Abstract
ObjectiveNonalcoholic fatty liver disease (NAFLD) is a well-recognized hepatic manifestation of metabolic disease in adults and has been associated with the development of gestational diabetes (GDM). Hepatic insulin resistance can result in increased release of glucose (from gluconeogenesis) and free fatty acids (due to enhanced lipolysis), which can lead in turn to fetal overgrowth. However, the relationship between maternal metabolic factors (such as circulating levels of triglycerides, free fatty acids [FFA], or adipokines) and excessive fetal birthweight in NAFLD has not been carefully examined. In this study, we evaluated the relationship between NAFLD and the subsequent risk of large-for-gestational-age (LGA) birthweight.MethodSingleton nondiabetic pregnant women were evaluated for the presence of fatty liver at 10–14 weeks of gestation by abdominal ultrasound. The degree of fatty liver was classified as Grade 0–3 steatosis. At the time of liver ultrasound, maternal blood was taken after fasting and measured for adiponectin and FFA. LGA was defined as birthweight >90th percentile for gestational age.ResultsA total of 623 women were included in the analysis. The frequency of LGA was 10.9% (68/623), and the frequency of NAFLD was 18.9%. The risk of LGA increased significantly in patients with Grade 2–3 steatosis in the first trimester. The relationship between Grade 2–3 steatosis and LGA remained significant after adjustment for maternal age, pre-pregnancy BMI, GDM, and maternal serum triglyceride levels. The concentration of maternal blood adiponectin at 10–14 weeks was significantly lower in cases with LGA than non-LGA, but the maternal blood FFA concentrations were not different between the groups.ConclusionThe presence of Grade 2–3 steatosis on ultrasound in early pregnancy was associated with the increased risk of delivering an LGA infant, even after adjustment for multiple confounding factors including GDM. Adiponectin may be the linking biomarker between NAFLD and LGA.
Highlights
Abnormal fetal growth—both fetal growth restriction and excessive fetal growth—is a risk factor for obesity and cardiovascular disease in later life.[1,2,3] Fetal growth is dependent on the adequate supply of nutrients across the placenta, but the exact mechanisms regulating fetal growth are not fully understood
The presence of Grade 2–3 steatosis on ultrasound in early pregnancy was associated with the increased risk of delivering an LGA infant, even after adjustment for multiple confounding factors including GDM
In the laboratory tests performed at the time of liver ultrasound, Women who delivered LGA neonates had higher level of triglyceride and homeostasis model assessmentinsulin resistance (HOMA-IR) than those who did not
Summary
Nonalcoholic fatty liver disease (NAFLD) is a well-recognized hepatic manifestation of metabolic disease in adults and has been associated with the development of gestational diabetes (GDM). Hepatic insulin resistance can result in increased release of glucose (from gluconeogenesis) and free fatty acids (due to enhanced lipolysis), which can lead in turn to fetal overgrowth. The relationship between maternal metabolic factors (such as circulating levels of triglycerides, free fatty acids [FFA], or adipokines) and excessive fetal birthweight in NAFLD has not been carefully examined. We evaluated the relationship between NAFLD and the subsequent risk of large-for-gestational-age (LGA) birthweight
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