Development of pancreatic islet cells in the extrahepatic bile ducts of rats with experimentally-induced metabolic syndrome.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-12-01 Epub Date: 2023-08-31 DOI:10.1080/13813455.2023.2252205

Maya Gulubova, Anna Tolekova, Dimitar Berbatov, Nurettin Aydogdu

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引用次数: 0

Abstract

Context: There is data about the existence of some endocrine cells in the epithelial layer of the bile duct in humans and rats.

Objective: We evaluated Ghrelin-, Insulin-, Glucagon- and Somatostatin-positive cells in peribiliary glands, mast cells, and nerve fibres.

Materials and methods: Wistar rats were used for dietary manipulation with a 15% fructose solution for 12 weeks. Tissue samples were elaborated with immunohistochemistry for Insulin, Glucagon, Ghrelin, and Somatostatin. Glucose and lipid parameters were studied.

Results: In treated animals, Ghrelin⁺ and Insulin⁺ cells in perybiliary glands (PBGs) were significantly increased. In the male fructose group there was a significant increase of the homeostasis model assessment insulin resistance (HOMA-IR).

Conclusions: Stem/progenitor cells in extrahepatic bile tree (EHBT) could be a source of Insulin-producing cells in metabolic syndrome. Fructose treatment induces the increase of Ghrelin⁺ and Insulin⁺ cells in PBGs and the elevation of Insulin and Ghrelin plasma concentration.

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实验性代谢综合征大鼠肝外胆管胰岛细胞的发育。

背景:有资料表明，人类和大鼠胆管上皮中存在一些内分泌细胞。目的:我们评估了生长素、胰岛素、胰高血糖素和生长抑素阳性细胞在胆道周围腺、肥大细胞和神经纤维中的作用。材料与方法:Wistar大鼠采用15%果糖溶液进行饮食操纵，为期12周。用免疫组化方法对组织样本进行胰岛素、胰高血糖素、生长素和生长抑素的检测。研究了葡萄糖和脂质参数。结果:治疗组小鼠胆道周围腺(PBGs)中Ghrelin+和胰岛素+细胞显著升高。在雄性果糖组中，评估胰岛素抵抗的稳态模型(HOMA-IR)显著增加。结论:肝外胆管树(EHBT)干细胞/祖细胞可能是代谢综合征中胰岛素生成细胞的来源。果糖处理诱导pbg中Ghrelin+和胰岛素+细胞增加，胰岛素和Ghrelin血浆浓度升高。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.