Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)
Diabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed...
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| Veröffentlicht in: | Lipids in health and disease 2016-11, Vol.15 (1), p.205-205, Article 205 |
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| creator | Dain, Alejandro Repossi, Gaston Diaz-Gerevini, Gustavo T Vanamala, Jairam Das, Undurti N Eynard, Aldo R |
| description | Diabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed the effects of supplementation of ω-3 and ω-6 polyunsaturated fatty acids (PUFAs) with or without nordihydroguaiaretic acid (NDGA) added, an antioxidant and lipoxygenase inhibitor, on metabolic and inflammatory parameters in eSS rats to evaluate whether they can delay development and/or prevent progression of DM.
After weaning, eSS rats received, intraperitoneally, once a month ω-3 (EPA 35% and DHA 40%-6.25 mg/Kg) or ω-6 (90% arachidonic acid- 6. 25 mg/Kg) for twelve months. Two additional groups of rats received 1.9 mg/kg NDGA added to ω-3 and ω-6 fatty acids. Blood samples were collected at day 40, and at the end of the 6th month and 12th month of age to determine plasma triglycerides (TGs), total plasma fatty acids (FA), A1C hemoglobin (HbA1C), C-reactive protein (CRP), gamma glutamyl transpeptidase (GGT), lipo and hydro peroxides, nitrites and IL-6 (in plasma and liver, kidney, and pancreas) and underwent oral glucose tolerance test (OGTT) as well. Wistar and eSS rats that received saline solution were used as controls.
Plasma lipids profile, TG, fasting and post-prandial blood glucose levels, and glycosylated HbA1C showed significant improvements in ω-3 and ω-3 + NDGA treated animals compared to eSS control group. ω-3 and ω-3 + NDGA groups showed an inverse correlation with fasting blood glucose and showed lower plasma levels of GGT, TG, and CRP. eSS rats treated with ω-3 LCPUFAs showed reduced level of inflammatory and oxidative indices in plasma and liver, kidney and pancreas tissues in comparison with eSS control (non-treated) and ω-6 treated groups.
eSS rats are a useful model to study type 2 DM pathophysiology and related inflammatory indices. ω-3 + NDGA supplementation, at the doses tested, ameliorated inflammatory, metabolic and oxidative stress markers studied. |
| doi_str_mv | 10.1186/s12944-016-0363-8 |
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After weaning, eSS rats received, intraperitoneally, once a month ω-3 (EPA 35% and DHA 40%-6.25 mg/Kg) or ω-6 (90% arachidonic acid- 6. 25 mg/Kg) for twelve months. Two additional groups of rats received 1.9 mg/kg NDGA added to ω-3 and ω-6 fatty acids. Blood samples were collected at day 40, and at the end of the 6th month and 12th month of age to determine plasma triglycerides (TGs), total plasma fatty acids (FA), A1C hemoglobin (HbA1C), C-reactive protein (CRP), gamma glutamyl transpeptidase (GGT), lipo and hydro peroxides, nitrites and IL-6 (in plasma and liver, kidney, and pancreas) and underwent oral glucose tolerance test (OGTT) as well. Wistar and eSS rats that received saline solution were used as controls.
Plasma lipids profile, TG, fasting and post-prandial blood glucose levels, and glycosylated HbA1C showed significant improvements in ω-3 and ω-3 + NDGA treated animals compared to eSS control group. ω-3 and ω-3 + NDGA groups showed an inverse correlation with fasting blood glucose and showed lower plasma levels of GGT, TG, and CRP. eSS rats treated with ω-3 LCPUFAs showed reduced level of inflammatory and oxidative indices in plasma and liver, kidney and pancreas tissues in comparison with eSS control (non-treated) and ω-6 treated groups.
eSS rats are a useful model to study type 2 DM pathophysiology and related inflammatory indices. ω-3 + NDGA supplementation, at the doses tested, ameliorated inflammatory, metabolic and oxidative stress markers studied.</description><identifier>ISSN: 1476-511X</identifier><identifier>EISSN: 1476-511X</identifier><identifier>DOI: 10.1186/s12944-016-0363-8</identifier><identifier>PMID: 27884155</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Animals ; Arachidonic Acid - pharmacology ; Biomarkers ; C-Reactive Protein - analysis ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - immunology ; Diabetes Mellitus, Type 2 - metabolism ; Dietary Supplements ; Disease Models, Animal ; Fatty Acids, Omega-3 - pharmacology ; gamma-Glutamyltransferase - blood ; Glycated Hemoglobin - analysis ; Inflammation - blood ; Inflammation - drug therapy ; Interleukin-6 - blood ; Male ; Masoprocol - pharmacology ; Rats ; Rats, Wistar ; Triglycerides - blood</subject><ispartof>Lipids in health and disease, 2016-11, Vol.15 (1), p.205-205, Article 205</ispartof><rights>Copyright BioMed Central 2016</rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4088-79256fbfab58948772a2f53fe17830716cd7f43295c6fbfd2380f5897d2962f63</citedby><cites>FETCH-LOGICAL-c4088-79256fbfab58948772a2f53fe17830716cd7f43295c6fbfd2380f5897d2962f63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5123226/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5123226/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27884155$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dain, Alejandro</creatorcontrib><creatorcontrib>Repossi, Gaston</creatorcontrib><creatorcontrib>Diaz-Gerevini, Gustavo T</creatorcontrib><creatorcontrib>Vanamala, Jairam</creatorcontrib><creatorcontrib>Das, Undurti N</creatorcontrib><creatorcontrib>Eynard, Aldo R</creatorcontrib><title>Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)</title><title>Lipids in health and disease</title><addtitle>Lipids Health Dis</addtitle><description>Diabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed the effects of supplementation of ω-3 and ω-6 polyunsaturated fatty acids (PUFAs) with or without nordihydroguaiaretic acid (NDGA) added, an antioxidant and lipoxygenase inhibitor, on metabolic and inflammatory parameters in eSS rats to evaluate whether they can delay development and/or prevent progression of DM.
After weaning, eSS rats received, intraperitoneally, once a month ω-3 (EPA 35% and DHA 40%-6.25 mg/Kg) or ω-6 (90% arachidonic acid- 6. 25 mg/Kg) for twelve months. Two additional groups of rats received 1.9 mg/kg NDGA added to ω-3 and ω-6 fatty acids. Blood samples were collected at day 40, and at the end of the 6th month and 12th month of age to determine plasma triglycerides (TGs), total plasma fatty acids (FA), A1C hemoglobin (HbA1C), C-reactive protein (CRP), gamma glutamyl transpeptidase (GGT), lipo and hydro peroxides, nitrites and IL-6 (in plasma and liver, kidney, and pancreas) and underwent oral glucose tolerance test (OGTT) as well. Wistar and eSS rats that received saline solution were used as controls.
Plasma lipids profile, TG, fasting and post-prandial blood glucose levels, and glycosylated HbA1C showed significant improvements in ω-3 and ω-3 + NDGA treated animals compared to eSS control group. ω-3 and ω-3 + NDGA groups showed an inverse correlation with fasting blood glucose and showed lower plasma levels of GGT, TG, and CRP. eSS rats treated with ω-3 LCPUFAs showed reduced level of inflammatory and oxidative indices in plasma and liver, kidney and pancreas tissues in comparison with eSS control (non-treated) and ω-6 treated groups.
eSS rats are a useful model to study type 2 DM pathophysiology and related inflammatory indices. ω-3 + NDGA supplementation, at the doses tested, ameliorated inflammatory, metabolic and oxidative stress markers studied.</description><subject>Animals</subject><subject>Arachidonic Acid - pharmacology</subject><subject>Biomarkers</subject><subject>C-Reactive Protein - analysis</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - immunology</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Dietary Supplements</subject><subject>Disease Models, Animal</subject><subject>Fatty Acids, Omega-3 - pharmacology</subject><subject>gamma-Glutamyltransferase - blood</subject><subject>Glycated Hemoglobin - analysis</subject><subject>Inflammation - blood</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin-6 - blood</subject><subject>Male</subject><subject>Masoprocol - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Triglycerides - blood</subject><issn>1476-511X</issn><issn>1476-511X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkl9rFDEUxQdRbK1-AF8k4Mvuw2iS-ZPMi7CsthUWFWrBt3B3kuymZpJtkhHmI_qtzLhtqT7lkvO7h3vgFMVrgt8Rwtv3kdCurktM2hJXbVXyJ8UpqVlbNoT8ePpoPilexHiDMcWsbZ8XJ5RxXpOmOS1-b7zboX4PxqGDt9PoIqQxQFISaUhpQtAbGdFis_52fb6KSwROIueDNPtJBr8bwUBQyfR_QbT48vFitUSDl6PNJmhQCbbeznLeM05bGAZIPkxogPBThZg_EaB48C6BU36MKE0HhSiSBrYqqZg9rDUpC9lVWbS4SsbaARy6ArsD6VE-Ny5fFs802Khe3b1nxfX5p-_ry3Lz9eLzerUp-xpzXrKONq3eatg2vKs5YxSobiqtCOMVZqTtJdN1RbumnzFJK451RpmkXUt1W50VH46-h3E7KNkrlwJYcQgmB5qEByP-VZzZi53_JRpCK0png8WdQfC3o4pJDCb2OeMxviC8rjGta9Zl9O1_6I0fg8vxZqrhjHJCMkWOVB98jEHph2MIFnNRxLEoIhdFzEURPO-8eZziYeO-GdUfONC8pQ</recordid><startdate>20161125</startdate><enddate>20161125</enddate><creator>Dain, Alejandro</creator><creator>Repossi, Gaston</creator><creator>Diaz-Gerevini, Gustavo T</creator><creator>Vanamala, Jairam</creator><creator>Das, Undurti N</creator><creator>Eynard, Aldo R</creator><general>BioMed Central</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>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161125</creationdate><title>Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)</title><author>Dain, Alejandro ; Repossi, Gaston ; Diaz-Gerevini, Gustavo T ; Vanamala, Jairam ; Das, Undurti N ; Eynard, Aldo R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4088-79256fbfab58948772a2f53fe17830716cd7f43295c6fbfd2380f5897d2962f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Arachidonic Acid - pharmacology</topic><topic>Biomarkers</topic><topic>C-Reactive Protein - analysis</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - immunology</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Dietary Supplements</topic><topic>Disease Models, Animal</topic><topic>Fatty Acids, Omega-3 - pharmacology</topic><topic>gamma-Glutamyltransferase - blood</topic><topic>Glycated Hemoglobin - analysis</topic><topic>Inflammation - blood</topic><topic>Inflammation - drug therapy</topic><topic>Interleukin-6 - blood</topic><topic>Male</topic><topic>Masoprocol - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Triglycerides - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dain, Alejandro</creatorcontrib><creatorcontrib>Repossi, Gaston</creatorcontrib><creatorcontrib>Diaz-Gerevini, Gustavo T</creatorcontrib><creatorcontrib>Vanamala, Jairam</creatorcontrib><creatorcontrib>Das, Undurti N</creatorcontrib><creatorcontrib>Eynard, Aldo R</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>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Lipids in health and disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dain, Alejandro</au><au>Repossi, Gaston</au><au>Diaz-Gerevini, Gustavo T</au><au>Vanamala, Jairam</au><au>Das, Undurti N</au><au>Eynard, Aldo R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats)</atitle><jtitle>Lipids in health and disease</jtitle><addtitle>Lipids Health Dis</addtitle><date>2016-11-25</date><risdate>2016</risdate><volume>15</volume><issue>1</issue><spage>205</spage><epage>205</epage><pages>205-205</pages><artnum>205</artnum><issn>1476-511X</issn><eissn>1476-511X</eissn><abstract>Diabetes mellitus (DM) is a complex disease with alterations in metabolic and inflammatory markers. Stillman Salgado rats (eSS) spontaneously develop type 2 DM by middle age showing progressive impairment of glucose tolerance with hyperglycemia, hypertriglyceridemia and hyperinsulinemia. We analyzed the effects of supplementation of ω-3 and ω-6 polyunsaturated fatty acids (PUFAs) with or without nordihydroguaiaretic acid (NDGA) added, an antioxidant and lipoxygenase inhibitor, on metabolic and inflammatory parameters in eSS rats to evaluate whether they can delay development and/or prevent progression of DM.
After weaning, eSS rats received, intraperitoneally, once a month ω-3 (EPA 35% and DHA 40%-6.25 mg/Kg) or ω-6 (90% arachidonic acid- 6. 25 mg/Kg) for twelve months. Two additional groups of rats received 1.9 mg/kg NDGA added to ω-3 and ω-6 fatty acids. Blood samples were collected at day 40, and at the end of the 6th month and 12th month of age to determine plasma triglycerides (TGs), total plasma fatty acids (FA), A1C hemoglobin (HbA1C), C-reactive protein (CRP), gamma glutamyl transpeptidase (GGT), lipo and hydro peroxides, nitrites and IL-6 (in plasma and liver, kidney, and pancreas) and underwent oral glucose tolerance test (OGTT) as well. Wistar and eSS rats that received saline solution were used as controls.
Plasma lipids profile, TG, fasting and post-prandial blood glucose levels, and glycosylated HbA1C showed significant improvements in ω-3 and ω-3 + NDGA treated animals compared to eSS control group. ω-3 and ω-3 + NDGA groups showed an inverse correlation with fasting blood glucose and showed lower plasma levels of GGT, TG, and CRP. eSS rats treated with ω-3 LCPUFAs showed reduced level of inflammatory and oxidative indices in plasma and liver, kidney and pancreas tissues in comparison with eSS control (non-treated) and ω-6 treated groups.
eSS rats are a useful model to study type 2 DM pathophysiology and related inflammatory indices. ω-3 + NDGA supplementation, at the doses tested, ameliorated inflammatory, metabolic and oxidative stress markers studied.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>27884155</pmid><doi>10.1186/s12944-016-0363-8</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arachidonic Acid - pharmacology Biomarkers C-Reactive Protein - analysis Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - immunology Diabetes Mellitus, Type 2 - metabolism Dietary Supplements Disease Models, Animal Fatty Acids, Omega-3 - pharmacology gamma-Glutamyltransferase - blood Glycated Hemoglobin - analysis Inflammation - blood Inflammation - drug therapy Interleukin-6 - blood Male Masoprocol - pharmacology Rats Rats, Wistar Triglycerides - blood |
| title | Long chain polyunsaturated fatty acids (LCPUFAs) and nordihydroguaiaretic acid (NDGA) modulate metabolic and inflammatory markers in a spontaneous type 2 diabetes mellitus model (Stillman Salgado rats) |
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