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BACKGROUND: Skeletal muscle insulin resistance is the key pathological link of type 2 diabetes. Static exercise can effectively improve skeletal muscle insulin resistance, but the mechanism remains unclear. OBJECTIVE: To explore the mechanism of static exercise on insulin resistance in the skeletal muscle of type 2 diabetic mice based on the phosphatidyl inositol 3-kinase (PI3K)/protein kinase B (AKT)/glucose transporter (GLUT4) signaling pathway. METHODS: After 1 week of adaptive feeding, 7 out of 40 C57BL/6 mice were randomly selected as blank group and fed common diet, while the other mice were fed high-fat diet and taken to prepare type 2 diabetes models through the low-dose streptozotocin intraperitoneal injection. Twenty-four mice were successfully modeled and they were randomly divided into model group (n=8), metformin group (n=8) and static exercise group (n=8), which continued to be fed high-fat diet. The metformin group was given 200 mg/kg metformin dissolved in normal saline (2 ml/kg) by gavage, once a day, for 6 weeks. The static exercise group was given normal saline daily by gavage and carried out static exercise, 30 minutes a day, 6 days per week. The model group was given the same dose of normal saline daily by gavage without exercise intervention. After the intervention, the fasting blood glucose of each group was detected, the intraperitoneal glucose tolerance test was performed, and the area under the glycemic curve was calculated. Glycosylated hemoglobin, serum insulin, insulin resistance index were detected by ELISA. Total cholesterol, triglyceride, high-density lipoprotein, low-density lipoprotein were detected using biochemical methods. The mRNA expression levels of PI3K, AKT and GLUT4 in the gastrocnemius of mice were detected by real-time quantitative PCR. Morphological changes of the gastrocnemius were observed by hematoxylin-eosin staining, and the cross-sectional area of muscle fibers was calculated. RESULTS AND CONCLUSION: Compared with the blank group, fasting blood glucose, glycosylated hemoglobin, area under the glycemic curve, insulin resistance index, total cholesterol, triglyceride and low-density lipoprotein levels were significantly increased in the model group (P < 0.01, P < 0.05). Whereas, these indicators were significantly lower in the static exercise and metformin group than the model group (P < 0.01, P < 0.05). Compared with the blank group, serum insulin and high-density lipoprotein levels were significantly declined in the model group (P < 0.01) and the mRNA expression of PI3K, AKT and GLUT4 in the gastrocnemius of mice were also significantly reduced (P < 0.01). These indicators were significantly elevated in the metformin group and static exercise group compared with the blank group (P < 0.01). Compared with the blank group, the muscle fibers in the model group were disordered, and the muscle cells atrophied and the muscle fiber gap widened. The cross-sectional area of muscle fibers was significantly decreased in the model group compared with the blank group (P < 0.01). Compared with the model group, atrophy of the gastrocnemius fibers and muscle fiber space were improved in the static exercise group and the metformin group, and the cross-sectional area of muscle fiber was significantly increased in both groups (P < 0.01). These findings indicate that static resistance training may promote glucose uptake and utilization by up-regulating the expression of PI3K, AKT and GLUT4 mRNA in skeletal muscle tissue, thereby improving the morphology and function of skeletal muscle tissue, alleviating insulin resistance and regulating glucose homeostasis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Because of the poor regeneration ability of chondrocytes after damage, the use of stem cells as a basic treatment for repairing cartilage damage has become a popular treatment method. OBJECTIVE: To observe the effect of psoralen combined with transforming growth factor β1 on the differentiation of rat bone marrow mesenchymal stem cells into chondrocytes. METHODS: Bone marrow mesenchymal stem cells were isolated from Sprague-Dawley rats and cultured by marrow adherent method. The effective concentration to promote bone marrow mesenchymal stem cells proliferation was selected by CCK-8 assay. Bone marrow mesenchymal stem cells were assigned to four groups. In the normal control group, cells were treated with low-sugar DMEM with 10% fetal bovine serum and 100 U/mL double antibodies. In the psoralen group, cells were treated with low-sugar DMEM with 10% fetal bovine serum, 100 U/mL double antibodies, 10-7 mol/L dexamethasone, 50 mg/L vitamin C, and 10 μmol/L psoralen. In the combination group, cells were treated with low-sugar DMEM with 10% fetal bovine serum, 100 U/mL double antibodies, 10 μg/L transforming growth factor β1, 10-7 mol/L dexamethasone, 50 mg/L vitamin C, and 10 μmol/L psoralen. In the positive control group, cells were treated with low-sugar DMEM with 10% fetal bovine serum, 100 U/mL double antibodies, 10 μg/L transforming growth factor β1, 10-7 mol/L dexamethasone, and 50 mg/L vitamin C. After 21 days, the expression of type ll collagen was detected by immunocytochemistry. RT-PCR and western blot assay were utilized to detect the expression levels of differentiation marker SOX-9 and type ll collagen mRNA and protein. RESULTS AND CONCLUSION: (1) Immunocytochemical staining showed that no positive cells were found in the normal control group, while type ll collagen positive cells were found in the other three groups. (2) Compared with the normal control group, the expression of SOX9 and type II collagen mRNA and protein increased significantly in the psoralen group, combination group and positive control group (P < 0.05), and the combination group had the best effect (P < 0.01), and it was significantly better than that in the positive control group and the psoralen group (P < 0.05). (3) The results show that within a certain concentration range, psoralen can promote the proliferation of bone marrow mesenchymal stem cells. Psoralen can induce bone marrow mesenchymal stem cells to differentiate into cartilage, and its combined use with transforming growth factor β1 has a synergistic promoting effect. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)