oa Effect Of Diabetes On Gastric Stem Cell Lineage In Rat Models

In 2013, it was estimated that over 382 million people throughout the world suffered from diabetes. Despite the numerous treatment approaches to manage this condition, diabetic patients continue to suffer from various symptoms and complications. These include, but are not limited to, retinopathy, nephropathy, peripheral and autonomic neuropathy, gastrointestinal, genitourinary, cardiovascular, and cerebral symptoms. In this study, we attempt to investigate the variations in the gastric stem cell lineage in order to further understand the gastrointestinal symptoms experienced by diabetic patients and reveal possible treatment promises. Using rats as an animal model, we divide them into different age groups of 3, 6, 9, and 12 months. For each age group, there were twelve animals, six of which were kept as control. The other six were injected with Streptozotocin to destroy the Beta cells of the Islet of Langerhans in the pancreas. The diabetic rats' plasma glucose was closely monitored; those that naturally recovered from diabetes were researched separately. Antibodies against KI-67 and Oct3/4 are used to examine cellular proliferation, Ghrelin for cells secreting this hormone, H,K-ATPase for parietal cells, UEA and GSII lectins for the surface and neck mucus cells respectively. For more quantitative results, qRT-PCR using primers specific for genes of gastric stem cell differentiation pathways was used. Statistical calculations including One-tailed T-test were used to determine whether the changes between the control and diabetic groups were significant. Results suggest an increase in the proliferation activity of stem cells number of some cells like surface mucus cells, and a decrease in the number of ghrelin secreting cells. Future tests to be used in order to support these results include antibodies against gastrin, CCK, and LGR5.