871&rft.pages=14871-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms232314871&rft_dat=%3Cproquest_pubme%3E2753309600%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2748548034&rft_id=info:pmid/36499198&rfr_iscdi=true |