Crocins from Crocus sativus L. in the Management of Hyperglycemia. In Vivo Evidence from Zebrafish.

Eleni Kakouri,Dimitris Beis,Adamantia Agalou,Charalabos Kanakis,Petros A Tarantilis

doi:10.3390/molecules25225223

Abstract

Diabetes mellitus is a disease characterized by persistent high blood glucose levels and accompanied by impaired metabolic pathways. In this study, we used zebrafish to investigate the effect of crocins isolated from Crocus sativus L., on the control of glucose levels and pancreatic β-cells. Embryos were exposed to an aqueous solution of crocins and whole embryo glucose levels were measured at 48 h post-treatment. We showed that the application of crocins reduces zebrafish embryo glucose levels and enhances insulin expression. We also examined whether crocins are implicated in the metabolic pathway of gluconeogenesis. We showed that following a single application of crocins and glucose level reduction, the expression of phosphoenolpyruvate carboxykinase 1 (pck1), a key gene involved in glucose metabolism, is increased. We propose a putative role for the crocins in glucose metabolism and insulin management.

Highlights

Diabetes mellitus (DM) is a chronic metabolic disease characterized by persistent high blood glucose levels and accompanied by impaired metabolic pathways of carbohydrates, proteins, and lipids.Diabetes is essentially caused either by the loss of β-cells, or of their ability to produce insulin
We aimed to investigate the effect of CRCs isolated from Crocus sativus L., on the control of glucose levels using zebrafish as an animal model
We examined whether the addition of crocins would regulate the levels of phosphoenolpyruvate carboxykinase 1, a key regulatory gene for the gluconeogenesis process that contributes to the maintenance of normoglycemia

Summary

Introduction

Diabetes mellitus (DM) is a chronic metabolic disease characterized by persistent high blood glucose levels and accompanied by impaired metabolic pathways of carbohydrates, proteins, and lipids. Diabetes is essentially caused either by the loss of β-cells, or of their ability to produce insulin (type I). Type II diabetes refers to the inability of the organism to properly regulate and sense insulin, known as resistance to insulin. Hyperglycemia is the result of both types. Since insulin is the main transporter, responsible for removing glucose from the blood-stream, its deficiency can inescapably lead to elevated blood glucose levels. Persistent hyperglycemia can lead to severe micro and macrovascular complications causing long-term damage to nerves and blood vessels, affecting different body organs

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