In the case of central obesity, visceral adipocytes release excess fatty acids and pro-inflammatory adipocytokines such as leptin and tumour necrosis factor-alpha into the portal circulation, leading to increased hepatic adiposity and insulin resistance, which further activates the renin–angiotensin–aldosterone system, increasing sympathetic activity, enhancing procoagulant activity, and inducing endothelial dysfunction, leading to hypertension and other cardiovascular diseases29–31. Here, LEP is linked to endothelial dysfunction.