Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status : a potential marker of fetal insulin resistance
Pregestational maternal diabetes increases obesity and diabetes risks in the offspring. Both conditions are characterized by insulin resistance, and diabetes is associated with low membrane arachidonic (AA) and docosahexaenoic (DHA) acids. We investigated whether type 1 and type 2 diabetes in pregna...
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creator | MIN, Yoeju LOWY, Clara GHEBREMESKEL, Kebreab THOMAS, Beverley OFFLEY-SHORE, Brigid CRAWFORD, Michael |
description | Pregestational maternal diabetes increases obesity and diabetes risks in the offspring. Both conditions are characterized by insulin resistance, and diabetes is associated with low membrane arachidonic (AA) and docosahexaenoic (DHA) acids.
We investigated whether type 1 and type 2 diabetes in pregnancy compromise maternal and fetal membrane essential fatty acids (FAs).
We studied 39 nondiabetic (control subjects), 32 type 1 diabetic, and 17 type 2 diabetic pregnant women and the infants they delivered. Maternal and cord blood samples were obtained at midgestation and at delivery, respectively. Plasma triacylglycerols and choline phosphoglycerides and red blood cell (RBC) choline and ethanolamine phosphoglyceride FAs were assessed.
The difference in maternal plasma triacylglycerol FAs between groups was not significant. However, the type 1 diabetes group had lower plasma choline phosphoglyceride DHA (3.7 +/- 0.9%; P < 0.01) than did the control group (5.2 +/- 1.6%). Likewise, RBC DHA was lower in the type 1 [choline: 3.4 +/- 1.5% (P < 0.01); ethanolamine: 5.9 +/- 2.5% (P < 0.05)] and type 2 [choline: 3.5 +/- 1.6% (P < 0.05)] diabetes groups than in the control group (choline: 5.5 +/- 2.2%; ethanolamine: 7.5 +/- 2.5%). Cord AA and DHA were lower in the plasma (type 1: P < 0.01) and RBC (type 2: P < 0.05) choline phosphoglycerides of the diabetics than of the control subjects, and cord RBC ethanolamine phosphoglycerides were lower in DHA (P < 0.05) in both diabetes groups than in the control group.
Diabetes (either type) compromises maternal RBC DHA and cord plasma and RBC AA and DHA. The association of these 2 FAs with insulin sensitivity may mean that the current finding explains the higher incidence of insulin resistance and diabetes in the offspring of diabetic women. |
doi_str_mv | 10.1093/ajcn/82.6.1162 |
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We investigated whether type 1 and type 2 diabetes in pregnancy compromise maternal and fetal membrane essential fatty acids (FAs).
We studied 39 nondiabetic (control subjects), 32 type 1 diabetic, and 17 type 2 diabetic pregnant women and the infants they delivered. Maternal and cord blood samples were obtained at midgestation and at delivery, respectively. Plasma triacylglycerols and choline phosphoglycerides and red blood cell (RBC) choline and ethanolamine phosphoglyceride FAs were assessed.
The difference in maternal plasma triacylglycerol FAs between groups was not significant. However, the type 1 diabetes group had lower plasma choline phosphoglyceride DHA (3.7 +/- 0.9%; P < 0.01) than did the control group (5.2 +/- 1.6%). Likewise, RBC DHA was lower in the type 1 [choline: 3.4 +/- 1.5% (P < 0.01); ethanolamine: 5.9 +/- 2.5% (P < 0.05)] and type 2 [choline: 3.5 +/- 1.6% (P < 0.05)] diabetes groups than in the control group (choline: 5.5 +/- 2.2%; ethanolamine: 7.5 +/- 2.5%). Cord AA and DHA were lower in the plasma (type 1: P < 0.01) and RBC (type 2: P < 0.05) choline phosphoglycerides of the diabetics than of the control subjects, and cord RBC ethanolamine phosphoglycerides were lower in DHA (P < 0.05) in both diabetes groups than in the control group.
Diabetes (either type) compromises maternal RBC DHA and cord plasma and RBC AA and DHA. The association of these 2 FAs with insulin sensitivity may mean that the current finding explains the higher incidence of insulin resistance and diabetes in the offspring of diabetic women.]]></description><identifier>ISSN: 0002-9165</identifier><identifier>EISSN: 1938-3207</identifier><identifier>DOI: 10.1093/ajcn/82.6.1162</identifier><identifier>PMID: 16332647</identifier><identifier>CODEN: AJCNAC</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Clinical Nutrition</publisher><subject>Adult ; Arachidonic Acid - analysis ; Arachidonic Acid - blood ; Associated diseases and complications ; Biological and medical sciences ; Biomarkers - blood ; Case-Control Studies ; Diabetes ; Diabetes Mellitus, Type 1 - blood ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes. Impaired glucose tolerance ; Docosahexaenoic Acids - analysis ; Docosahexaenoic Acids - blood ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Erythrocyte Membrane - chemistry ; Erythrocyte Membrane - metabolism ; Fatty acids ; Fatty Acids, Essential - analysis ; Fatty Acids, Essential - blood ; Fatty Acids, Essential - metabolism ; Female ; Fetal Blood - chemistry ; Fetal Blood - metabolism ; Fetuses ; Glycerylphosphorylcholine - chemistry ; Humans ; Insulin Resistance - physiology ; Maternal-Fetal Exchange ; Medical sciences ; Phosphatidylethanolamines - chemistry ; Pregnancy ; Pregnancy in Diabetics - blood ; Pregnancy in Diabetics - metabolism ; Pregnancy Trimester, Second - blood ; Pregnancy Trimester, Second - metabolism ; Pregnancy Trimester, Third - blood ; Pregnancy Trimester, Third - metabolism ; Triglycerides - blood ; Triglycerides - chemistry</subject><ispartof>The American journal of clinical nutrition, 2005-12, Vol.82 (6), p.1162-1168</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright American Society for Clinical Nutrition, Inc. Dec 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-3acddc7984d5e048a94f4234473e5a36a47cf3e36eba8c1aba8aa91fc678be233</citedby><cites>FETCH-LOGICAL-c456t-3acddc7984d5e048a94f4234473e5a36a47cf3e36eba8c1aba8aa91fc678be233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17345644$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16332647$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MIN, Yoeju</creatorcontrib><creatorcontrib>LOWY, Clara</creatorcontrib><creatorcontrib>GHEBREMESKEL, Kebreab</creatorcontrib><creatorcontrib>THOMAS, Beverley</creatorcontrib><creatorcontrib>OFFLEY-SHORE, Brigid</creatorcontrib><creatorcontrib>CRAWFORD, Michael</creatorcontrib><title>Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status : a potential marker of fetal insulin resistance</title><title>The American journal of clinical nutrition</title><addtitle>Am J Clin Nutr</addtitle><description><![CDATA[Pregestational maternal diabetes increases obesity and diabetes risks in the offspring. Both conditions are characterized by insulin resistance, and diabetes is associated with low membrane arachidonic (AA) and docosahexaenoic (DHA) acids.
We investigated whether type 1 and type 2 diabetes in pregnancy compromise maternal and fetal membrane essential fatty acids (FAs).
We studied 39 nondiabetic (control subjects), 32 type 1 diabetic, and 17 type 2 diabetic pregnant women and the infants they delivered. Maternal and cord blood samples were obtained at midgestation and at delivery, respectively. Plasma triacylglycerols and choline phosphoglycerides and red blood cell (RBC) choline and ethanolamine phosphoglyceride FAs were assessed.
The difference in maternal plasma triacylglycerol FAs between groups was not significant. However, the type 1 diabetes group had lower plasma choline phosphoglyceride DHA (3.7 +/- 0.9%; P < 0.01) than did the control group (5.2 +/- 1.6%). Likewise, RBC DHA was lower in the type 1 [choline: 3.4 +/- 1.5% (P < 0.01); ethanolamine: 5.9 +/- 2.5% (P < 0.05)] and type 2 [choline: 3.5 +/- 1.6% (P < 0.05)] diabetes groups than in the control group (choline: 5.5 +/- 2.2%; ethanolamine: 7.5 +/- 2.5%). Cord AA and DHA were lower in the plasma (type 1: P < 0.01) and RBC (type 2: P < 0.05) choline phosphoglycerides of the diabetics than of the control subjects, and cord RBC ethanolamine phosphoglycerides were lower in DHA (P < 0.05) in both diabetes groups than in the control group.
Diabetes (either type) compromises maternal RBC DHA and cord plasma and RBC AA and DHA. The association of these 2 FAs with insulin sensitivity may mean that the current finding explains the higher incidence of insulin resistance and diabetes in the offspring of diabetic women.]]></description><subject>Adult</subject><subject>Arachidonic Acid - analysis</subject><subject>Arachidonic Acid - blood</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Case-Control Studies</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - blood</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Docosahexaenoic Acids - analysis</subject><subject>Docosahexaenoic Acids - blood</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Erythrocyte Membrane - chemistry</subject><subject>Erythrocyte Membrane - metabolism</subject><subject>Fatty acids</subject><subject>Fatty Acids, Essential - analysis</subject><subject>Fatty Acids, Essential - blood</subject><subject>Fatty Acids, Essential - metabolism</subject><subject>Female</subject><subject>Fetal Blood - chemistry</subject><subject>Fetal Blood - metabolism</subject><subject>Fetuses</subject><subject>Glycerylphosphorylcholine - chemistry</subject><subject>Humans</subject><subject>Insulin Resistance - physiology</subject><subject>Maternal-Fetal Exchange</subject><subject>Medical sciences</subject><subject>Phosphatidylethanolamines - chemistry</subject><subject>Pregnancy</subject><subject>Pregnancy in Diabetics - blood</subject><subject>Pregnancy in Diabetics - metabolism</subject><subject>Pregnancy Trimester, Second - blood</subject><subject>Pregnancy Trimester, Second - metabolism</subject><subject>Pregnancy Trimester, Third - blood</subject><subject>Pregnancy Trimester, Third - metabolism</subject><subject>Triglycerides - blood</subject><subject>Triglycerides - chemistry</subject><issn>0002-9165</issn><issn>1938-3207</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkV9rFDEUxUNR2m311UcJQn2bbf5tkvFNSq1CwRf7HO5kbmDW2cyaZIT9HH5hM-5AwZfkwv2dE3IOIe8423LWyjvY-3hnxVZvOdfigmx4K20jBTOvyIYxJpqW690Vuc55zxgXyupLcsW1lEIrsyF_nmOA31OCbkSKIaAvdAq0nI5IOYXYn0dB-wE6LJjpFOkBCqYI4799wFInzBljGeoUoJQTBT_0NBcoc6afKNDjVNb9AdJPTMsjZ-UQ8zwOkSbMQxVEj2_I6wBjxrfrfUOevzz8uP_aPH1__Hb_-anxaqdLI8H3vTetVf0OmbLQqqCEVMpI3IHUoIwPEqXGDqznUE-Algevje1QSHlDPp59j2n6NWMu7jBkj-MIEac5O22tUYabCn74D9xP8xJAdkLWwLnRi9v2DPk05ZwwuGMa6mdPjjO3dOWWrpwVTrulqyp4v7rO3QH7F3wtpwK3KwDZwxhSDWfIL5yRNQel5F9VyJ6q</recordid><startdate>20051201</startdate><enddate>20051201</enddate><creator>MIN, Yoeju</creator><creator>LOWY, Clara</creator><creator>GHEBREMESKEL, Kebreab</creator><creator>THOMAS, Beverley</creator><creator>OFFLEY-SHORE, Brigid</creator><creator>CRAWFORD, Michael</creator><general>American Society for Clinical Nutrition</general><general>American Society for Clinical Nutrition, Inc</general><scope>IQODW</scope><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>7QP</scope><scope>7T7</scope><scope>7TS</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20051201</creationdate><title>Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status : a potential marker of fetal insulin resistance</title><author>MIN, Yoeju ; LOWY, Clara ; GHEBREMESKEL, Kebreab ; THOMAS, Beverley ; OFFLEY-SHORE, Brigid ; CRAWFORD, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-3acddc7984d5e048a94f4234473e5a36a47cf3e36eba8c1aba8aa91fc678be233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Arachidonic Acid - analysis</topic><topic>Arachidonic Acid - blood</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Case-Control Studies</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - blood</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Docosahexaenoic Acids - analysis</topic><topic>Docosahexaenoic Acids - blood</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Erythrocyte Membrane - chemistry</topic><topic>Erythrocyte Membrane - metabolism</topic><topic>Fatty acids</topic><topic>Fatty Acids, Essential - analysis</topic><topic>Fatty Acids, Essential - blood</topic><topic>Fatty Acids, Essential - metabolism</topic><topic>Female</topic><topic>Fetal Blood - chemistry</topic><topic>Fetal Blood - metabolism</topic><topic>Fetuses</topic><topic>Glycerylphosphorylcholine - chemistry</topic><topic>Humans</topic><topic>Insulin Resistance - physiology</topic><topic>Maternal-Fetal Exchange</topic><topic>Medical sciences</topic><topic>Phosphatidylethanolamines - chemistry</topic><topic>Pregnancy</topic><topic>Pregnancy in Diabetics - blood</topic><topic>Pregnancy in Diabetics - metabolism</topic><topic>Pregnancy Trimester, Second - blood</topic><topic>Pregnancy Trimester, Second - metabolism</topic><topic>Pregnancy Trimester, Third - blood</topic><topic>Pregnancy Trimester, Third - metabolism</topic><topic>Triglycerides - blood</topic><topic>Triglycerides - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MIN, Yoeju</creatorcontrib><creatorcontrib>LOWY, Clara</creatorcontrib><creatorcontrib>GHEBREMESKEL, Kebreab</creatorcontrib><creatorcontrib>THOMAS, Beverley</creatorcontrib><creatorcontrib>OFFLEY-SHORE, Brigid</creatorcontrib><creatorcontrib>CRAWFORD, Michael</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The American journal of clinical nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MIN, Yoeju</au><au>LOWY, Clara</au><au>GHEBREMESKEL, Kebreab</au><au>THOMAS, Beverley</au><au>OFFLEY-SHORE, Brigid</au><au>CRAWFORD, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status : a potential marker of fetal insulin resistance</atitle><jtitle>The American journal of clinical nutrition</jtitle><addtitle>Am J Clin Nutr</addtitle><date>2005-12-01</date><risdate>2005</risdate><volume>82</volume><issue>6</issue><spage>1162</spage><epage>1168</epage><pages>1162-1168</pages><issn>0002-9165</issn><eissn>1938-3207</eissn><coden>AJCNAC</coden><abstract><![CDATA[Pregestational maternal diabetes increases obesity and diabetes risks in the offspring. Both conditions are characterized by insulin resistance, and diabetes is associated with low membrane arachidonic (AA) and docosahexaenoic (DHA) acids.
We investigated whether type 1 and type 2 diabetes in pregnancy compromise maternal and fetal membrane essential fatty acids (FAs).
We studied 39 nondiabetic (control subjects), 32 type 1 diabetic, and 17 type 2 diabetic pregnant women and the infants they delivered. Maternal and cord blood samples were obtained at midgestation and at delivery, respectively. Plasma triacylglycerols and choline phosphoglycerides and red blood cell (RBC) choline and ethanolamine phosphoglyceride FAs were assessed.
The difference in maternal plasma triacylglycerol FAs between groups was not significant. However, the type 1 diabetes group had lower plasma choline phosphoglyceride DHA (3.7 +/- 0.9%; P < 0.01) than did the control group (5.2 +/- 1.6%). Likewise, RBC DHA was lower in the type 1 [choline: 3.4 +/- 1.5% (P < 0.01); ethanolamine: 5.9 +/- 2.5% (P < 0.05)] and type 2 [choline: 3.5 +/- 1.6% (P < 0.05)] diabetes groups than in the control group (choline: 5.5 +/- 2.2%; ethanolamine: 7.5 +/- 2.5%). Cord AA and DHA were lower in the plasma (type 1: P < 0.01) and RBC (type 2: P < 0.05) choline phosphoglycerides of the diabetics than of the control subjects, and cord RBC ethanolamine phosphoglycerides were lower in DHA (P < 0.05) in both diabetes groups than in the control group.
Diabetes (either type) compromises maternal RBC DHA and cord plasma and RBC AA and DHA. The association of these 2 FAs with insulin sensitivity may mean that the current finding explains the higher incidence of insulin resistance and diabetes in the offspring of diabetic women.]]></abstract><cop>Bethesda, MD</cop><pub>American Society for Clinical Nutrition</pub><pmid>16332647</pmid><doi>10.1093/ajcn/82.6.1162</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Arachidonic Acid - analysis Arachidonic Acid - blood Associated diseases and complications Biological and medical sciences Biomarkers - blood Case-Control Studies Diabetes Diabetes Mellitus, Type 1 - blood Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - metabolism Diabetes. Impaired glucose tolerance Docosahexaenoic Acids - analysis Docosahexaenoic Acids - blood Endocrine pancreas. Apud cells (diseases) Endocrinopathies Erythrocyte Membrane - chemistry Erythrocyte Membrane - metabolism Fatty acids Fatty Acids, Essential - analysis Fatty Acids, Essential - blood Fatty Acids, Essential - metabolism Female Fetal Blood - chemistry Fetal Blood - metabolism Fetuses Glycerylphosphorylcholine - chemistry Humans Insulin Resistance - physiology Maternal-Fetal Exchange Medical sciences Phosphatidylethanolamines - chemistry Pregnancy Pregnancy in Diabetics - blood Pregnancy in Diabetics - metabolism Pregnancy Trimester, Second - blood Pregnancy Trimester, Second - metabolism Pregnancy Trimester, Third - blood Pregnancy Trimester, Third - metabolism Triglycerides - blood Triglycerides - chemistry |
title | Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status : a potential marker of fetal insulin resistance |
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