Abstract
Pregnant rats were fed a high fat diet (HFD) for the first (HF1), second (HF2), third (HF3) or all three weeks (HFG) of gestation. Maintenance on a HFD during specific periods of gestation was hypothesized to alter fetal glycemia, insulinemia, induce insulin resistance; and alter fetal plasma and hepatic fatty acid (FA) profiles. At day 20 of gestation, fetal plasma and hepatic FA profiles were determined by gas chromatography; body weight, fasting glycemia, insulinemia and the Homeostasis Model Assessment (HOMA-insulin resistance) were also determined. HF3 fetuses were heaviest concomitant with elevated glycemia and insulin resistance (p < 0.05). HFG fetuses had elevated plasma linoleic (18:2 n-6) and arachidonic (20:4 n-6) acid proportions (p < 0.05). In the liver, HF3 fetuses displayed elevated linoleic, eicosatrienoic (20:3 n-6) and arachidonic acid proportions (p < 0.05). HFG fetuses had reduced hepatic docosatrienoic acid (22:5 n-3) proportions (p < 0.05). High fat maintenance during the final week of fetal life enhances hepatic omega-6 FA profiles in fetuses concomitant with hyperglycemia and insulin resistance thereby presenting a metabolically compromised phenotype.
Highlights
Fetal metabolism, and fetal growth, directly depends on the nutrients crossing the placenta, and the mother adapts her metabolism to support this continuous draining of substrates [1].Fatty acids (FAs) are important for fetal growth and development
A high fat diet (HFD) was shown to contribute to the development of obesity, insulin resistance, type 2 diabetes and the impairment of the glucose signaling system in the beta cells [5,6,7,8]; in neonates, these effects were dependent on the period of fetal life when the HFD was administered [5]
The hyperglycemia and insulin resistance in fetuses maintained on a HFD for the final week of fetal life concomitant with increased hepatic omega-6 FA proportions were the main findings
Summary
Fetal growth, directly depends on the nutrients crossing the placenta, and the mother adapts her metabolism to support this continuous draining of substrates [1]. Linoleic acid (18:2 n-6) and α-linolenic acid (ALA, 18:3 n-3) are the essential fatty acids (EFAs), which together with their long-chain polyunsaturated FA (LCPUFA) derivatives are essential for fetal and postnatal development. The fetus obtains both EFAs and LCPUFAs from maternal circulation by transfer across the placenta [2,3]. A high fat diet (HFD) was shown to contribute to the development of obesity, insulin resistance, type 2 diabetes and the impairment of the glucose signaling system in the beta cells [5,6,7,8]; in neonates, these effects were dependent on the period of fetal life when the HFD was administered [5]. We investigated, in fetal rats, how exposure to a HFD during specific weeks of fetal life influences plasma and hepatic FA profiles, glycemia, insulinemia and insulin resistance
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