
By 2030, approximately one billion people are predicted to suffer from obesity. Leptin, an adipokine produced by adipose tissue, plays a role in cardiovascular risk. Leptin stimulates the synthesis of vascular endothelial growth factor (VEGF). This review examines recent studies on the interaction between leptin and VEGF in obesity and related conditions. The crosstalk between leptin and VEGF promotes cancer progression. Animal research indicates that a high-fat diet enhances leptin-VEGF interaction. Genetic and epigenetic mechanisms, as well as procreator-offspring programming, may play a role in leptin-VEGF crosstalk. Some female-specific characteristics of the leptin-VEGF relationship in obesity have been observed. Human studies have shown that elevated leptin and VEGF synthesis, along with leptin-VEGF crosstalk, are factors connecting obesity to increased cardiovascular risk. Recent studies have shed new light on the relationship between obesity, leptin-VEGF crosstalk, and heightened cardiovascular risk.
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