Intestinal Microbiota Determine Severity of Myocardial Infarction in Rats

We read with great interest the recent paper by Lam et al. (1). This novel paper demonstrated that alteration of the gut microbiome by vancomycin significantly reduced leptin levels and subsequently led to an increased myocardial ischemia tolerance. They confirmed that leptin was directly involved in myocardial ischemia tolerance by demonstrating that pretreatment with leptin abolished the cardioprotection seen with vancomycin treatment. There is, however, conflicting evidence of the role of leptin in myocardial ischemia tolerance, with other groups reporting that leptin may be beneficial (2–4). Receptors for leptin are known to be present on both the myocardium and the kidney (5), which prompted us to examine whether tissue protection induced by vancomycin treatment could be extended to other organs. We replicated the experimental protocol described by Lam et al. (1) in 24 male Wistar rats, which were divided into control and vancomycin (0.5 mg/ml)treated groups. After 1 week, all animals underwent a right nephrectomy and a 45-min left renal artery occlusion, followed by reperfusion for 48 h, at which point, the animals were killed. Serum leptin concentrations and the degree of renal failure were measured. We confirmed the finding by Lam et al. (1)—that 1 week of vancomycin treatment led to a significant reduction in serum leptin levels (Table 1). Despite a 41% reduction in serum leptin levels by vancomycin, no difference in renal injury was seen between the treated and untreated groups, as measured by serum urea, creatinine, phosphate, potassium, or AST. We conclude that this novel effect of leptin-mediated, reduced ischemia tolerance appears to be tissue-specific and currently limited to the myocardium. REFERENCES