Preweaning Growth Hormone Treatment Ameliorates Adipose Tissue Insulin Resistance and Inflammation in Adult Male Offspring Following Maternal Undernutrition
It is well established that early-life nutritional alterations lead to increased risk of obesity and metabolic disorders in adult life. Although it is clear that obesity gives rise to chronic low-grade inflammation, there is little evidence regarding the role of inflammation in the adipose tissue of...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2013-08, Vol.154 (8), p.2676-2686 |
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| description | It is well established that early-life nutritional alterations lead to increased risk of obesity and metabolic disorders in adult life. Although it is clear that obesity gives rise to chronic low-grade inflammation, there is little evidence regarding the role of inflammation in the adipose tissue of undernourished (UN) offspring. GH reduces fat mass and has antiinflammatory properties. The present study examined the effect of maternal UN on adipose inflammation in adult offspring and whether GH treatment during a critical period of developmental plasticity could ameliorate metabolic dysfunction associated with a poor start to life. Sprague Dawley rats were assigned to chow (C) or UN (50% ad libitum; UN) diet throughout gestation. Male C and UN pups received saline (control saline [CS]/UN) or GH (2.5 μg/g/d; control growth hormone [CGH]/undernourished growth hormone [UNGH]) from days 3–21. Postweaning males were further randomized and fed either chow or high-fat diet until day 160. An ex vivo glucose uptake assay demonstrated adipose tissue from UN offspring displayed attenuated insulin-stimulated glucose uptake compared with CS, CGH, and UNGH. This was associated with increased insulin receptor, glucose transporter 4, and insulin receptor substrate 1 gene expression. Furthermore, UN demonstrated enhanced TNFα and IL-1β secretion from adipose explants and stromal vascular fraction cultures accompanied by increased adipose tissue gene expression of several key proinflammatory genes and markers of macrophage infiltration. Overall, UN offspring displayed a more potent immunophenotype, which correlated with decreased insulin sensitivity. Preweaning GH treatment negates these detrimental effects, indicating the potential for reversing metabolic dysfunction in UN adult offspring. |
| doi_str_mv | 10.1210/en.2013-1146 |
| format | Article |
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M ; Li, M ; Gray, C ; Vickers, M. H</creator><creatorcontrib>Reynolds, C. M ; Li, M ; Gray, C ; Vickers, M. H</creatorcontrib><description>It is well established that early-life nutritional alterations lead to increased risk of obesity and metabolic disorders in adult life. Although it is clear that obesity gives rise to chronic low-grade inflammation, there is little evidence regarding the role of inflammation in the adipose tissue of undernourished (UN) offspring. GH reduces fat mass and has antiinflammatory properties. The present study examined the effect of maternal UN on adipose inflammation in adult offspring and whether GH treatment during a critical period of developmental plasticity could ameliorate metabolic dysfunction associated with a poor start to life. Sprague Dawley rats were assigned to chow (C) or UN (50% ad libitum; UN) diet throughout gestation. Male C and UN pups received saline (control saline [CS]/UN) or GH (2.5 μg/g/d; control growth hormone [CGH]/undernourished growth hormone [UNGH]) from days 3–21. Postweaning males were further randomized and fed either chow or high-fat diet until day 160. An ex vivo glucose uptake assay demonstrated adipose tissue from UN offspring displayed attenuated insulin-stimulated glucose uptake compared with CS, CGH, and UNGH. This was associated with increased insulin receptor, glucose transporter 4, and insulin receptor substrate 1 gene expression. Furthermore, UN demonstrated enhanced TNFα and IL-1β secretion from adipose explants and stromal vascular fraction cultures accompanied by increased adipose tissue gene expression of several key proinflammatory genes and markers of macrophage infiltration. Overall, UN offspring displayed a more potent immunophenotype, which correlated with decreased insulin sensitivity. Preweaning GH treatment negates these detrimental effects, indicating the potential for reversing metabolic dysfunction in UN adult offspring.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2013-1146</identifier><identifier>PMID: 23715866</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Chevy Chase, MD: Endocrine Society</publisher><subject>Adipose tissue ; Adipose Tissue - drug effects ; Adipose Tissue - metabolism ; Adipose Tissue - physiopathology ; Animals ; Animals, Newborn ; Anti-inflammatory agents ; Biological and medical sciences ; Blood Glucose - metabolism ; Body fat ; Body Weight - drug effects ; Critical period ; Cytokines - blood ; Developmental plasticity ; Diet ; Diet, High-Fat ; Explants ; Female ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression - drug effects ; Glucose ; Glucose transporter ; Glucose Transporter Type 4 - genetics ; Growth Hormone - administration & dosage ; Growth Hormone - pharmacology ; Growth hormones ; High fat diet ; Inflammation ; Inflammation - genetics ; Inflammation - physiopathology ; Inflammation - prevention & control ; Insulin ; Insulin - blood ; Insulin receptor substrate 1 ; Insulin Receptor Substrate Proteins - genetics ; Insulin receptors ; Insulin Resistance ; Macrophages ; Male ; Males ; Malnutrition ; Maternal Nutritional Physiological Phenomena ; Medical sciences ; Metabolic diseases ; Metabolic disorders ; Metabolism ; Obesity ; Offspring ; Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...) ; Pregnancy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptor, Insulin - genetics ; Receptors ; Reverse Transcriptase Polymerase Chain Reaction ; Undernutrition ; Vertebrates: endocrinology ; Weaning</subject><ispartof>Endocrinology (Philadelphia), 2013-08, Vol.154 (8), p.2676-2686</ispartof><rights>Copyright © 2013 by The Endocrine Society</rights><rights>Copyright © 2013 by The Endocrine Society 2013</rights><rights>2014 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-5e5fe5fe290180aa646550ac36053e2ca9782e61e4a6f48cf1aee19d3c1636183</citedby><cites>FETCH-LOGICAL-c463t-5e5fe5fe290180aa646550ac36053e2ca9782e61e4a6f48cf1aee19d3c1636183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27574355$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23715866$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reynolds, C. M</creatorcontrib><creatorcontrib>Li, M</creatorcontrib><creatorcontrib>Gray, C</creatorcontrib><creatorcontrib>Vickers, M. H</creatorcontrib><title>Preweaning Growth Hormone Treatment Ameliorates Adipose Tissue Insulin Resistance and Inflammation in Adult Male Offspring Following Maternal Undernutrition</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>It is well established that early-life nutritional alterations lead to increased risk of obesity and metabolic disorders in adult life. Although it is clear that obesity gives rise to chronic low-grade inflammation, there is little evidence regarding the role of inflammation in the adipose tissue of undernourished (UN) offspring. GH reduces fat mass and has antiinflammatory properties. The present study examined the effect of maternal UN on adipose inflammation in adult offspring and whether GH treatment during a critical period of developmental plasticity could ameliorate metabolic dysfunction associated with a poor start to life. Sprague Dawley rats were assigned to chow (C) or UN (50% ad libitum; UN) diet throughout gestation. Male C and UN pups received saline (control saline [CS]/UN) or GH (2.5 μg/g/d; control growth hormone [CGH]/undernourished growth hormone [UNGH]) from days 3–21. Postweaning males were further randomized and fed either chow or high-fat diet until day 160. An ex vivo glucose uptake assay demonstrated adipose tissue from UN offspring displayed attenuated insulin-stimulated glucose uptake compared with CS, CGH, and UNGH. This was associated with increased insulin receptor, glucose transporter 4, and insulin receptor substrate 1 gene expression. Furthermore, UN demonstrated enhanced TNFα and IL-1β secretion from adipose explants and stromal vascular fraction cultures accompanied by increased adipose tissue gene expression of several key proinflammatory genes and markers of macrophage infiltration. Overall, UN offspring displayed a more potent immunophenotype, which correlated with decreased insulin sensitivity. Preweaning GH treatment negates these detrimental effects, indicating the potential for reversing metabolic dysfunction in UN adult offspring.</description><subject>Adipose tissue</subject><subject>Adipose Tissue - drug effects</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - physiopathology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Anti-inflammatory agents</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Body fat</subject><subject>Body Weight - drug effects</subject><subject>Critical period</subject><subject>Cytokines - blood</subject><subject>Developmental plasticity</subject><subject>Diet</subject><subject>Diet, High-Fat</subject><subject>Explants</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression - drug effects</subject><subject>Glucose</subject><subject>Glucose transporter</subject><subject>Glucose Transporter Type 4 - genetics</subject><subject>Growth Hormone - administration & dosage</subject><subject>Growth Hormone - pharmacology</subject><subject>Growth hormones</subject><subject>High fat diet</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - physiopathology</subject><subject>Inflammation - prevention & control</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin receptor substrate 1</subject><subject>Insulin Receptor Substrate Proteins - genetics</subject><subject>Insulin receptors</subject><subject>Insulin Resistance</subject><subject>Macrophages</subject><subject>Male</subject><subject>Males</subject><subject>Malnutrition</subject><subject>Maternal Nutritional Physiological Phenomena</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Metabolic disorders</subject><subject>Metabolism</subject><subject>Obesity</subject><subject>Offspring</subject><subject>Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)</subject><subject>Pregnancy</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Insulin - genetics</subject><subject>Receptors</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Undernutrition</subject><subject>Vertebrates: endocrinology</subject><subject>Weaning</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kVuL1TAQx4so7nH1zWcJiOiDXTO5tX08LO4FdlmR3ecS26lmSZOaaTn4XfywppyjC6IQyGTmN7f8i-Il8BMQwD9gOBEcZAmgzKNiA43SZQUVf1xs-OqvhKiOimdE9_mplJJPiyMhK9C1MZvi56eEO7TBha_sPMXd_I1dxDTGgOw2oZ1HDDPbjuhdTHZGYtveTZFy1BEtyC4DLd4F9hnJ0WxDh8yGPrsHb8fRzi4GlsPbfvEzu7Ye2c0w0JTWfmfR-7hbretcOgXr2V3os7HMya2Zz4sng_WELw73cXF39vH29KK8ujm_PN1elZ0yci416mE9ouFQc2uNMlpz20nDtUTR2aaqBRpAZc2g6m4AiwhNLzsw0kAtj4t3-7pTit8XpLkdHXXovQ0YF2pBARhRmYZn9PVf6H1c1tGplSC5EQJAZur9nupSJEo4tHnj0aYfLfB2Va3F0K6qtatqGX91KLp8GbH_A_-WKQNvDoClzvoh5Y929MBVulJS68y93XNxmf7Xsjy0lHsSQx-7LAdOCYketvnnoL8ANvW-eg</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Reynolds, C. 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H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-5e5fe5fe290180aa646550ac36053e2ca9782e61e4a6f48cf1aee19d3c1636183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adipose tissue</topic><topic>Adipose Tissue - drug effects</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - physiopathology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Anti-inflammatory agents</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Body fat</topic><topic>Body Weight - drug effects</topic><topic>Critical period</topic><topic>Cytokines - blood</topic><topic>Developmental plasticity</topic><topic>Diet</topic><topic>Diet, High-Fat</topic><topic>Explants</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Gene Expression - drug effects</topic><topic>Glucose</topic><topic>Glucose transporter</topic><topic>Glucose Transporter Type 4 - genetics</topic><topic>Growth Hormone - administration & dosage</topic><topic>Growth Hormone - pharmacology</topic><topic>Growth hormones</topic><topic>High fat diet</topic><topic>Inflammation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - physiopathology</topic><topic>Inflammation - prevention & control</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Insulin receptor substrate 1</topic><topic>Insulin Receptor Substrate Proteins - genetics</topic><topic>Insulin receptors</topic><topic>Insulin Resistance</topic><topic>Macrophages</topic><topic>Male</topic><topic>Males</topic><topic>Malnutrition</topic><topic>Maternal Nutritional Physiological Phenomena</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Metabolic disorders</topic><topic>Metabolism</topic><topic>Obesity</topic><topic>Offspring</topic><topic>Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...)</topic><topic>Pregnancy</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Insulin - genetics</topic><topic>Receptors</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Undernutrition</topic><topic>Vertebrates: endocrinology</topic><topic>Weaning</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reynolds, C. 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M</au><au>Li, M</au><au>Gray, C</au><au>Vickers, M. H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preweaning Growth Hormone Treatment Ameliorates Adipose Tissue Insulin Resistance and Inflammation in Adult Male Offspring Following Maternal Undernutrition</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2013-08-01</date><risdate>2013</risdate><volume>154</volume><issue>8</issue><spage>2676</spage><epage>2686</epage><pages>2676-2686</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>It is well established that early-life nutritional alterations lead to increased risk of obesity and metabolic disorders in adult life. Although it is clear that obesity gives rise to chronic low-grade inflammation, there is little evidence regarding the role of inflammation in the adipose tissue of undernourished (UN) offspring. GH reduces fat mass and has antiinflammatory properties. The present study examined the effect of maternal UN on adipose inflammation in adult offspring and whether GH treatment during a critical period of developmental plasticity could ameliorate metabolic dysfunction associated with a poor start to life. Sprague Dawley rats were assigned to chow (C) or UN (50% ad libitum; UN) diet throughout gestation. Male C and UN pups received saline (control saline [CS]/UN) or GH (2.5 μg/g/d; control growth hormone [CGH]/undernourished growth hormone [UNGH]) from days 3–21. Postweaning males were further randomized and fed either chow or high-fat diet until day 160. An ex vivo glucose uptake assay demonstrated adipose tissue from UN offspring displayed attenuated insulin-stimulated glucose uptake compared with CS, CGH, and UNGH. This was associated with increased insulin receptor, glucose transporter 4, and insulin receptor substrate 1 gene expression. Furthermore, UN demonstrated enhanced TNFα and IL-1β secretion from adipose explants and stromal vascular fraction cultures accompanied by increased adipose tissue gene expression of several key proinflammatory genes and markers of macrophage infiltration. Overall, UN offspring displayed a more potent immunophenotype, which correlated with decreased insulin sensitivity. Preweaning GH treatment negates these detrimental effects, indicating the potential for reversing metabolic dysfunction in UN adult offspring.</abstract><cop>Chevy Chase, MD</cop><pub>Endocrine Society</pub><pmid>23715866</pmid><doi>10.1210/en.2013-1146</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Oxford University Press Journals All Titles (1996-Current); Alma/SFX Local Collection |
| subjects | Adipose tissue Adipose Tissue - drug effects Adipose Tissue - metabolism Adipose Tissue - physiopathology Animals Animals, Newborn Anti-inflammatory agents Biological and medical sciences Blood Glucose - metabolism Body fat Body Weight - drug effects Critical period Cytokines - blood Developmental plasticity Diet Diet, High-Fat Explants Female Fundamental and applied biological sciences. Psychology Gene expression Gene Expression - drug effects Glucose Glucose transporter Glucose Transporter Type 4 - genetics Growth Hormone - administration & dosage Growth Hormone - pharmacology Growth hormones High fat diet Inflammation Inflammation - genetics Inflammation - physiopathology Inflammation - prevention & control Insulin Insulin - blood Insulin receptor substrate 1 Insulin Receptor Substrate Proteins - genetics Insulin receptors Insulin Resistance Macrophages Male Males Malnutrition Maternal Nutritional Physiological Phenomena Medical sciences Metabolic diseases Metabolic disorders Metabolism Obesity Offspring Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...) Pregnancy Random Allocation Rats Rats, Sprague-Dawley Receptor, Insulin - genetics Receptors Reverse Transcriptase Polymerase Chain Reaction Undernutrition Vertebrates: endocrinology Weaning |
| title | Preweaning Growth Hormone Treatment Ameliorates Adipose Tissue Insulin Resistance and Inflammation in Adult Male Offspring Following Maternal Undernutrition |
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