Analysis of the Localization of Connexin 36 in the Endocrine Part of Pancreatic Tissue in Modeling Various Subtypes of Gestational Diabetes Mellitus in Rats

Introduction. Gestational diabetes mellitus (GDM) is heterogeneous disease that includes several subtypes: subtype with predominant insulin resistance (IR) and subtype with predominant dysfunction of β-cell of pancreas. It was revealed that pancreatic cells express a gap junction protein, connexin 36, and gap junctions containing this protein normally coordinate the pulsating dynamics of Ca ²⁺ and the release of insulin, and disruption of this process may be one of the pathogenetic mechanisms of GDM.

The aim of work was to study distribution of connexin 36 in pancreatic tissue when modeling various subtypes of GDM in rats.

Materials and methods. Prospective study was conducted on white nonlinear rats: 50 females and 15 males. Female rats were divided into 3 groups: I — 15 pregnant rats (control); II — 12 pregnant rats (pancreatic β-cell dysfunction); III — 12 pregnant rats (IR). All rats underwent histomorphological examination on paraffin sections using primary rabbit polyclonal antibodies to connexin 36 (Invitrogen, USA).

Results. In study of pancreatic samples of group III, a sharp decrease in level of connexin 36 expression was noted. In samples of group II, it was revealed that in endocrine regions of gland, membrane reaction between cells is negative. Morphometric examination revealed a significant decrease in both the specific density of immune complexes and their average area in groups III and II (p < 0.050).

Discussion. An immunohistochemical study of the distribution of connexin 36 indicates a decrease in electrotonic connectivity through gap contacts both in model of GDM subtype with predominant IR and pancreatic beta-cell dysfunction.

Conclusion. Results obtained suggest that reduction of connexin 36 may accompany development of pathogenetic mechanisms of GDM.

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