Restoration of metabolic inflammation-related ghrelin resistance by weight loss
High-fat diet (HFD)-induced metabolic inflammation in the central and peripheral organs contributes to the pathogenesis of obesity. Long-term HFD blunts signaling by ghrelin, a gastric-derived orexigenic peptide, in the vagal afferent nerve via a mechanism involving in situ activation of inflammatio...
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| Veröffentlicht in: | Journal of molecular endocrinology 2018-02, Vol.60 (2), p.109-118 |
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| container_title | Journal of molecular endocrinology |
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| creator | Naznin, Farhana Toshinai, Koji Waise, T M Zaved Okada, Tadashi Sakoda, Hideyuki Nakazato, Masamitsu |
| description | High-fat diet (HFD)-induced metabolic inflammation in the central and peripheral organs contributes to the pathogenesis of obesity. Long-term HFD blunts signaling by ghrelin, a gastric-derived orexigenic peptide, in the vagal afferent nerve via a mechanism involving in situ activation of inflammation. This study was undertaken to investigate whether ghrelin resistance is associated with progressive development of metabolic inflammation. In mice, ghrelin’s orexigenic activity was abolished 2–4 weeks after the commencement of HFD (60% of energy from fat), consistent with the timing of accumulation and activation of macrophages and microglia in the nodose ganglion and hypothalamus. Calorie-restricted weight loss after 12-week HFD feeding restored ghrelin responsiveness and alleviated the upregulation of macrophage/microglia activation markers and inflammatory cytokines. HSP72, a chaperone protein, was upregulated in the hypothalamus of HFD-fed mice, potentially contributing to prevention of irreversible neuron damage. These results demonstrate that ghrelin resistance is reversible following reversal of the HFD-induced inflammation and obesity phenotypes. |
| doi_str_mv | 10.1530/JME-17-0192 |
| format | Article |
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Long-term HFD blunts signaling by ghrelin, a gastric-derived orexigenic peptide, in the vagal afferent nerve via a mechanism involving in situ activation of inflammation. This study was undertaken to investigate whether ghrelin resistance is associated with progressive development of metabolic inflammation. In mice, ghrelin’s orexigenic activity was abolished 2–4 weeks after the commencement of HFD (60% of energy from fat), consistent with the timing of accumulation and activation of macrophages and microglia in the nodose ganglion and hypothalamus. Calorie-restricted weight loss after 12-week HFD feeding restored ghrelin responsiveness and alleviated the upregulation of macrophage/microglia activation markers and inflammatory cytokines. HSP72, a chaperone protein, was upregulated in the hypothalamus of HFD-fed mice, potentially contributing to prevention of irreversible neuron damage. These results demonstrate that ghrelin resistance is reversible following reversal of the HFD-induced inflammation and obesity phenotypes.</description><identifier>ISSN: 0952-5041</identifier><identifier>EISSN: 1479-6813</identifier><identifier>DOI: 10.1530/JME-17-0192</identifier><identifier>PMID: 29233861</identifier><language>eng</language><publisher>England: Bioscientifica Ltd</publisher><subject>Body weight loss ; Cell activation ; Cytokines ; Ghrelin ; High fat diet ; Hsp72 protein ; Hypothalamus ; Inflammation ; Macrophages ; Metabolism ; Microglia ; Nodose ganglion ; Obesity ; Phenotypes ; Rodents ; Sensory neurons ; Vagus nerve ; Weight control</subject><ispartof>Journal of molecular endocrinology, 2018-02, Vol.60 (2), p.109-118</ispartof><rights>2018 The authors</rights><rights>2018 The authors.</rights><rights>Copyright Society for Endocrinology & BioScientifica Ltd. 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Long-term HFD blunts signaling by ghrelin, a gastric-derived orexigenic peptide, in the vagal afferent nerve via a mechanism involving in situ activation of inflammation. This study was undertaken to investigate whether ghrelin resistance is associated with progressive development of metabolic inflammation. In mice, ghrelin’s orexigenic activity was abolished 2–4 weeks after the commencement of HFD (60% of energy from fat), consistent with the timing of accumulation and activation of macrophages and microglia in the nodose ganglion and hypothalamus. Calorie-restricted weight loss after 12-week HFD feeding restored ghrelin responsiveness and alleviated the upregulation of macrophage/microglia activation markers and inflammatory cytokines. HSP72, a chaperone protein, was upregulated in the hypothalamus of HFD-fed mice, potentially contributing to prevention of irreversible neuron damage. These results demonstrate that ghrelin resistance is reversible following reversal of the HFD-induced inflammation and obesity phenotypes.</description><subject>Body weight loss</subject><subject>Cell activation</subject><subject>Cytokines</subject><subject>Ghrelin</subject><subject>High fat diet</subject><subject>Hsp72 protein</subject><subject>Hypothalamus</subject><subject>Inflammation</subject><subject>Macrophages</subject><subject>Metabolism</subject><subject>Microglia</subject><subject>Nodose ganglion</subject><subject>Obesity</subject><subject>Phenotypes</subject><subject>Rodents</subject><subject>Sensory neurons</subject><subject>Vagus nerve</subject><subject>Weight control</subject><issn>0952-5041</issn><issn>1479-6813</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kcFLHDEUxoNYdLU9eZcBL4JMzUteJjMXQRarLRahtOeQZDK7kZmJJrOW_e-bda1YDz29B-_Hx_e-j5AjoJ9BcHr-7ftVCbKk0LAdMgOUTVnVwHfJjDaClYIi7JODlO4pBQES98g-axjndQUzcvfDpSlEPfkwFqErBjdpE3pvCz92vR6G50sZXa8n1xaLZd78WESXfJr0aF1h1sVv5xfLqehDSh_Jh073yX16mYfk15ern_Ob8vbu-uv88rY02cJUMuw6Y5hmRkjZmopaqAWzgnGJaHUjtLBMG9YaiUagrZDKDmvJERow2PJDcrHVfViZwbXWjVPUvXqIftBxrYL26t_L6JdqEZ6UkA2XwLLA6YtADI-rHIIafLKu7_XowiopaGSFWKGkGT15h96HVRzze4pRFBwrUdeZOttSNuYcoutezQBVm6JULkqBVJuiMn381v8r-7eZDMAWMD4k6_MXvvNW_1f0D196nxI</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Naznin, Farhana</creator><creator>Toshinai, Koji</creator><creator>Waise, T M Zaved</creator><creator>Okada, Tadashi</creator><creator>Sakoda, Hideyuki</creator><creator>Nakazato, Masamitsu</creator><general>Bioscientifica Ltd</general><general>Society for Endocrinology & BioScientifica Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180201</creationdate><title>Restoration of metabolic inflammation-related ghrelin resistance by weight loss</title><author>Naznin, Farhana ; Toshinai, Koji ; Waise, T M Zaved ; Okada, Tadashi ; Sakoda, Hideyuki ; Nakazato, Masamitsu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b517t-24ffbb2a2b577db60c1852c523744ca95a5c2ab2db74b54c6407f48734191b4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Body weight loss</topic><topic>Cell activation</topic><topic>Cytokines</topic><topic>Ghrelin</topic><topic>High fat diet</topic><topic>Hsp72 protein</topic><topic>Hypothalamus</topic><topic>Inflammation</topic><topic>Macrophages</topic><topic>Metabolism</topic><topic>Microglia</topic><topic>Nodose ganglion</topic><topic>Obesity</topic><topic>Phenotypes</topic><topic>Rodents</topic><topic>Sensory neurons</topic><topic>Vagus nerve</topic><topic>Weight control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Naznin, Farhana</creatorcontrib><creatorcontrib>Toshinai, Koji</creatorcontrib><creatorcontrib>Waise, T M Zaved</creatorcontrib><creatorcontrib>Okada, Tadashi</creatorcontrib><creatorcontrib>Sakoda, Hideyuki</creatorcontrib><creatorcontrib>Nakazato, Masamitsu</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of molecular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Naznin, Farhana</au><au>Toshinai, Koji</au><au>Waise, T M Zaved</au><au>Okada, Tadashi</au><au>Sakoda, Hideyuki</au><au>Nakazato, Masamitsu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Restoration of metabolic inflammation-related ghrelin resistance by weight loss</atitle><jtitle>Journal of molecular endocrinology</jtitle><addtitle>J Mol Endocrinol</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>60</volume><issue>2</issue><spage>109</spage><epage>118</epage><pages>109-118</pages><issn>0952-5041</issn><eissn>1479-6813</eissn><abstract>High-fat diet (HFD)-induced metabolic inflammation in the central and peripheral organs contributes to the pathogenesis of obesity. 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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Society for Endocrinology Journals |
| subjects | Body weight loss Cell activation Cytokines Ghrelin High fat diet Hsp72 protein Hypothalamus Inflammation Macrophages Metabolism Microglia Nodose ganglion Obesity Phenotypes Rodents Sensory neurons Vagus nerve Weight control |
| title | Restoration of metabolic inflammation-related ghrelin resistance by weight loss |
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