Endocrine Abstracts

Introduction: β cells are a major target of therapeutic strategies to treat diabetes and are extensively studied in terms of their differentiation, function, and maintenance. β cell mass dynamically changes in response to altered metabolic demands in an organism. Many therapies are suggested including transplantation of pancreas or islet cells for type 1 diabetes patients, however these procedures are associated with significant risks and costs. Hence, search for new therapeutic modalities is extremely actual.

Design: Stretozotocin was used as diabetogenic agent. As an antidiabetic compound was used Embryonal antitumor modulator, created by Prof. L. Mkrtchyan (EATM-LM). Preparation of primary mouse β cell culture was conducted as described by Skelin et al. (2010). Pancreatic islet and β cell identity was confirmed by morphological studies of cell suspension and fixed cells stained with AzurII-eozin and immunostained with anti-insulin antibodies using light and fluorescent microscopy. Cells were counted in the Neubauer counting chamber with 600× magnification) and the results expressed by means of β cells count ×10⁵/ml. Tripan blue (TB) exclusion method was used to evaluate the effect of tested agents on cells viability. Agarose gel electrophoresis was used to assay of DNA damage value and character.

Results: EATM revealed pronounced protective activity in stretozotocin–induced damage of pancreatic β cells. In a primary culture of mouse pancreatic β cells EATM prevented stretozotocin action in different concentrations (0.01–0.1 mg/ml). EATM promoted survival of β cells damaged by stretozotocin. Moreover, EATM prevented the decrease of insulin production and DNA destruction in stretozotocin-damaged β cells.

Conclusions: The data obtained support the idea of the the appropriateness of EATM in diabetes therapy.