The elevated GLP-1 in systemic inflammatory conditions, such as sepsis, might be another anti-inflammatory mechanism to compensate for exaggerated inflammation as decreasing glucose intake during bacterial infections leading to sepsis onset protects from lethality, including neuronal damage [40] and dietary glucose intake is one of the other macronutrients regulating gastric and neuronal GLP-1 release. The gene discussed is GLP1R; the disease is bacterial infectious disease.