The prevalence of maternal obesity is rapidly increasing, which represents a major public health concern worldwide. Currently more than 50% of all adult women are overweight or obese, and this trend is reflected in women of child-bearing age. Maternal obesity is characterized by metabolic dysfunction and chronic inflammation, and is associated with health problems in both the mother and the offspring. Intrauterine programming occurs during embryonic and fetal development, a critical period not only for the formation of tissues and organs but also for the etiology of diseases later in life. The principal mechanisms underlying fetal programming in the offspring of obese mothers appear to involve DNA methylation and chromatin remodeling within progenitor cells. Aberrant DNA methylation patterns have been identified in genes involved in insulin signaling, lipid metabolism, and appetite regulation in the placenta and fetal tissues. Histone modifications, such as acetylation and methylation of histone tails, may also play a crucial role in modulating chromatin structure and accessibility of transcriptional machinery to DNA. The persistence of such modifications throughout life, and potentially across generations, can lead to permanent alterations in gene expression, thereby contributing to the intergenerational transmission of metabolic disorders. The aim of this paper is to present an overview of the current knowledge regarding the effects of maternal obesity on fetal development and the occurrence of fetal complications, as well as long-term complications observed in adulthood related to intrauterine exposure to maternal obesity, including hypertension and cardiovascular diseases, impaired insulin secretion and resistance, diabetes mellitus, and metabolic syndrome. The mechanisms underlying fetal programming are also discussed.

Fatty acid-binding protein 4 (FABP4) is an adipokine involved in regulating lipid metabolism, glucose homeostasis, and inflammatory processes. Altered circulating FABP4 concentrations have been associated with insulin resistance, adipose tissue dysfunction, and endothelial abnormalities. Growing evidence suggests that FABP4 dysregulation may contribute to impaired maternal metabolic and vascular adaptation during pregnancy, although the underlying mechanisms remain incompletely understood. FABP4 has been implicated in the pathophysiology of several pregnancy-related conditions, including maternal obesity, gestational diabetes mellitus, hypertensive disorders of pregnancy, preeclampsia, and recurrent pregnancy loss. Circulating FABP4 has also emerged as a potential biomarker for the early identification of women at increased risk of pregnancy-related metabolic and vascular complications, potentially improving risk assessment and providing earlier preventive or therapeutic interventions. This review summarizes current evidence on the role of FABP4 during pregnancy and its potential involvement in the pathophysiology of pregnancy-related complications, with particular emphasis on its biological functions, diagnostic and prognostic potential, and emerging therapeutic implications. Further mechanistic and prospective clinical studies are needed to determine whether FABP4 is a clinically useful biomarker and to clarify its potential as a therapeutic target in the management of pregnancy-related complications.