Neonatal and fetal exposure to trans-fatty acids retards early growth and adiposity while adversely affecting glucose in mice.
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.
Kavanagh
Kylie
K
Department of Pathology, Section on Comparative Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA. kkavanag@wfubmc.edu
Sajadian
Soraya
S
Jenkins
Kurt A
KA
Wilson
Martha D
MD
Carr
J Jeffery
JJ
Wagner
Janice D
JD
Rudel
Lawrence L
LL
D050153:Abdominal Fat / Q000378:metabolism; D050154:Adiposity / Q000187:drug effects; D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000378:metabolism*; D004041:Dietary Fats / Q000008:administration & dosage*; D005260:Female; D006128:Growth / Q000187:drug effects*; D006130:Growth Disorders / Q000209:etiology* / Q000378:metabolism; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007774:Lactation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008895:Milk, Human / Q000737:chemistry; D009765:Obesity / Q000378:metabolism / Q000517:prevention & control*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism; D044242:Trans Fatty Acids / Q000494:pharmacology*
D001786:Blood Glucose; D004041:Dietary Fats; D044242:Trans Fatty Acids; D007334:Insulin-Like Growth Factor I