Unfavorable effect of type 1 and type 2 diabetes on maternal and fetal essential fatty acid status: a potential marker of fetal insulin resistance.
BACKGROUND
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.


OBJECTIVE
We investigated whether type 1 and type 2 diabetes in pregnancy compromise maternal and fetal membrane essential fatty acids (FAs).


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Min
Yoeju
Y
Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, United Kingdom. y.min@londonmet.ac.uk
Lowy
Clara
C
Ghebremeskel
Kebreab
K
Thomas
Beverley
B
Offley-Shore
Brigid
B
Crawford
Michael
M
D000328:Adult; D016718:Arachidonic Acid / Q000032:analysis / Q000097:blood; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000378:metabolism; D004281:Docosahexaenoic Acids / Q000032:analysis / Q000097:blood; D004910:Erythrocyte Membrane / Q000737:chemistry / Q000378:metabolism; D005228:Fatty Acids, Essential / Q000032:analysis / Q000097:blood* / Q000378:metabolism; D005260:Female; D005312:Fetal Blood / Q000737:chemistry / Q000378:metabolism; D005997:Glycerylphosphorylcholine / Q000737:chemistry; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D008431:Maternal-Fetal Exchange; D010714:Phosphatidylethanolamines / Q000737:chemistry; D011247:Pregnancy; D011262:Pregnancy Trimester, Second / Q000097:blood / Q000378:metabolism; D011263:Pregnancy Trimester, Third / Q000097:blood / Q000378:metabolism; D011254:Pregnancy in Diabetics / Q000097:blood* / Q000378:metabolism; D014280:Triglycerides / Q000097:blood / Q000737:chemistry
D015415:Biomarkers; D005228:Fatty Acids, Essential; D010714:Phosphatidylethanolamines; D014280:Triglycerides; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid; D005997:Glycerylphosphorylcholine