Mulberry Bark Alleviates Effect of STZ Inducing Diabetic Mice through Negatively Regulating FoxO1

Dysfunction of insulin secretion and hyperglycaemia were commonly found due to damaged β cells of pancreas. In our previous research, it was found that mulberry branch bark powder (MBBP) was effective in treating diabetes in mice which were induced by STZ and high fat diet. The present study was des...

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Bibliographic Details
Published in:Evidence-based complementary and alternative medicine 2019-01, Vol.2019 (2019), p.1-9
Main Authors: Zhang, Yu-Qing, Liu, Hua-Yu, Wang, Jiang, Qiu, Fan
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Antioxidants
Apoptosis
Bark
Blood glucose
Body weight loss
Diabetes
Diabetes mellitus
Evidence-based medicine
Feeds
Flavonoids
FOXO1 protein
Gene expression
Genetic screening
Glucose
High fat diet
Hyperglycemia
Insulin
Insulin resistance
Insulin secretion
Kinases
Laboratories
Leaves
Liver
Medicine
Metabolism
Metabolites
Oxidative stress
Pancreas
Phosphorylation
Powder
Proteins
Secretion
Signal transduction
Toxicity
Transcription factors
Weight loss
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Summary:Dysfunction of insulin secretion and hyperglycaemia were commonly found due to damaged β cells of pancreas. In our previous research, it was found that mulberry branch bark powder (MBBP) was effective in treating diabetes in mice which were induced by STZ and high fat diet. The present study was designed to evaluate the protective effect of MBBP on STZ-induced β cells injury and investigate underlying mechanisms. By preventive administration of branch bark powder, the damage caused by STZ injection was found to be alleviated. In MBBP feed groups, pathological weight loss was inhibited, fasting blood glucose was controlled, the incidence of diabetes decreased, and blood lipid level and antioxidant capacities were restored. The PI3K/AKT/FoxO1 signal pathway was found to be activated by key proteins expression and gene testing. In liver, the increased PI3K and phosphorylated AKT, the phosphorylated, and inactivated FoxO1, which regulates the expression of gluconeogenic gene and explains the effect of relieving insulin resistance of MBBP. Therefore, the MBBP improves the tolerance of pancreas to the toxicity of STZ involving the PI3K/AKT/FoxO1 signalling pathway.
ISSN:1741-427X
1741-4288
DOI:10.1155/2019/2182865