Cholecalciferol ameliorates insulin signalling and insulin regulation of enzymes involved in glucose metabolism in the rat heart.

IF 2.5 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Tamara Ivkovic, Tijana Culafic, Snezana Tepavcevic, Snjezana Romic, Mojca Stojiljkovic, Milan Kostic, Jelena Stanisic, Goran Koricanac
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引用次数: 0

Abstract

Context: The evidence on potential cross-talk of vitamin D and insulin in the regulation of cardiac metabolism is very scanty.

Objective: Cholecalciferol was administered to male Wistar rats for six weeks to study its effects on cardiac glucose metabolism regulation.

Materials and methods: An expression, phosphorylation and/or subcellular localisation of insulin signalling molecules, glucose transport and metabolism key proteins were studied.

Results: Circulating non-esterified fatty acids (NEFA) level was lower after cholecalciferol administration. Cholecalciferol decreased cardiac insulin receptor substrate 1 Ser307 phosphorylation, while insulin-stimulated Akt Thr308 phosphorylation was increased. Cardiac 6-phosphofructo-2-kinase protein, hexokinase 2 mRNA level and insulin-stimulated glycogen synthase kinase 3β Ser9 phosphorylation were also increased. Finally, FOXO1 transcription factor cytosolic level was reduced.

Conclusion: Vitamin D-related improvement of insulin signalling and insulin regulation of glucose metabolism in the rat heart is accompanied by the decrease of blood NEFA level and dysregulation of cardiac FOXO1 signalling.

胆钙化醇可改善胰岛素信号和胰岛素对大鼠心脏葡萄糖代谢酶的调节。
背景:关于维生素 D 和胰岛素在调节心脏代谢过程中潜在交叉作用的证据非常少:给雄性 Wistar 大鼠注射胆钙化醇六周,研究其对心脏糖代谢调节的影响:研究胰岛素信号分子、葡萄糖转运和代谢关键蛋白的表达、磷酸化和/或亚细胞定位:结果:服用胆钙化醇后,循环中的非酯化脂肪酸(NEFA)水平降低。胆钙化醇降低了心脏胰岛素受体底物 1 Ser307 的磷酸化,而胰岛素刺激的 Akt Thr308 磷酸化增加。心脏 6-磷酸果糖-2-激酶蛋白、己糖激酶 2 mRNA 水平和胰岛素刺激的糖原合酶激酶 3β Ser9 磷酸化也增加了。最后,FOXO1 转录因子的细胞水平降低:结论:维生素 D 改善了大鼠心脏的胰岛素信号传导和胰岛素对糖代谢的调节,同时降低了血液中 NEFA 的水平,并导致心脏 FOXO1 信号传导失调。
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来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
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.
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