Glucose transporters and insulin action--implications for insulin resistance and diabetes mellitus.

The chemical composition of pectin production wastewater and its toxicity during biological treatment were investigated. Samples of wastewater from different steps of a pectin production wastewater biological treatment plant were investigated including the influent of the treatment (1), after denitrification tank (2), after anaerobic treatment (3) and final effluent (4). The conventional physicochemical characteristics of samples did not indicate wastewater toxicity. However, toxicity assessments carried out on Vibrio fischeri and Scenedesmus subspicatus indicated low EC50 values. The fractionation of the samples using an XAD resin showed that the toxicity was associated with the organic matter. Wastewater apparent molecular mass distributions were 14.3, 25.0, 24.4 and 29.6 kDa for samples 1-4, respectively. Finally, characteristics of the sample by pyrolisis-gas chromatography-mass spectrometry (Py-CG-MS) demonstrated its polyphenolic nature and a 23% increase in the levels of such compounds after the first biological treatment step.

New model of diabetes mellitus

Streptozotocin-induced pancreatic insulitis

Multiple small injections of streptozotocin in mice produce pancreatic insulitis, with progression to nearly complete beta cell destruction and diabetes mellitus. The timing and appearance of the inflammatory islet lesions suggest but do not prove that streptozotocin acts by initiating a cell-mediated immune reaction. Ultrastructural evidence of abundant type C viruses within beta cells of treated mice suggests that streptozotocin may activate murine leukemia virus in vivo in susceptible hosts.

Anti-CD3 Monoclonal Antibody in New-Onset Type 1 Diabetes Mellitus

Introduction

Type 1 diabetes mellitus is a chronic autoimmune disease caused by the pathogenic action of T lymphocytes on insulin-producing beta cells. Previous clinical studies have shown that continuous immune suppression temporarily slows the loss of insulin production. Preclinical studies suggested that a monoclonal antibody against CD3 could reverse hyperglycemia at presentation and induce tolerance to recurrent disease.

result of the study

Treatment with the monoclonal antibody maintained or improved insulin production after one year in 9 of the 12 patients in the treatment group, whereas only 2 of the 12 controls had a sustained response (P=0.01). The treatment effect on insulin responses lasted for at least 12 months after diagnosis. Glycosylated hemoglobin levels and insulin doses were also reduced in the monoclonal-antibody group. No severe side effects occurred, and the most common side effects were fever, rash, and anemia. Clinical responses were associated with a change in the ratio of CD4+ T cells to CD8+ T cells 30 and 90 days after treatment.

Treatment with hOKT3γ1(Ala-Ala) mitigates the deterioration in insulin production and improves metabolic control during the first year of type 1 diabetes mellitus in the majority of patients. The mechanism of action of the anti-CD3 monoclonal antibody may involve direct effects on pathogenic T cells, the induction of populations of regulatory cells, or both.