Obesity is a well-known public health issue around the world.
Sepsis is a lethal clinical syndrome that causes multiorgan failure.
Obesity may aggravate
inflammation in septic patients.
Glutamine (GLN) is a nutrient with immune regulatory and anti-inflammatory properties. Since
sepsis is a common contributing factor for
acute kidney injury (AKI), this study investigated the effects of GLN administration on
sepsis-induced
inflammation and AKI in obese mice. A high-fat diet which consists of 60% of calories from fat was provided for 10 weeks to induce
obesity in the mice. Then, the obese mice were subdivided into
sepsis with saline (SS) or GLN (SG) groups. Cecal
ligation and
puncture (CLP) was performed to produce
sepsis. The SS group was intravenously injected with saline while the SG group was administered GLN one or two doses after CLP. Obese mice with
sepsis were sacrificed at 12, 24, or 48 h post-CLP. Results revealed that
sepsis resulted in upregulated high-mobility group box protein-1 pathway-associated gene expression in obese mice. Also, expressions of macrophage/neutrophil infiltration markers and inflammatory
cytokines in kidneys were elevated. Obese mice treated with GLN after
sepsis reversed the depletion of plasma GLN, reduced production of
lipid peroxides, and downregulated macrophage/neutrophil infiltration and the inflammatory-associated pathway whereas tight junction gene expression increased in the kidneys. These findings suggest that intravenously administered GLN to obese mice after
sepsis alleviated
inflammation and attenuated AKI. This model may have clinical application to obese patients with a risk for
infection in abdominal surgery.