Diabetes, Vol 48, Issue 1 112-116, Copyright © 1999 by American Diabetes Association

ARTICLES

Relationships between maternal risk of insulin resistance and the child's muscle membrane fatty acid composition

LA Baur, J O'Connor, DA Pan and LH Storlien
Department of Paediatrics and Child Health, University of Sydney, Australia. lbaur@usyd.edu.au

In adult humans, insulin resistance is associated with relatively low proportions of polyunsaturated fatty acids (PUFAs) in muscle membrane structural lipid. The aim of the present study was to determine the relationship between young children's muscle membrane fatty acid (FA) composition and indices of insulin resistance in their mothers. Muscle biopsy specimens obtained at the time of elective surgery from 83 children (54 boys), aged 0.78 +/- 0.05 year (mean +/- SE), were analyzed for phospholipid FA composition. Fasting blood samples were collected from the mothers of the children, and maternal BMIs were calculated. Stepwise multiple regression analysis showed that after accounting for the effect of breast-feeding, log maternal insulin levels were inversely associated with the child's muscle membrane docosahexaenoic acid (22:6 n-3; R2 = 0.29, P = 0.0006) and the sum of the n-3 PUFAs (R2 = 0.23, P = 0.0016) but positively associated with the sum of the n-6 PUFAs (R2 = 0.05, P = 0.03) and the n-6/n-3 PUFA ratio (R2 = 0.20, P = 0.007). Independent of breast-feeding, log maternal triglyceride levels were inversely associated with the child's muscle membrane unsaturation index (a measure of unsaturation) (R2 = 0.08, P = 0.005). Maternal BMI; total, LDL, and HDL cholesterol; and the child's age, sex, and birth weight were not significant predictors of the child's muscle membrane FA composition. Thus, maternal fasting insulin and triglyceride levels are significant predictors of the FA composition of the child's muscle membrane. The less unsaturated muscle membranes in children whose mothers have higher fasting insulin and triglyceride levels may reflect a genetic reluctance to incorporate PUFAs into membranes, thus predisposing them to insulin resistance syndromes.
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