A low-protein diet during pregnancy prevents modifications in intercellular communication proteins in rat islets.

Ana Flávia Marçal-Pessoa,Cristiana Dos Santos Barbosa Salvatierra,Luiz Fabrizio Stoppiglia,Marise Auxiliadora De Barros Reis,Letícia Martins Ignacio-Souza,Roberto Vilela Veloso,Márcia Queiroz Latorraca,Vanessa Cristina Arantes,Sílvia Regina De Lima Reis,Carmen Lucia Bassi-Branco,Antonio Carlos Boschero,Everardo Magalhães Carneiro

doi:10.1186/0717-6287-48-3

Ana Flávia Marçal-Pessoa, Cristiana Dos Santos Barbosa Salvatierra + Show 10 more

Open Access

https://doi.org/10.1186/0717-6287-48-3

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Abstract

BackgroundGap junctions between β-cells participate in the precise regulation of insulin secretion. Adherens junctions and their associated proteins are required for the formation, function and structural maintenance of gap junctions. Increases in the number of the gap junctions between β-cells and enhanced glucose-stimulated insulin secretion are observed during pregnancy. In contrast, protein restriction produces structural and functional alterations that result in poor insulin secretion in response to glucose. We investigated whether protein restriction during pregnancy affects the expression of mRNA and proteins involved in gap and adherens junctions in pancreatic islets. An isoenergetic low-protein diet (6% protein) was fed to non-pregnant or pregnant rats from day 1–15 of pregnancy, and rats fed an isocaloric normal-protein diet (17% protein) were used as controls.ResultsThe low-protein diet reduced the levels of connexin 36 and β-catenin protein in pancreatic islets. In rats fed the control diet, pregnancy increased the levels of phospho-[Ser279/282]-connexin 43, and it decreased the levels of connexin 36, β-catenin and beta-actin mRNA as well as the levels of connexin 36 and β-catenin protein in islets. The low-protein diet during pregnancy did not alter these mRNA and protein levels, but avoided the increase of levels of phospho-[Ser279/282]-connexin 43 in islets. Insulin secretion in response to 8.3 mmol/L glucose was higher in pregnant rats than in non-pregnant rats, independently of the nutritional status.ConclusionShort-term protein restriction during pregnancy prevented the Cx43 phosphorylation, but this event did not interfer in the insulin secretion.

Highlights

Gap junctions between β-cells participate in the precise regulation of insulin secretion
Because the regulation of gap junction communication can occur at both the transcriptional and translational levels, we investigated the effect of protein restriction during pregnancy on the gene and protein expression of gap and adherens junction-associated proteins (Cx36, Cx43, β-catenin and β-actin) in pancreatic islets
Pregnancy enhanced the food intake in the two nutritional status groups, and the low-protein pregnant (LPP) group ate the same amount of food as the control pregnant (CP) group

Summary

Introduction

Gap junctions between β-cells participate in the precise regulation of insulin secretion. Increases in the number of the gap junctions between β-cells and enhanced glucose-stimulated insulin secretion are observed during pregnancy. Pregnancy increases glucose-stimulated insulin secretion and reduces the threshold for stimulation of insulin secretion by glucose [1,2] This effect is attributed to enhanced glucose metabolism, increased activity of the cAMP and PLC pathways [1,3,4,5], high β-cell proliferation and increased islet volume [6], insulin synthesis [7] and gap junction coupling among β-cells [8]. Connexin proteins form membrane channels at gap junctions, allowing β-cells to rapidly exchange cytoplasmic ions and metabolites, signaling the activity state of neighboring cells This direct communication allows for a coordinated and synchronized response of the islet cell [16,18,19,20]. Both homozygous and heterozygous transgenic mice that overexpresses Cx43 present increases in the islet size, and heterozygous mice exhibit an increase in insulin levels [25]

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