Persistent inflammation, immuno-suppression and catabolism syndrome (PICS) occurs at the later stage of sepsis, characterized by T cell dysfunction with severe poor outcome. Recent studies found that T cell function be largely affected by its metabolic status. In sepsis, a variety of signaling molecules, including the nutrients, could trigger T cell to undergo metabolic reprogramming that from oxidative phosphorylation to aerobic glycolysis via phosphatidylinositol 3-kinase (PI3K)-serine/threonine kinases (Akt)-mammalian target of rapamycin (mTOR) pathway, leading to severe alterations of its immune phenotype. Glucagon-like peptide-1 (GLP-1) is a kind of incretin hormone that could regulate nutrients and energy metabolism in the body. It can reduce blood glucose level, suppress the immune and inflammatory responses. Plasma GLP-1 levels were rapidly elevated in sepsis and correlated closely with the outcome in critical care. GLP-1 receptor (GLP-1R) agonist could block the glycolysis of T cells, reduce glucose transporter type 1 mRNA expression, and inhibit T cell proliferation. Therefore, the elevated GLP-1 level may represent the metabolic switch toward "aerobic glycolysis", reflecting the pathological status of PICS. Here, the review elucidates the regulation of GLP-1 on the immune function and metabolic reprogramming of T cells and provides strategies for the prevention and treatment of T cell immune dysfunction in sepsis via GLP-1 receptor.