aeruginosa, and ligation followed by puncture of the cecum, the administration of human LECT2 improved survival. LECTT2 acted by directly stimulating the CD209 receptor on mouse macrophages thereby mobilizing their protective functions. Knockout of the Lect2 gene in mice increase the mortality caused by staphylococcal enterotoxin A; human LECT2 reduced this morality increase. Blood levels of LECT2 in patients suffering bacterial sepsis correlated inversely with the severity of systemic inflammation suggesting that LECT2 blood levels may be a reliable diagnostic indicator of human inflammatory diseases. Diabetes Deletion of the Lect2 gene in mice improves peripheral glucose entry into tissues. These studies suggest that mouse Lect2 suppresses insulin signaling in skeletal muscle but not adipose or liver tissues of Lect2-deficient mice and thereby may contribute to the development of insulin resistance. Indeed, serum levels of LECT2 are increased in animal models of insulin-resistant diabetes as well as in individual diabetics demonstrating insulin resistance. These data suggest that inhibiting LECT2 production or action may be clinically useful means for treating diabetes. In support of this notion, Gemigliptin, an anti-diabetic drug, has been shown reduce insulin resistance and concurrently inhibit Lect2 production in a mouse model of dietary-induces insulin resistance. Studies conducted on cultured myocytes, a form of muscle cell, indicates that LECT2 impairs insulin signaling by activating a c-Jun N-terminal kinases cell signaling pathway. Metabolic syndrome Mice made deficient in the Lect2 gene were compared to wild-type mice in a model of high fatty acid diet-induced obesity and the metabolic syndrome. Lect2-deficient mice appeared to be protected from developing certain characteristics of the metabolic syndrome: they exhibited less weight gain; lower blood glucose and insulin levels following feeding; and better results for glucose and insulin tolerance tests. In a study of 200 individuals in Japan, serum LECT2 levels correlated positively with (i.e. increased in proportion to increases in) several clinical features of the metabolic syndrome viz., body mass index, waist circumference, systolic blood pressure, selenoprotein P serum levels, and hemoglobin A1c blood levels. Levels of LECT2 are also elevated in individuals not only with diagnosed metabolic syndrome but also with a characteristic of and possible precursor to the metabolic syndrome, non-alcoholic fatty liver disease. LEPT2 has been suggested to be a potential therapeutic target for treating the metabolic syndrome. Cancer Circulating levels of LECT2 are elevated in >90% of individuals with hepatoblastoma and >20% of individuals with Hepatocellular carcinoma. In the latter