155 Leptin, hunger and fat 5 INTRODUCTION Since survival rates of pediatric acute lymphoblastic leukemia (ALL) have increased to over 90% in high-income countries, more attention is being paid to acute and late toxicities.1 These toxicities are due to the disease itself, but also to the intensity and type of treatment. Dexamethasone is an important component of ALL treatment, but is notorious for its numerous side effects.2,3 Dyslipidemia and adiposity are well-known side effects of dexamethasone, as well as increased fatigue and sleep problems.4-6 Additionally, increased appetite and consequent unhealthy eating behavior are reported acute side effects of dexamethasone treatment.7-9 Previous pediatric ALL studies showed that merely four or five days of glucocorticoid treatment increased blood pressure as well as fasting glucose and lipid levels, and significantly induced insulin resistance.6,10 This illustrates that the high dose glucocorticoid pulses, which are frequently administered in ALL treatment, trigger significant metabolic changes, which in turn may precede long-term metabolic side effects with its attendant health consequences.11 Figure 1. Regulation of energy balance through leptin pathway Leptin is produced by adipose tissue and exerts its effect on both intake and energy expenditure through the hypothalamus. Low levels of leptin induce a physiological response including feeling of hunger and decreases energy expenditure. High leptin levels reduce food intake and increases energy expenditure. The exact effect of dexamethasone and sleep and fatigue is unknown. Created with BioRender.com
RkJQdWJsaXNoZXIy MTk4NDMw