Both acetyl-CoA carboxylase 1 (ACC1) and acetyl-CoA carboxylase 2

Both acetyl-CoA carboxylase 1 (ACC1) and acetyl-CoA carboxylase 2 (ACC2), which are crucial biotin-dependent

enzymes, catalyze the incorporation of bicarbonate into acetyl-CoA to form malonyl-CoA. The malonylcarnitine level might reflect malonyl-CoA homeostasis. In Polish newborns with CL/P low malonylcarnitine levels (≤ 0.047μmol/L) were 1.7 times more predominant than in healthy individuals, p=0.03. The findings may suggest that the metabolic pathway of malonyl-CoA is disturbed in CL/P-affected individuals, however the potential role of biotindependent carboxylases has yet to be elucidated [28]. Moreover, further studies are needed to clarify the relation between maternal carnitine (so-called vitamin BT, which is a hydrophilic molecule) and its derivatives

(e.g. acylcarnitines) BYL719 E7080 price status and clefting risk [28, 46]. Carnitine plays an indispensable role in fatty acid oxidation. It is noteworthy that there is strong evidence for the utilization of lipids as an energy substrate by early embryos [47]. The formation of acylcarnitine conjugates is the basis of expanded newborn screening for inborn errors of metabolism based on tandem mass spectrometry (MS/MS). The functions of zinc in the human and experimental animals’ reproduction have been studied extensively and reviewed recently by Shah and Sachdev [48]. At least in rodent models in the face of an acute dietary zinc deficiency, maternal mobilization of zinc stores is inadequate to supply the needs of the conceptus. In rats the deficiency of zinc results in offspring that are characterized by anomalies

affecting nearly every organ. In the years 2004–2005 low zinc level was independently reported as a maternal risk factor for orofacial clefts in the Netherlands (in erythrocytes) [49], the Philippines (in plasma) [50], and Poland (in serum) [22]. DOCK10 In mothers of children with CL/P mean serum zinc level was lower than in women who gave birth to children without a birth defect, 511μg/L (SD 121) vs. 572 μg/L (SD 76), p=0.01, respectively [22]. The second Polish study, in which zinc was analyzed in whole blood, confirmed an association between low maternal zinc and increased risk of CL/P in offspring [25]. A maternal whole blood zinc concentration of 47.1μmol/L or less increased the risk of CL/P 2.5-times more than higher concentrations (95%CI:1.03–6.23, p=0.04). Zinc transporters SLC30A1 and SLC30A5 play a key role in regulation the delivery of maternal zinc to the developing embryo. Embryonic nutrition is determined not only by the mother’s dietary intakes and nutrient stores, but also by transfer capabilities. Cadmium exposure down-regulates Slc30a1 expression, indicating that maternal cadmium exposure may alter zinc homeostasis in the conceptus [51]. Experimental and epidemiological studies have reported an association between prenatal exposure to cadmium and structural malformations [51, 52].

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