Epidemiological investigations have confirmed that prenatal caffeine intake could increase the incidence rate of intrauterine growth retardation (IUGR) and multiple diseases after birth. Based on liquid chromatography-mass spectrometry, we analyzed serum metabolic profiles of offspring rats before and after birth in IUGR model induced by prenatal caffeine exposure (PCE). We discovered that differential metabolites in PCE fetuses mainly manifested as amino acids and lipid metabolism. In adulthood, PCE offspring showed less and inconsistent types of differential metabolites compared to those in utero, which still exhibited gender differences. The main differential metabolites induced by PCE, including phospholipids, platelet-activating factor, arachidonic acid, bile acid, sphingosine-1-phosphoric acid, indoxyl sulfuric acid, and cortexolone, may participate in the pathological and physiological processes of organ toxicities. This study demonstrated the short- and long-term developmental toxicity and gender differences of caffeine, providing new ideas for exploring the early warning and drug intervention targets of IUGR offspring.
Keywords: Developmental toxicity; Fetal-origin disease; Lipid metabolism; Metabolomics; Prenatal caffeine exposure.
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