Maternal lipids and steatosis in the offspring

Abstract

The relationship between maternal hypertriglyceridemia and fetal hepatic steatosis is framed within the complex metabolic interaction of the fetoplacental unit, especially in the context of maternal pathologies such as obesity, gestational diabetes, and primary dyslipidemias.

During normal pregnancy, the mother experiences physiological hypertriglyceridemia in the second and third trimesters, designed to ensure maternal energy supply and the essential fatty acids necessary for fetal growth.

However, when pre-existing maternal hypertriglyceridemia is added to this physiological change, the excess lipids generate a massive increase in the flow of free fatty acids into the fetal circulation through the placenta. As a result, the fetal liver receives a lipid supply that exceeds its metabolic capacity to oxidize or export them in the form of very low-density lipoproteins (VLDL).

• Pathophysiological mechanism. Excess unmetabolized fatty acids are re-esterified and stored as triglyceride droplets within fetal hepatocytes, triggering fetal hepatic steatosis.
• Fetal Programming. This lipotoxic environment alters liver development and predisposes the individual in the long term to metabolic syndrome and MASLD (Metabolic Dysfunction-Associated Steatotic Liver Disease) and cardiovascular diseases in adulthood.

Furthermore, there is a significant obstetric risk associated with severe maternal hypertriglyceridemia, which is independently linked to an increased risk of preeclampsia, premature birth, fetal macrosomia, and, in cases of severe hypertriglyceridemia, acute maternal pancreatitis, which poses a serious risk to the lives of both mother and fetus.