Metabolic syndrome improves cardiovascular dysfunction and survival during cecal ligation and puncture-induced mild sepsis in mice

Sepsis is a potentially fatal systemic inflammatory response and its underlying pathophysiology is still poorly understood. Studies suggest that obesity, a component of metabolic syndrome (MS), is associated with sepsis survival. Therefore, this study focused on investigating the influence of MS on mortality and cardiovascular dysfunction induced by sublethal cecal ligation and puncture (SL-CLP). Newborn Swiss mice received monosodium glutamate (MSG) (4 mg kg−1 day−1, s.c.) during the first 5 d of life for MS induction, while the control pups received equimolar saline solution. On the 75th day, SL-CLP was used to induce mild sepsis (M-CLP) in the MS (MS-M-CLP) and control (SAL-M-CLP) mice. The effect of MS on sepsis in mice was assessed by determining the survival rate and quantification of nitric oxide (NO) in the plasma, and associating this data with hematological and cardiovascular parameters. MS improved the survival of septic mice, preventing impairment to hematological and cardiovascular parameters. In addition, MS attenuated plasmatic NO increase, which is a typical feature of sepsis. These findings provide new insights into the relationship between obesity and mild sepsis in mice, thus revealing an approach in favor of the “obesity paradox.” •Metabolic syndrome protects mice from CLP-induced mild sepsis in mice.•Hypotension during sepsis is blunted in mice with metabolic syndrome.•Metabolic syndrome attenuates NO increase during sepsis.•Hematological profile favors MS animals to survive due to sepsis.