Abstract

BackgroundMulberry (Morus alba L.) leaf tea benefits the control of diabetes in Asian nations. This study was aim to investigate if the flavonoids, which extracts from mulberry leaves, could regulate the metabolism of glycolipid, and to investigate if flavonoids could regulate IRS1/PI3K/AKT pathway signal to affect the expression of FAS and membrane transfer capacity GLUT4 in 3T3-L1 adipocytes.ResultsResults revealed that flavonoids decreased the levels of free fatty acid and increased the glucose consumption and the levels of adiponectin and leptin in a dose-dependent manner, and remarkably increased the protein expression levels of p-IRS1, p-PI3K, p-Akt, total GLUT4, and membrane GLUT4, and decreased the protein expression levels of PTEN and FAS in 3T3-L1 adipocytes IR model. On the other hand, wortmannin (2 nM), a selective and irreversible PI3K inhibitor, significantly decreased the glucose consumption and the adiponectin and leptin levels, and increased the free fatty acid level in flavonoids treated 3T3-L1 adipocytes IR model. Furthermore, wortmannin (2 nM) partly eliminated the activation of PI3K/AKT signaling, the suppression of FAS, and the up-regulated membrane transfer capacity of GLUT4 in flavonoids treated 3T3-L1 adipocytes IR model.ConclusionIn conclusion, our results illustrated that mulberry leaf extracts flavonoids alleviated the glycolipid metabolic abnormalities in 3T3-L1 adipocytes IR model, and the effect was associated with the activation of IRS1/PI3K/AKT pathway, the suppression of FAS, and the up-regulation of membrane transfer capacity of GLUT4.

Highlights

  • As one of the main factors in the pathogenesis of type 2 diabetes mellitus (T2DM), insulin resistance (IR) is characterized by the decline of insulin sensitivity in insulinMeng et al Chin Med (2020) 15:1 a cause of IR and T2DM [6]

  • We used a mouse embryonic fibroblast (3T3-L1) adipocytes IR model to evaluate the effects of the flavonoids on the metabolism of glycolipid, and to investigate if the flavonoids could regulate IRS1/PI3K/AKT pathway signal to affect the expression of fatty acid synthetase (FAS) and the membrane transfer capacity of glucose transporter type 4 (GLUT4)

  • On the eighth day after induction of differentiation, and the cells were stained with oil red O dye, showing that the 3T3-L1 preadipocytes had been differentiated into mature fat cells (Fig. 2a)

Read more

Summary

Introduction

As one of the main factors in the pathogenesis of type 2 diabetes mellitus (T2DM), insulin resistance (IR) is characterized by the decline of insulin sensitivity in insulinMeng et al Chin Med (2020) 15:1 a cause of IR and T2DM [6]. Study reports that mulberry leaf extract stimulates glucose uptake and GLUT4 translocation in rat adipocytes [9], the mechanism of the hypoglycemic effects of the flavonoids that came from mulberry leaves in adipocytes was still unclear. We used a 3T3-L1 adipocytes IR model to evaluate the effects of the flavonoids on the metabolism of glycolipid, and to investigate if the flavonoids could regulate IRS1/PI3K/AKT pathway signal to affect the expression of FAS and the membrane transfer capacity of GLUT4. This study was aim to investigate if the flavonoids, which extracts from mulberry leaves, could regulate the metabolism of glycolipid, and to investigate if flavonoids could regulate IRS1/PI3K/AKT pathway signal to affect the expression of FAS and membrane transfer capacity GLUT4 in 3T3-L1 adipocytes

Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.