Circulating docosahexaenoic acid levels are associated with fetal insulin sensitivity.
BACKGROUND
Arachidonic acid (AA; C20∶4 n-6) and docosahexaenoic acid (DHA; C22∶6 n-3) are important long-chain polyunsaturated fatty acids (LC-PUFA) in maintaining pancreatic beta-cell structure and function. Newborns of gestational diabetic mothers are more susceptible to the development of type 2 diabetes in adulthood. It is not known whether low circulating AA or DHA is involved in perinatally "programming" this susceptibility. This study aimed to assess whether circulating concentrations of AA, DHA and other fatty acids are associated with fetal insulin sensitivity or beta-cell function, and whether low circulating concentrations of AA or DHA are involved in compromised fetal insulin sensitivity in gestational diabetic pregnancies.


RESULTS
In a prospective singleton pregnancy cohort, maternal (32-35 weeks gestation) and cord plasma fatty acids were assessed in relation to surrogate indicators of fetal insulin sensitivity (cord plasma glucose-to-insulin ratio, proinsulin concentration) and beta-cell function (proinsulin-to-insulin ratio) in 108 mother-newborn pairs. Cord plasma DHA levels (in percentage of total fatty acids) were lower comparing newborns of gestational diabetic (n = 24) vs. non-diabetic pregnancies (2.9% vs. 3.5%, P = 0.01). Adjusting for gestational age at blood sampling, lower cord plasma DHA levels were associated with lower fetal insulin sensitivity (lower glucose-to-insulin ratio, r = 0.20, P = 0.036; higher proinsulin concentration, r = -0.37, P <0.0001). The associations remained after adjustment for maternal and newborn characteristics. Cord plasma saturated fatty acids C18∶0 and C20∶0 were negatively correlated with fetal insulin sensitivity, but their levels were not different between gestational diabetic and non-diabetic pregnancies. Cord plasma AA levels were not correlated with fetal insulin sensitivity.


CONCLUSIONS
Low circulating DHA levels are associated with compromised fetal insulin sensitivity, and may be involved in perinatally "programming" the susceptibility to type 2 diabetes in the offspring of gestational diabetic mothers.
Department of Obstetrics and Gynecology, University of Montreal, Montreal, Quebec, Canada.
Jin-Ping
JP
Zhao
Department of Nutrition, University of Montreal, Montreal, Quebec, Canada.
Emile
E
Levy
Department of Obstetrics and Gynecology, University of Montreal, Montreal, Quebec, Canada.
William D
WD
Fraser
Endocrinology and Nephrology, Laval University Hospital Research Centre, and Department of Medicine, Laval University, Quebec City, Quebec, Canada.
Pierre
P
Julien
Department of Biochemistry, University of Montreal, Montreal, Quebec, Canada.
Edgard
E
Delvin
Department of Nutrition, University of Montreal, Montreal, Quebec, Canada.
Alain
A
Montoudis
Department of Nutrition, University of Montreal, Montreal, Quebec, Canada.
Schohraya
S
Spahis
Department of Nutrition, University of Montreal, Montreal, Quebec, Canada.
Carole
C
Garofalo
Department of Pediatrics, Sainte-Justine Hospital Research Center, University of Montreal, Montreal, Quebec, Canada.
Anne Monique
AM
Nuyt
Department of Obstetrics and Gynecology, University of Montreal, Montreal, Quebec, Canada ; Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health, Xinhua Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Zhong-Cheng
ZC
Luo
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D016640:Diabetes, Gestational / Q000097:blood; D004281:Docosahexaenoic Acids / Q000097:blood*; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005333:Fetus / Q000378:metabolism*; D006801:Humans; D007231:Infant, Newborn; D007328:Insulin / Q000097:blood*; D011247:Pregnancy
D001786:Blood Glucose; D007328:Insulin; D004281:Docosahexaenoic Acids