Leptin, a regulator of eating behavior, is secreted by adipocytes and affects energy homeostasis in health and disease. Specifically, leptin is implicated in modulating multiple pathways controlling energy intake, energy expenditure and the allocation of precious nutrients between conversion, storage, and consumption. Whereas leptin has been shown to be a major determinant of anorexia in uremic animals, human data are so far unclear. Regardless, multiple studies have demonstrated that patients with chronic kidney function impairment have elevated leptin levels, although these levels still correlate strongly with body fat mass. In the present publication, we will review the current evidence for the pathophysiological role of leptin, focusing on chronic kidney disease (CKD) patients.
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