Maternal high-fat diet and risk of cardiovascular disease in offspring: a review of mechanisms, controversies, and interventions

FIGURE 1. Cellular and molecular mechanisms of early atherosclerotic plaque formation. The schematic illustrates the initiation of atherosclerosis driven by subendothelial LDL retention and modification. Monocytes tether to endothelial adhesion molecules and transmigrate into the intima, differentiating into macrophages under the influence of GM-CSF and M-CSF. Macrophages engulf modified lipoproteins through scavenger receptors and are transformed into cholesterol crystal-laden foam cells. The subsequent secretion of pro-inflammatory cytokines by foam cells, notably IL-1β, amplifies local intimal inflammation, alters medial smooth muscle cell activity, and drives the release of IL-6.

FIGURE 2. Animal experimental studies confirming the impact of HFD on coronary artery function. The intake of HFD leads to significant cardiac dysfunction, manifested as prolonged QRS interval, increased heart rate, and significantly reduced LVDP. Coronary microvascular injury is an early pathological event before myocardial dysfunction in HFD-induced cardiac injury.

FIGURE 3. Effects of a high-fat diet on the cardiovascular system through metabolic disturbances and gene expression alterations. A high-fat diet also significantly disrupts cardiac metabolism and alters gene expression. In a metabolic syndrome rat model, administration of puerarin significantly ameliorated systemic inflammatory responses. Supplementation with L-arginine in HFD-fed male Wistar rats reduced circulating leptin levels and enhanced phosphatidylinositol 3-kinase (PIK3) activity.

FIGURE 4. Role of the early-life nutritional environment in shaping the long-term health trajectory of offspring. Maternal dietary patterns during pregnancy not only directly influence fetal intrauterine development, but they also exert profound and lasting programming effects on offspring cardiovascular health through complex biological mechanisms.

FIGURE 5. The impact of a high-fat diet on coronary artery health remains controversial. High fat diet intake elevates circulating low-density lipoprotein cholesterol levels, thereby increasing the risk of atherosclerotic arterial cardiovascular disease. However, other studies propose alternative explanations, suggesting that the saturated fatty acid-induced elevation of low-density lipoprotein cholesterol may reflect a physiological homeostatic adaptation response aimed at maintaining cell membrane fluidity and cellular function, rather than a pathological reaction in metabolically healthy individuals.