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One of the proposed mechanisms is that HTY may support wound healing by influencing growth factors and cytokines involved in tissue repair, including vascular endothelial growth factor receptor 2 (VEGFR2) [103, 104]

Alternatively, preclinical studies using leptin-deficient animals ( ob/ob mice) demonstrated that restoring plasma leptin concentration to normal improved heart function after MI, and that these beneficial effects were associated with reductions in cardiac inflammation and apoptosis [13, 14] and activation of anti-hypertrophic pathways in obese animals with left ventricle (LV) hypertrophy [8]

These tissue changes create a depot that traps medication, releasing it erratically rather than smoothly