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Prolonged oxidative stress can cause enzyme inactivation, lipid peroxidation (LPOx), deoxyribonucleic acid (DNA) damage, and lead to apoptosis or cell necrosis
These therapies interact with natural pathways involved in appetite and glucose balance, and are prescribed following a medical evaluation
Accordingly, the prevention of declining leptin levels via exogenous leptin treatment attenuates starvation-induced suppression of gonadal and thyroid axes in mice and humans 1, 3
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