concanavalin-a and Metabolic-Syndrome

Metabolic syndrome (MetS), a cluster of various metabolic conditions, has become epidemic and causes increased morbidity and mortality.. The aim of this study was to compare lymphocyte proliferation under two different stimuli, Concanavalin A (ConA) and insulin, in a group of patients with MetS (Group 1) and a healthy group (Group 2).. Group 1 consisted of 53 patients who met the diagnostic criteria for MetS. Group 2 consisted of 63 patients without MetS. All individuals were evaluated for lipid profile and glycemia. Lymphocyte extraction and culture were performed for each subject and lymphocyte proliferation was assessed using the Alamar blue technique.. There was no gender difference between both groups, but in terms of age, there was a significant difference. The use of Con A at concentrations of 1 and 5 µg/mL induced a high lymphocyte proliferation in both groups. In contrast, when different concentrations of insulin were added, no significant changes in lymphocyte proliferation were observed. However, the proliferation of lymphocytes was significantly higher in Group 1 compared to Group 2 under insulin stimulus, which did not happen under ConA stimulation. Even after age and gender correction, this difference was maintained.. The increased lymphocyte proliferative response to insulin in patients with MetS found in this study suggests a role of the lymphocyte response to insulin in the pathophysiology of MetS. This response may be used as an immuno-biological marker for MetS, although further studies to evaluate its clinical usefulness need to be conducted.

Topics: Adult; Aged; Cell Proliferation; Concanavalin A; Female; Humans; Hypoglycemic Agents; Insulin; Male; Metabolic Syndrome; Middle Aged; Mitogens; T-Lymphocytes

To determine the immune-modulatory and the hepatoprotective effects of oral administration of two soy extracts in immune mediated liver injury and non-alcoholic steatohepatitis (NASH).. Two soy extracts, M1 and OS, were orally administered to mice with concanavalin A (ConA) immune-mediated hepatitis, to high-fat diet (HFD) mice and to methionine and choline reduced diet combined with HFD mice. Animals were followed for disease and immune biomarkers.. Oral administration of OS and M1 had an additive effect in alleviating ConA hepatitis manifested by a decrease in alanine aminotransferase and aspartate aminotransferase serum levels. Oral administration of the OS and M1 soy derived fractions, ameliorated liver injury in the high fat diet model of NASH, manifested by a decrease in hepatic triglyceride levels, improvement in liver histology, decreased serum cholesterol and triglycerides and improved insulin resistance. In the methionine and choline reduced diet combined with the high fat diet model, we noted a decrease in hepatic triglycerides and improvement in blood glucose levels and liver histology. The effects were associated with reduced serum tumor necrosis factor alpha and alteration of regulatory T cell distribution.. Oral administration of the combination of OS and M1 soy derived extracts exerted an adjuvant effect in the gut-immune system, altering the distribution of regulatory T cells, and alleviating immune mediated liver injury, hyperlipidemia and insulin resistance.

Topics: Administration, Oral; Animals; Biomarkers; Blood Glucose; Chemical and Drug Induced Liver Injury; Choline Deficiency; Concanavalin A; Cytoprotection; Diet, High-Fat; Disease Models, Animal; Glycine max; Immunologic Factors; Insulin; Insulin Resistance; Lipids; Liver; Metabolic Syndrome; Methionine; Mice; Non-alcoholic Fatty Liver Disease; Plant Extracts; T-Lymphocytes, Regulatory; Time Factors; Tumor Necrosis Factor-alpha

To determine the metabolic and immunological effects of the oral administration of DT56a, an enzymatic isolate of soybeans.. DT56a was orally administered to mice in three animal models: leptin deficiency, high-fat diet (HFD) supplementation and immune-mediated hepatitis. Liver damage and immunological status were assessed.. Oral administration of DT56a to leptin-deficient (ob/ob) and HFD mice led to a significant reduction in serum triglyceride (TG) and total cholesterol (TC) levels. DT56a-treated mice in both models exhibited a significant reduction in hepatic levels of TG and marked alleviation of glycemic control as indicated by significant decreases in fasting blood glucose levels and glucose tolerance tests. The levels of liver enzymes were reduced. These metabolic effects were associated with altered distributions of regulatory T (Tregs) and natural killer T (NKT) cells. DT56a suppressed the immune-mediated liver damage induced by concanavalin A indicated by decreased liver enzymes and serum interferon-γ levels and by improved histology and decreased hepatic apoptosis. Oral administration of DT56a also alleviated immune-mediated hepatitis and affected Tregs and NKT cells.. Oral administration of DT56a promotes a hepatoprotective effect associated with an alteration in the distribution of Tregs and NKT cells.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Blood Glucose; Cholesterol; Concanavalin A; Dietary Fats; Fatty Liver; Glucose Tolerance Test; Hepatitis, Autoimmune; Interferon-gamma; Leptin; Liver; Lymphocyte Count; Male; Metabolic Syndrome; Mice; Mice, Inbred C57BL; Mice, Knockout; Natural Killer T-Cells; Plant Extracts; T-Lymphocytes, Regulatory; Triglycerides