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Application of tectorigenin and derivatives thereof in medicines for preventing and treating insulin resistance diseases

A technology for insulin resistance and irisin, applied in diseases, metabolic diseases, bone diseases, etc.

Inactive Publication Date: 2018-12-25
NORTHEAST NORMAL UNIVERSITY
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0010] So far, there have been no research reports on irisin and its derivatives improving insulin target tissues and organs, such as muscle, liver and fat, etc.

Method used

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  • Application of tectorigenin and derivatives thereof in medicines for preventing and treating insulin resistance diseases
  • Application of tectorigenin and derivatives thereof in medicines for preventing and treating insulin resistance diseases
  • Application of tectorigenin and derivatives thereof in medicines for preventing and treating insulin resistance diseases

Examples

Experimental program
Comparison scheme
Effect test

Embodiment 1

[0036] Example 1. Effects of irisin and its derivatives on insulin-mediated uptake of glucose by cells such as skeletal muscle, fat and liver

[0037] Skeletal muscle, fat, and liver are the main target organs / tissues of insulin action, and they are also the most important tissues and organs that metabolize glucose in the body. Insulin resistance refers to a state in which the sensitivity of insulin target tissues to insulin decreases, resulting in lower than normal biological effects of normal doses of insulin, that is, decreased glucose uptake and utilization. In view of this, we first explored whether iridinin and its derivatives can promote insulin-mediated glucose uptake.

[0038] Materials: Myoblast C2C12 cells, preadipocyte cell line 3T3-L1, and liver cell line L02 were subcultured in our laboratory; DMEM medium, high-glucose DMEM medium and fetal bovine serum (FBS) were purchased from Gibco; Recombinant insulin (product number, 91077C), Isobutylmethylxanthine (IBMX; p...

Embodiment 2

[0052] Example 2. Effect of irisin on insulin sensitivity of normal and insulin-resistant skeletal muscle cells

[0053] Insulin binds and activates its insulin receptor, thereby activating the intracellular PI3K / AKT signaling pathway, increasing the level of phosphorylated AKT (phospho-AKT, P-AKT), and reactivating downstream target molecules to mediate metabolism including glucose uptake Biological effects included. Therefore, within a certain range, the insulin-mediated intracellular phosphorylated AKT level is directly proportional to the sensitivity of cells to insulin. When insulin resistance occurs, insulin will not be able to effectively raise phosphorylated AKT levels. Since Example 1 proves that irisin and its derivatives can promote insulin-mediated glucose uptake, next we will explore whether irisin and its derivatives can improve the sensitivity of cells to insulin in the case of insulin resistance.

[0054] Materials: For the acquisition and cultivation of C1C1...

Embodiment 3

[0057] Example 3, the preventive effect of irisin on high-fat diet-induced insulin resistance mice

[0058] We determined in vitro that irisinin can promote insulin-mediated glucose uptake in skeletal muscle, adipose and hepatic cells, and can improve the insulin resistance state of insulin-target tissue-derived cells. In order to further confirm the anti-insulin resistance effect of irisin in vivo, we used mice to construct an insulin resistance model, and first tested the preventive effect of irisin on insulin resistance.

[0059] Materials: Neutral insulin injection was purchased from Jiangsu Wanbang Biochemical Pharmaceutical Co., Ltd.; 45% high-fat feed (article number, MD12032) was purchased from Jiangsu Medisen Biomedical Co., Ltd.; blood glucose meter was purchased from Abbott; mouse insulin ( INS) ELISA kit (product number, m1001983) was purchased from Shanghai Enzyme Biotechnology Co., Ltd. Dissolve irisin in DMSO, dilute with normal saline, the proportion of DMSO s...

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Abstract

The invention relates to application of tectorigenin and derivatives thereof in medicines for preventing and treating insulin resistance diseases, and belongs to the field of biomedicine. The tectorigenin and the derivatives thereof have the effects of preventing and treating the insulin resistance diseases, can promote the glucose uptake capability of insulin target tissues, and enhance the sensitivity of insulin resistance cells to insulin; for insulin resistance mice induced by high-fat diet, the tectorigenin and the derivatives thereof can improve the insulin resistance state of the mice and the resulting hyperglycaemia and hyperinsulinemia, and has definite preventive and therapeutic effects on insulin resistance.

Description

technical field [0001] The invention belongs to the field of biomedicine, in particular to the use of iridinin and its derivatives in the preparation of drugs for preventing and treating insulin resistance-related diseases. Background technique [0002] Insulin resistance (Insulin Resistance, IR) refers to the weakening of the cellular effect produced by a unit concentration of insulin, that is, the target organs and tissues of insulin action, such as skeletal muscle, fat and liver, etc., are less responsive or sensitive to insulin, resulting in insulin-mediated Reduced cellular ability to uptake and metabolize glucose. Insulin activates the PI3K / AKT signaling pathway in the cell by binding to the insulin receptor on the surface of the target cell, and the activated AKT activates the substrate and finally promotes the translocation of glucose transporters (GLUT) to the cell membrane surface for uptake into the blood glucose and transport it into the cell for metabolism (SAL...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): A61K31/352A61K31/7048A61P5/50A61P3/04A61P3/10A61P3/06A61P9/12A61P9/10A61P19/06A61P15/08A61P1/16
CPCA61K31/352A61K31/7048A61P1/16A61P3/04A61P3/06A61P3/10A61P5/50A61P9/10A61P9/12A61P15/08A61P19/06
Inventor 孙陆果李玉新姚新蕾于春雷刘磊鲍永利王淑跃
Owner NORTHEAST NORMAL UNIVERSITY
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