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Is Leptin A Key to Metabolic Inflammation in Trauma and Sepsis?

The study by Negrin et al. (1) focuses on an understudied area involving the link between metabolism and inflammation. The obesity epidemic brought to the forefront the link between inflammation and metabolism, in part, by the association of obesity with chronic inflammation. Leptin is a key adipocytederived cytokine (adipokine) and is elevated in patients with obesity (2). Leptin functions as a neuro-endocrine hormone and is important in appetite regulation but also has effects on the innate and adaptive immune response (3). The objective of the study by Negrin et al. was to evaluate whether there was a dose-dependent therapeutic effect of exogenous leptin on mortality in a two-hit trauma and sepsis model and whether these effects were dependent on IL-6. The findings suggest that leptin administration reduces mortality in a murine model of trauma and sepsis. The authors also suggest that the reported effect is mediated by IL-6 and conclude that leptin may be considered a therapeutic agent for the prevention or treatment of sepsis post trauma. New pathways by which the immune system influences outcomes of trauma and sepsis and identifying potential therapeutics are important for critical care investigators. While the study provides some important mechanistic information on leptin and IL-6 in trauma and sepsis, some interesting but puzzling data still need to be explained. The authors demonstrate that higher-dose leptin administration improved survival in wild-type mice but not in IL-6 knockout mice after trauma/sepsis. While there was a survival benefit with leptin treatment, leptin treatment did not affect the activity level in mice after trauma/sepsis. It is difficult to understand how there is a survival benefit without a difference in activity level between the groups. An explanation for these discrepant findings may relate to the method of measurement. Activity level was scored once per day, scoring only live animals. No score was given to dead mice. Therefore, the activity level score does not reflect the group as a whole it only reflects the survivors’ activity level score. The lack of difference in activity level could also be explained by differences in food intake. At the examination of the body weights of these groups, the leptin-treated mice had lower body weights on days 4 to 6 after trauma/sepsis. An explanation for the weight differences could relate to less food intake in the leptin-treated mice compared with vehicle since leptin is known to suppress appetite. However, this was not examined in this study. Less food intake leading to weight loss may cause a relative