Analysis of the activity of c-kit immunopositive alpha-cells of the pancreas in exogenous infusions and endogenously formed pathology

Abstract

There are a number of factors and agents that change the population of endocrinocytes and their secretory activity depending on various conditions and experimentally formed pathologies. These include the impact of intermittent hypoxic hypoxia; experimentally formed pathology (diabetes); genetically formed pathology (arterial hypertension), direct effect on endocrinocytes of the pancreas with their own pathophysiological mechanism. In this context, it is interesting to analyze the state of the progenitor potential of alpha cells depending on the living conditions of the organism, its effects, and developing pathological conditions in it. The aim of the work is to determine the activity of the proliferative factor c-kit in alpha cells under exogenous factors – intermittent hypoxic hypoxia and endogenously formed pathology – arterial hypertension and diabetes. Materials and methods. The study was conducted on the pancreas of SHR and Wistar rats. Glucagon and c-kit in pancreatic islets were determined by the immunofluorescence method. The immunofluorescence reaction was studied with an AxioImager-M2 fluorescence microscope. Results. Analysis of the c-kit positive alpha-cell index in rats with diabetes showed a 5-fold increase. This was explained by the fact, that the development of hyperglycemia in diabetes mellitus was characterized not only by an increased level of glucose in the blood due to insufficient insulin production but also due to an increase in the number of alpha cells, their active proliferation and possible transdifferentiation from beta cells. The number of c-kit positive alpha cells in SHR rats decreased. This may indicate that these changes were not so related to a violation of the modulation of the transcription factor, but to the participation of neurogenic mechanisms. The decrease in c-kit positive alpha cells in animals with hypoxic hypoxia can be explained by transdifferentiation (remodeling) changes, aimed at suppressing proliferative processes in alpha endocrinocytes. Conclusions. The increase in the number of c-kit positive alpha cells in rats with diabetes is explained by the fact, that the development of hyperglycemia in diabetes is characterized not only by an increased level of glucose in the blood due to insufficient insulin production but also by an increase in the number of alpha cells, their active proliferation and possible transdifferentiation from beta cells. A decrease in the number of c-kit positive alpha cells in SHR rats may indicate that these changes are not so much related to a violation of the modulation of the transcription factor, but to the participation of neurogenic mechanisms. The decrease in c-kit positive alpha cells in animals with hypoxic hypoxia can be explained by transdifferentiation (remodeling) changes, aimed at suppressing proliferative processes in alpha endocrinocytes.