Age-Dependent Control of Energy Homeostasis by Brown Adipose Tissue in Progeny Subjected to Maternal Diet-Induced Fetal Programming
Epidemiological and animal studies show that deleterious maternal environments predispose aging offspring to metabolic disorders and type 2 diabetes. Young progenies in a rat model of maternal low-protein (LP) diet are normoglycemic despite collapsed insulin secretion. However, without further worse...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2017-03, Vol.66 (3), p.627-639 |
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| creator | Dumortier, Olivier Roger, Estelle Pisani, Didier F Casamento, Virginie Gautier, Nadine Lebrun, Patricia Johnston, Hereroa Lopez, Pascal Amri, Ez-Zoubir Jousse, Céline Fafournoux, Pierre Prentki, Marc Hinault, Charlotte Van Obberghen, Emmanuel |
| description | Epidemiological and animal studies show that deleterious maternal environments predispose aging offspring to metabolic disorders and type 2 diabetes. Young progenies in a rat model of maternal low-protein (LP) diet are normoglycemic despite collapsed insulin secretion. However, without further worsening of the insulin secretion defect, glucose homeostasis deteriorates in aging LP descendants. Here we report that normoglycemic and insulinopenic 3-month-old LP progeny shows increased body temperature and energy dissipation in association with enhanced brown adipose tissue (BAT) activity. In addition, it is protected against a cold challenge and high-fat diet (HFD)-induced obesity with associated insulin resistance and hyperglycemia. Surgical BAT ablation in 3-month-old LP offspring normalizes body temperature and causes postprandial hyperglycemia. At 10 months, BAT activity declines in LP progeny with the appearance of reduced protection to HFD-induced obesity; at 18 months, LP progeny displays a BAT activity comparable to control offspring and insulin resistance and hyperglycemia occur. Together our findings identify BAT as a decisive physiological determinant of the onset of metabolic dysregulation in offspring predisposed to altered β-cell function and hyperglycemia and place it as a critical regulator of fetal programming of adult metabolic disease. |
| doi_str_mv | 10.2337/db16-0956 |
| format | Article |
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Young progenies in a rat model of maternal low-protein (LP) diet are normoglycemic despite collapsed insulin secretion. However, without further worsening of the insulin secretion defect, glucose homeostasis deteriorates in aging LP descendants. Here we report that normoglycemic and insulinopenic 3-month-old LP progeny shows increased body temperature and energy dissipation in association with enhanced brown adipose tissue (BAT) activity. In addition, it is protected against a cold challenge and high-fat diet (HFD)-induced obesity with associated insulin resistance and hyperglycemia. Surgical BAT ablation in 3-month-old LP offspring normalizes body temperature and causes postprandial hyperglycemia. At 10 months, BAT activity declines in LP progeny with the appearance of reduced protection to HFD-induced obesity; at 18 months, LP progeny displays a BAT activity comparable to control offspring and insulin resistance and hyperglycemia occur. Together our findings identify BAT as a decisive physiological determinant of the onset of metabolic dysregulation in offspring predisposed to altered β-cell function and hyperglycemia and place it as a critical regulator of fetal programming of adult metabolic disease.</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db16-0956</identifier><identifier>PMID: 27927722</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>United States: American Diabetes Association</publisher><subject>Adipose Tissue, Brown - metabolism ; Adipose Tissue, Brown - surgery ; Age Factors ; Animals ; Blood Glucose - metabolism ; Blotting, Western ; Body Temperature Regulation ; Diabetes ; Diabetes Mellitus, Type 2 - metabolism ; Diet, High-Fat ; Diet, Protein-Restricted ; Energy Metabolism ; Epidemiology ; Female ; Fetal Development ; Food and Nutrition ; Glucose ; Glucose Tolerance Test ; Homeostasis ; Hyperglycemia ; Hyperglycemia - metabolism ; Immunohistochemistry ; Insulin - metabolism ; Insulin Resistance ; Life Sciences ; Lipolysis ; Male ; Obesity - metabolism ; Postprandial Period ; Pregnancy ; Prenatal Exposure Delayed Effects - metabolism ; Rats ; Rats, Wistar ; Real-Time Polymerase Chain Reaction ; Santé publique et épidémiologie ; Triglycerides - metabolism</subject><ispartof>Diabetes (New York, N.Y.), 2017-03, Vol.66 (3), p.627-639</ispartof><rights>2017 by the American Diabetes Association.</rights><rights>Copyright American Diabetes Association Mar 1, 2017</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-74eb88a5aa91c78287c499f4dc67a6831921abd9f1618ec0dadcbc90c7c1bc9c3</citedby><cites>FETCH-LOGICAL-c448t-74eb88a5aa91c78287c499f4dc67a6831921abd9f1618ec0dadcbc90c7c1bc9c3</cites><orcidid>0000-0001-5879-8527 ; 0000-0002-3146-249X ; 0000-0002-9914-4252 ; 0000-0002-4900-4331 ; 0000-0001-8426-5396</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27927722$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01594882$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Dumortier, Olivier</creatorcontrib><creatorcontrib>Roger, Estelle</creatorcontrib><creatorcontrib>Pisani, Didier F</creatorcontrib><creatorcontrib>Casamento, Virginie</creatorcontrib><creatorcontrib>Gautier, Nadine</creatorcontrib><creatorcontrib>Lebrun, Patricia</creatorcontrib><creatorcontrib>Johnston, Hereroa</creatorcontrib><creatorcontrib>Lopez, Pascal</creatorcontrib><creatorcontrib>Amri, Ez-Zoubir</creatorcontrib><creatorcontrib>Jousse, Céline</creatorcontrib><creatorcontrib>Fafournoux, Pierre</creatorcontrib><creatorcontrib>Prentki, Marc</creatorcontrib><creatorcontrib>Hinault, Charlotte</creatorcontrib><creatorcontrib>Van Obberghen, Emmanuel</creatorcontrib><title>Age-Dependent Control of Energy Homeostasis by Brown Adipose Tissue in Progeny Subjected to Maternal Diet-Induced Fetal Programming</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Epidemiological and animal studies show that deleterious maternal environments predispose aging offspring to metabolic disorders and type 2 diabetes. Young progenies in a rat model of maternal low-protein (LP) diet are normoglycemic despite collapsed insulin secretion. However, without further worsening of the insulin secretion defect, glucose homeostasis deteriorates in aging LP descendants. Here we report that normoglycemic and insulinopenic 3-month-old LP progeny shows increased body temperature and energy dissipation in association with enhanced brown adipose tissue (BAT) activity. In addition, it is protected against a cold challenge and high-fat diet (HFD)-induced obesity with associated insulin resistance and hyperglycemia. Surgical BAT ablation in 3-month-old LP offspring normalizes body temperature and causes postprandial hyperglycemia. At 10 months, BAT activity declines in LP progeny with the appearance of reduced protection to HFD-induced obesity; at 18 months, LP progeny displays a BAT activity comparable to control offspring and insulin resistance and hyperglycemia occur. Together our findings identify BAT as a decisive physiological determinant of the onset of metabolic dysregulation in offspring predisposed to altered β-cell function and hyperglycemia and place it as a critical regulator of fetal programming of adult metabolic disease.</description><subject>Adipose Tissue, Brown - metabolism</subject><subject>Adipose Tissue, Brown - surgery</subject><subject>Age Factors</subject><subject>Animals</subject><subject>Blood Glucose - metabolism</subject><subject>Blotting, Western</subject><subject>Body Temperature Regulation</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diet, High-Fat</subject><subject>Diet, Protein-Restricted</subject><subject>Energy Metabolism</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Fetal Development</subject><subject>Food and Nutrition</subject><subject>Glucose</subject><subject>Glucose Tolerance Test</subject><subject>Homeostasis</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - metabolism</subject><subject>Immunohistochemistry</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance</subject><subject>Life Sciences</subject><subject>Lipolysis</subject><subject>Male</subject><subject>Obesity - metabolism</subject><subject>Postprandial Period</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Santé publique et épidémiologie</subject><subject>Triglycerides - metabolism</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkV1rFDEUhoNY7Fq98A9IwBu9mJqP2UlyuW5bt7BFwQrehUxyZs0yk2yTjLLX_nFnaK1QzsUL5zznixehN5ScM87FR9fSpiJq2TxDC6q4qjgTP56jBSGUVVQocYpe5rwnhDRTvECnTCgmBGML9Ge1g-oCDhAchILXMZQUexw7fBkg7Y54EweIuZjsM26P-FOKvwNeOX-IGfCtz3kE7AP-muIOwhF_G9s92AIOl4hvTIEUTI8vPJTqOrjRToUrKFNqbkhmGHzYvUInnekzvH7QM_T96vJ2vam2Xz5fr1fbyta1LJWooZXSLI1R1ArJpLC1Ul3tbCNMIzlVjJrWqY42VIIlzjjbWkWssHRSy8_Qh_u5P02vD8kPJh11NF5vVls95whdqlpK9otO7Pt79pDi3Qi56MFnC31vAsQxayprISVlqpnQd0_QfRznt2dKcM4aRuv_y22KOSfoHi-gRM8u6tlFPbs4sW8fJo7tAO6R_Gcb_wsEnZd2</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Dumortier, Olivier</creator><creator>Roger, Estelle</creator><creator>Pisani, Didier F</creator><creator>Casamento, Virginie</creator><creator>Gautier, Nadine</creator><creator>Lebrun, Patricia</creator><creator>Johnston, Hereroa</creator><creator>Lopez, Pascal</creator><creator>Amri, Ez-Zoubir</creator><creator>Jousse, Céline</creator><creator>Fafournoux, Pierre</creator><creator>Prentki, Marc</creator><creator>Hinault, Charlotte</creator><creator>Van Obberghen, Emmanuel</creator><general>American Diabetes Association</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-5879-8527</orcidid><orcidid>https://orcid.org/0000-0002-3146-249X</orcidid><orcidid>https://orcid.org/0000-0002-9914-4252</orcidid><orcidid>https://orcid.org/0000-0002-4900-4331</orcidid><orcidid>https://orcid.org/0000-0001-8426-5396</orcidid></search><sort><creationdate>20170301</creationdate><title>Age-Dependent Control of Energy Homeostasis by Brown Adipose Tissue in Progeny Subjected to Maternal Diet-Induced Fetal Programming</title><author>Dumortier, Olivier ; Roger, Estelle ; Pisani, Didier F ; Casamento, Virginie ; Gautier, Nadine ; Lebrun, Patricia ; Johnston, Hereroa ; Lopez, Pascal ; Amri, Ez-Zoubir ; Jousse, Céline ; Fafournoux, Pierre ; Prentki, Marc ; Hinault, Charlotte ; Van Obberghen, Emmanuel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-74eb88a5aa91c78287c499f4dc67a6831921abd9f1618ec0dadcbc90c7c1bc9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adipose Tissue, Brown - metabolism</topic><topic>Adipose Tissue, Brown - surgery</topic><topic>Age Factors</topic><topic>Animals</topic><topic>Blood Glucose - metabolism</topic><topic>Blotting, Western</topic><topic>Body Temperature Regulation</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diet, High-Fat</topic><topic>Diet, Protein-Restricted</topic><topic>Energy Metabolism</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Fetal Development</topic><topic>Food and Nutrition</topic><topic>Glucose</topic><topic>Glucose Tolerance Test</topic><topic>Homeostasis</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - metabolism</topic><topic>Immunohistochemistry</topic><topic>Insulin - metabolism</topic><topic>Insulin Resistance</topic><topic>Life Sciences</topic><topic>Lipolysis</topic><topic>Male</topic><topic>Obesity - metabolism</topic><topic>Postprandial Period</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Santé publique et épidémiologie</topic><topic>Triglycerides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dumortier, Olivier</creatorcontrib><creatorcontrib>Roger, Estelle</creatorcontrib><creatorcontrib>Pisani, Didier F</creatorcontrib><creatorcontrib>Casamento, Virginie</creatorcontrib><creatorcontrib>Gautier, Nadine</creatorcontrib><creatorcontrib>Lebrun, Patricia</creatorcontrib><creatorcontrib>Johnston, Hereroa</creatorcontrib><creatorcontrib>Lopez, Pascal</creatorcontrib><creatorcontrib>Amri, Ez-Zoubir</creatorcontrib><creatorcontrib>Jousse, Céline</creatorcontrib><creatorcontrib>Fafournoux, Pierre</creatorcontrib><creatorcontrib>Prentki, Marc</creatorcontrib><creatorcontrib>Hinault, Charlotte</creatorcontrib><creatorcontrib>Van Obberghen, Emmanuel</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 Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dumortier, Olivier</au><au>Roger, Estelle</au><au>Pisani, Didier F</au><au>Casamento, Virginie</au><au>Gautier, Nadine</au><au>Lebrun, Patricia</au><au>Johnston, Hereroa</au><au>Lopez, Pascal</au><au>Amri, Ez-Zoubir</au><au>Jousse, Céline</au><au>Fafournoux, Pierre</au><au>Prentki, Marc</au><au>Hinault, Charlotte</au><au>Van Obberghen, Emmanuel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Age-Dependent Control of Energy Homeostasis by Brown Adipose Tissue in Progeny Subjected to Maternal Diet-Induced Fetal Programming</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><addtitle>Diabetes</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>66</volume><issue>3</issue><spage>627</spage><epage>639</epage><pages>627-639</pages><issn>0012-1797</issn><eissn>1939-327X</eissn><coden>DIAEAZ</coden><abstract>Epidemiological and animal studies show that deleterious maternal environments predispose aging offspring to metabolic disorders and type 2 diabetes. Young progenies in a rat model of maternal low-protein (LP) diet are normoglycemic despite collapsed insulin secretion. However, without further worsening of the insulin secretion defect, glucose homeostasis deteriorates in aging LP descendants. Here we report that normoglycemic and insulinopenic 3-month-old LP progeny shows increased body temperature and energy dissipation in association with enhanced brown adipose tissue (BAT) activity. In addition, it is protected against a cold challenge and high-fat diet (HFD)-induced obesity with associated insulin resistance and hyperglycemia. Surgical BAT ablation in 3-month-old LP offspring normalizes body temperature and causes postprandial hyperglycemia. At 10 months, BAT activity declines in LP progeny with the appearance of reduced protection to HFD-induced obesity; at 18 months, LP progeny displays a BAT activity comparable to control offspring and insulin resistance and hyperglycemia occur. Together our findings identify BAT as a decisive physiological determinant of the onset of metabolic dysregulation in offspring predisposed to altered β-cell function and hyperglycemia and place it as a critical regulator of fetal programming of adult metabolic disease.</abstract><cop>United States</cop><pub>American Diabetes Association</pub><pmid>27927722</pmid><doi>10.2337/db16-0956</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-5879-8527</orcidid><orcidid>https://orcid.org/0000-0002-3146-249X</orcidid><orcidid>https://orcid.org/0000-0002-9914-4252</orcidid><orcidid>https://orcid.org/0000-0002-4900-4331</orcidid><orcidid>https://orcid.org/0000-0001-8426-5396</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetes (New York, N.Y.), 2017-03, Vol.66 (3), p.627-639 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Adipose Tissue, Brown - metabolism Adipose Tissue, Brown - surgery Age Factors Animals Blood Glucose - metabolism Blotting, Western Body Temperature Regulation Diabetes Diabetes Mellitus, Type 2 - metabolism Diet, High-Fat Diet, Protein-Restricted Energy Metabolism Epidemiology Female Fetal Development Food and Nutrition Glucose Glucose Tolerance Test Homeostasis Hyperglycemia Hyperglycemia - metabolism Immunohistochemistry Insulin - metabolism Insulin Resistance Life Sciences Lipolysis Male Obesity - metabolism Postprandial Period Pregnancy Prenatal Exposure Delayed Effects - metabolism Rats Rats, Wistar Real-Time Polymerase Chain Reaction Santé publique et épidémiologie Triglycerides - metabolism |
| title | Age-Dependent Control of Energy Homeostasis by Brown Adipose Tissue in Progeny Subjected to Maternal Diet-Induced Fetal Programming |
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