Industrially produced
trans-fatty acids (TFAs) consumed in Western diets are incorporated into maternal and fetal tissues and are passed linearly to offspring via breast milk. We hypothesized that TFA exposure in utero and during lactation in infants would promote
obesity and poor
glycemic control as compared with unmodified
fatty acids. We further hypothesized that in utero exposure alone may program for these outcomes in adulthood. To test this hypothesis, we fed female C57/BL6 mice identical Western diets that differed only in cis- or trans-isomers of C18:1 and then aimed to determine whether maternal transfer of TFAs through pregnancy and lactation alters growth, body composition, and
glucose metabolism. Mice were unexposed, exposed during pregnancy, during lactation, or throughout pregnancy and lactation to TFA.
Body weight and composition (by computed tomography) and
glucose metabolism were assessed at weaning and adulthood.
Trans-fatty acid exposure through breast milk caused significant early growth retardation (P < .001) and higher fasting
glucose (P = .01), but
insulin sensitivity was not different. Elevated plasma
insulin-like growth factor-1 in mice consuming TFA-enriched milk (P = .02) may contribute to later catch-up growth and
leanness and preserved peripheral
insulin sensitivity observed in these mice. Mice exposed to TFA in utero underwent rapid early neonatal growth with TFA-free breast milk and had significantly impaired
insulin sensitivity (P < .05) and greater abdominal fat (P = .01). We conclude that very early catch-up growth resulted in impaired peripheral
insulin sensitivity in this model of diet-related fetal and neonatal programming.
Trans-fatty acid surprisingly retarded growth and adiposity while still adversely affecting
glucose metabolism.