Early life stress induces type 2 diabetes-like features in ageing mice
•Maternal separation is a risk factor for glucose intolerance in ageing mice.•Maternal separation induces microbiota dysbiosis in favor to pathobionts.•Maternal separation-induced glucose intolerance is associated with decrease of intestinal IL-17 and IL-22 responses. Early life stress is known to i...
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| Veröffentlicht in: | Brain, behavior, and immunity behavior, and immunity, 2019-08, Vol.80, p.452-463 |
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| creator | Ilchmann-Diounou, Hanna Olier, Maïwenn Lencina, Corinne Riba, Ambre Barretto, Sharon Nankap, Michèle Sommer, Caroline Guillou, Hervé Ellero-Simatos, Sandrine Guzylack-Piriou, Laurence Théodorou, Vassilia Ménard, Sandrine |
| description | •Maternal separation is a risk factor for glucose intolerance in ageing mice.•Maternal separation induces microbiota dysbiosis in favor to pathobionts.•Maternal separation-induced glucose intolerance is associated with decrease of intestinal IL-17 and IL-22 responses.
Early life stress is known to impair intestinal barrier through induction of intestinal hyperpermeability, low-grade inflammation and microbiota dysbiosis in young adult rodents. Interestingly, those features are also observed in metabolic disorders (obesity and type 2 diabetes) that appear with ageing. Based on the concept of Developmental Origins of Health and Diseases, our study aimed to investigate whether early life stress can trigger metabolic disorders in ageing mice.
Maternal separation (MS) is a well-established model of early life stress in rodent. In this study, MS increased fasted blood glycemia, induced glucose intolerance and decreased insulin sensitivity in post-natal day 350 wild type C3H/HeN male mice fed a standard diet without affecting body weight. MS also triggered fecal dysbiosis favoring pathobionts and significantly decreased IL-17 and IL-22 secretion in response to anti-CD3/CD28 stimulation in small intestine lamina propria. Finally, IL-17 secretion in response to anti-CD3/CD28 stimulation was also diminished at systemic level (spleen).
For the first time, we demonstrate that early life stress is a risk factor for metabolic disorders development in ageing wild type mice under normal diet. |
| doi_str_mv | 10.1016/j.bbi.2019.04.025 |
| format | Article |
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Early life stress is known to impair intestinal barrier through induction of intestinal hyperpermeability, low-grade inflammation and microbiota dysbiosis in young adult rodents. Interestingly, those features are also observed in metabolic disorders (obesity and type 2 diabetes) that appear with ageing. Based on the concept of Developmental Origins of Health and Diseases, our study aimed to investigate whether early life stress can trigger metabolic disorders in ageing mice.
Maternal separation (MS) is a well-established model of early life stress in rodent. In this study, MS increased fasted blood glycemia, induced glucose intolerance and decreased insulin sensitivity in post-natal day 350 wild type C3H/HeN male mice fed a standard diet without affecting body weight. MS also triggered fecal dysbiosis favoring pathobionts and significantly decreased IL-17 and IL-22 secretion in response to anti-CD3/CD28 stimulation in small intestine lamina propria. Finally, IL-17 secretion in response to anti-CD3/CD28 stimulation was also diminished at systemic level (spleen).
For the first time, we demonstrate that early life stress is a risk factor for metabolic disorders development in ageing wild type mice under normal diet.</description><identifier>ISSN: 0889-1591</identifier><identifier>EISSN: 1090-2139</identifier><identifier>DOI: 10.1016/j.bbi.2019.04.025</identifier><identifier>PMID: 30981713</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Diabetes Mellitus, Type 2 - complications ; DOHaD ; Dysbiosis - metabolism ; Female ; Gastrointestinal Microbiome - physiology ; Glucose Intolerance - etiology ; Glucose Intolerance - metabolism ; Glucose Intolerance - physiopathology ; Inflammation - metabolism ; Insulin Resistance - physiology ; Intestinal barrier ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - microbiology ; Intestines - microbiology ; Life Sciences ; Male ; Maternal Deprivation ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Microbiota - physiology ; Microbiota dysbiosis ; Non-communicable diseases ; Obesity - metabolism ; Stress, Psychological - physiopathology</subject><ispartof>Brain, behavior, and immunity, 2019-08, Vol.80, p.452-463</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</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-c430t-d9327d1015d6d8f2cb6a17ac432065a6f8ddf82486b3b10c768f4068a85767373</citedby><cites>FETCH-LOGICAL-c430t-d9327d1015d6d8f2cb6a17ac432065a6f8ddf82486b3b10c768f4068a85767373</cites><orcidid>0000-0002-0052-5435 ; 0000-0001-8867-199X ; 0000-0001-7214-1134 ; 0000-0002-9282-1804 ; 0000-0002-6078-1705</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbi.2019.04.025$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,778,782,883,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30981713$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.inrae.fr/hal-02627238$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Ilchmann-Diounou, Hanna</creatorcontrib><creatorcontrib>Olier, Maïwenn</creatorcontrib><creatorcontrib>Lencina, Corinne</creatorcontrib><creatorcontrib>Riba, Ambre</creatorcontrib><creatorcontrib>Barretto, Sharon</creatorcontrib><creatorcontrib>Nankap, Michèle</creatorcontrib><creatorcontrib>Sommer, Caroline</creatorcontrib><creatorcontrib>Guillou, Hervé</creatorcontrib><creatorcontrib>Ellero-Simatos, Sandrine</creatorcontrib><creatorcontrib>Guzylack-Piriou, Laurence</creatorcontrib><creatorcontrib>Théodorou, Vassilia</creatorcontrib><creatorcontrib>Ménard, Sandrine</creatorcontrib><title>Early life stress induces type 2 diabetes-like features in ageing mice</title><title>Brain, behavior, and immunity</title><addtitle>Brain Behav Immun</addtitle><description>•Maternal separation is a risk factor for glucose intolerance in ageing mice.•Maternal separation induces microbiota dysbiosis in favor to pathobionts.•Maternal separation-induced glucose intolerance is associated with decrease of intestinal IL-17 and IL-22 responses.
Early life stress is known to impair intestinal barrier through induction of intestinal hyperpermeability, low-grade inflammation and microbiota dysbiosis in young adult rodents. Interestingly, those features are also observed in metabolic disorders (obesity and type 2 diabetes) that appear with ageing. Based on the concept of Developmental Origins of Health and Diseases, our study aimed to investigate whether early life stress can trigger metabolic disorders in ageing mice.
Maternal separation (MS) is a well-established model of early life stress in rodent. In this study, MS increased fasted blood glycemia, induced glucose intolerance and decreased insulin sensitivity in post-natal day 350 wild type C3H/HeN male mice fed a standard diet without affecting body weight. MS also triggered fecal dysbiosis favoring pathobionts and significantly decreased IL-17 and IL-22 secretion in response to anti-CD3/CD28 stimulation in small intestine lamina propria. Finally, IL-17 secretion in response to anti-CD3/CD28 stimulation was also diminished at systemic level (spleen).
For the first time, we demonstrate that early life stress is a risk factor for metabolic disorders development in ageing wild type mice under normal diet.</description><subject>Animals</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>DOHaD</subject><subject>Dysbiosis - metabolism</subject><subject>Female</subject><subject>Gastrointestinal Microbiome - physiology</subject><subject>Glucose Intolerance - etiology</subject><subject>Glucose Intolerance - metabolism</subject><subject>Glucose Intolerance - physiopathology</subject><subject>Inflammation - metabolism</subject><subject>Insulin Resistance - physiology</subject><subject>Intestinal barrier</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - microbiology</subject><subject>Intestines - microbiology</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Maternal Deprivation</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Microbiota - physiology</subject><subject>Microbiota dysbiosis</subject><subject>Non-communicable diseases</subject><subject>Obesity - metabolism</subject><subject>Stress, Psychological - physiopathology</subject><issn>0889-1591</issn><issn>1090-2139</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LAzEQhoMotlZ_gBfJ1cOuk2Q3yeKpSGuFghc9h2wyW1O3H2y2hf57U6o9ehqYeZ5h5iXknkHOgMmnZV7XIefAqhyKHHh5QYYMKsg4E9UlGYLWVcbKig3ITYxLACgF09dkIKDSTDExJNOJ7doDbUODNPYdxkjD2u8cRtoftkg59cHW2GPM2vCNtEHb7xKWKGoXGNYLugoOb8lVY9uId791RD6nk4-XWTZ_f317Gc8zVwjoM18Jrny6vfTS64a7WlqmbBpykKWVjfa-0bzQshY1A6ekbgqQ2upSSSWUGJHH094v25ptF1a2O5iNDWY2nptjD7jkigu9Z4llJ9Z1mxg7bM4CA3PMzyxNys8c8zNQJLVMzsPJ2e7qFfqz8RdYAp5PAKYv9wE7E13AtUMfOnS98Zvwz_ofeZ9-Dg</recordid><startdate>20190801</startdate><enddate>20190801</enddate><creator>Ilchmann-Diounou, Hanna</creator><creator>Olier, Maïwenn</creator><creator>Lencina, Corinne</creator><creator>Riba, Ambre</creator><creator>Barretto, Sharon</creator><creator>Nankap, Michèle</creator><creator>Sommer, Caroline</creator><creator>Guillou, Hervé</creator><creator>Ellero-Simatos, Sandrine</creator><creator>Guzylack-Piriou, Laurence</creator><creator>Théodorou, Vassilia</creator><creator>Ménard, Sandrine</creator><general>Elsevier Inc</general><general>Elsevier</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>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0002-0052-5435</orcidid><orcidid>https://orcid.org/0000-0001-8867-199X</orcidid><orcidid>https://orcid.org/0000-0001-7214-1134</orcidid><orcidid>https://orcid.org/0000-0002-9282-1804</orcidid><orcidid>https://orcid.org/0000-0002-6078-1705</orcidid></search><sort><creationdate>20190801</creationdate><title>Early life stress induces type 2 diabetes-like features in ageing mice</title><author>Ilchmann-Diounou, Hanna ; 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Early life stress is known to impair intestinal barrier through induction of intestinal hyperpermeability, low-grade inflammation and microbiota dysbiosis in young adult rodents. Interestingly, those features are also observed in metabolic disorders (obesity and type 2 diabetes) that appear with ageing. Based on the concept of Developmental Origins of Health and Diseases, our study aimed to investigate whether early life stress can trigger metabolic disorders in ageing mice.
Maternal separation (MS) is a well-established model of early life stress in rodent. In this study, MS increased fasted blood glycemia, induced glucose intolerance and decreased insulin sensitivity in post-natal day 350 wild type C3H/HeN male mice fed a standard diet without affecting body weight. MS also triggered fecal dysbiosis favoring pathobionts and significantly decreased IL-17 and IL-22 secretion in response to anti-CD3/CD28 stimulation in small intestine lamina propria. Finally, IL-17 secretion in response to anti-CD3/CD28 stimulation was also diminished at systemic level (spleen).
For the first time, we demonstrate that early life stress is a risk factor for metabolic disorders development in ageing wild type mice under normal diet.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>30981713</pmid><doi>10.1016/j.bbi.2019.04.025</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0052-5435</orcidid><orcidid>https://orcid.org/0000-0001-8867-199X</orcidid><orcidid>https://orcid.org/0000-0001-7214-1134</orcidid><orcidid>https://orcid.org/0000-0002-9282-1804</orcidid><orcidid>https://orcid.org/0000-0002-6078-1705</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Brain, behavior, and immunity, 2019-08, Vol.80, p.452-463 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Diabetes Mellitus, Type 2 - complications DOHaD Dysbiosis - metabolism Female Gastrointestinal Microbiome - physiology Glucose Intolerance - etiology Glucose Intolerance - metabolism Glucose Intolerance - physiopathology Inflammation - metabolism Insulin Resistance - physiology Intestinal barrier Intestinal Mucosa - metabolism Intestinal Mucosa - microbiology Intestines - microbiology Life Sciences Male Maternal Deprivation Mice Mice, Inbred C3H Mice, Inbred C57BL Microbiota - physiology Microbiota dysbiosis Non-communicable diseases Obesity - metabolism Stress, Psychological - physiopathology |
| title | Early life stress induces type 2 diabetes-like features in ageing mice |
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