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Effects of Whole Body Vibration in Adult Individuals with Metabolic Syndrome
Published in Redha Taiar, Christiano Bittencourt Machado, Xavier Chiementin, Mario Bernardo-Filho, Whole Body Vibrations, 2019
D. da Cunha de Sá-Caputo, M. Fritsch Neves, Mario Bernardo-Filho
In addition, an IDF publication (2006) pointed out that (a) genetics, (b) physical inactivity, (c) ageing, (d) proinflammatory state, and (e) hormonal changes may also have a causal effect, but the role of these may vary depending on ethnic group. Furthermore, IR occurs when cells (liver, skeletal muscle, and adipose/fat tissue) become less sensitive and eventually resistant to insulin that facilitates the glucose absorption. Glucose, which remains in the blood, leads the necessity of more and more insulin (hyperinsulinemia). When the pancreas does not produce enough insulin, there is hyperglycemia characterizing the diagnosis of T2DM. Before the presence of T2DM occurs a build-up of triglycerides which further impairs insulin sensitivity. The glucose transporter type-4 (GLUT4) is a protein that plays a relevant role in the tissue and plasma glucose balance. Moreover, it is involved in the facilitated diffusion of glucose in insulin-sensitive tissues. Changes in the expression and/or translocation of the glucose transporter, especially in adipose and skeletal muscle cells, has been directly associated with IR (Klip, 2009; Klip et al., 2009; Caponi et al., 2013).
Enzyme Nanocapsules for Glucose Sensing and Insulin Delivery
Published in Grunwald Peter, Biocatalysis and Nanotechnology, 2017
Insulin circulates throughout the blood stream until it binds to an insulin receptor. Binding to insulin causes a conformational change of the insulin receptor that activates its kinase domain and induces the autophosphorylation of tyrosine residues on the C-terminus of the receptor, leading to internal signal cascade that allows the glucose transporter 4 (GLUT4) to transport glucose into cells (Fig. 16.1 c) (Yang, 2010). The key consequence of intracellular signal transduction is the increased expression of GLUT4 in the plasma membrane and the immediate activation of glycogen synthase. By the facilitative transport of glucose into the cells, the glucose transporters effectively remove glucose from the blood stream. The glycogen synthase converts the glucose into glycogen and stores it in cells as the glucose reservoir (Halse et al., 2001). The insulin receptors promote the uptake of glucose into various tissues but mainly muscle cells (myocytes) and fat cells (adipocytes) (Czech et al., 1978). When glucose concentration comes down to normal level, the insulin secretion from beta cells slows and stops. The insulin action will be terminated by endocytosis and degradation of GLUT4, which leads to a decrease and finally to an abolished glucose uptake in myoctes and adipocytes (Yang, 2010).
Optimizing 3D Models of Engineered Skeletal Muscle
Published in Karen J.L. Burg, Didier Dréau, Timothy Burg, Engineering 3D Tissue Test Systems, 2017
Megan E. Kondash, Brittany N. J. Davis, George A. Truskey
Glucose enters skeletal muscle cells primarily via two glucose transporters, GLUT1 and GLUT4, that allow selective movement of glucose down its concentration gradient into the cell. GLUT1 is responsible for constitutive, basal glucose uptake in skeletal muscle, whereas GLUT4 is responsible for insulin-stimulated glucose uptake. However, the ratio of GLUT1 to GLUT4 expression increases when cells are taken from a 3D physiological environment and plated in a 2D culture system, causing a change in the metabolic behavior of cells cultured in vitro. In vivo, rat muscle has a GLUT1/GLUT4 protein ratio value that varies from 0.1 to 0.6 (Sarabia et al. 1992; Kraegen et al. 1993), whereas rat constructs in vitro showed a GLUT1/GLUT4 protein ratio of 6.3:1 (Baker et al. 2003). In vivo, human muscle was found to have a GLUT1:GLUT4 total cell mRNA expression ratio of 0.6:1 (Stuart et al. 2000), whereas total cell mRNA expression levels in myotubes in vitro showed a ratio of 12:1 (Al-Khalili et al. 2003). The high GLUT1 content seen in cultured cells contributes to a high basal uptake rate that dilutes the insulin responsive glucose uptake by the relatively less abundant GLUT4 transporters.
Amphiphilic block versus random copolymer nanoparticles with reactive oxygen species responsiveness as berberine vehicles
Published in Journal of Biomaterials Science, Polymer Edition, 2021
Honglei Guo, Qianqian Guo, Tianyu Lan, Yongjun Luo, Xiuhao Pan, Yifang Yao, Yafei Li, Ya Feng, Yujia Liu, Ling Tao, Xiangchun Shen
Insulin can stimulate Glut4 translocation to the plasma membrane for transporting glucose into cells, thereby reducing the blood glucose level [50]. Since BBR can increase insulin sensitivity to facilitate the cell uptake of glucose [11, 12, 51], a 2-DOG uptake assay was performed to evaluate the effect of BBR on insulin. Figure 10 shows Glut4 immunofluorescence staining in mouse podocytes with different agents. It was found that BBR did not differ from the control group, indicating that BBR was ineffective for Glut4 translocation. Insulin improved Glut4 translocation to the cell membrane and promoted glucose transport into the cells. The combination of insulin with BBR also improved Glut4 translocation, and the fluorescent intensity was stronger than that in the insulin group. The block and random nanoparticles did not differ from the control group, indicating that blank nanoparticles were ineffective for Glut4 translocation. By comparison, the combination of insulin with BBR-loaded nanoparticle groups showed higher fluorescence intensity, revealing a significant increase in the glucose uptake of cells. These results show that BBR and BBR-loaded nanoparticles can enhance the effect of insulin on improving Glut4 translocation to the plasma membrane.
Biochanin A prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced adipocyte dysfunction in cultured 3T3-L1 cells
Published in Journal of Environmental Science and Health, Part A, 2019
Eun Mi Choi, Kwang Sik Suh, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Suk Chon
In the present study, biochanin A significantly increased insulin-stimulated glucose uptake in the presence of TCDD. Glucose uptake by adipose tissue occurs through glucose transporters and is a major mechanism for reducing the blood glucose level.[30] Insulin induces the translocation of GLUT4 to the cell membrane through the IRS-1 pathway in adipose tissue. Impaired GLUT4 translocation plays a pivotal role in the pathogenesis of insulin resistance as an early defect during the development of type 2 diabetes.[31] GLUT4 provides insulin-stimulated glucose transport in adipocytes,[32] and phosphorylation of IRS-1 is a key event linking inflammation and insulin resistance.[33,34] In the present study, we observed that TCDD attenuated IRS-1 and GLUT4 levels, while biochanin A reversed these changes, leading to improved glucose uptake. This positive effect of biochanin A on insulin signaling improved glucose tolerance under TCDD-induced disease conditions. Many inflammatory molecules attenuate insulin-mediated tyrosine phosphorylation of IRS1, leading to insulin resistance.[34] We observed a significant increase in PGE2, as well as a decrease in IRS-1, in 3T3-L1 adipocytes exposed to TCDD; all of these changes were partially reversed by biochanin A. These results confirm that biochanin A has anti-inflammatory effects in adipose cells that are in line with its influence on insulin signaling.
Applications of omega-3 polyunsaturated fatty acid supplementation for sport performance
Published in Research in Sports Medicine, 2019
Jordan D. Philpott, Oliver C. Witard, Stuart D.R. Galloway
Dietary intake of n-3PUFA also are known to alter membrane fatty acid composition in skeletal (Andersson, Nälsén, Tengblad, & Vessby, 2002) and myocardial (Charnock, McLennan, & Abeywardena, 1992) muscle tissue. These changes in membrane composition can lead to changes in insulin sensitivity (Borkman et al., 1993) via a yet to be determined mechanism. However, a pre-clinical rodent study demonstrated that the addition of n-3PUFA to a high fat diet increased the protein expression of Glucose transporter type-4 (GLUT4; Lanza et al., 2013). GLUT4 is present only in skeletal muscle and adipose tissue and plays a key role in transporting extracellular glucose into cells that are insulin sensitive (Huang & Czech, 2007). In humans, n-3PUFA supplementation also has been shown to improve insulin sensitivity in skeletal muscle (Borkman et al., 1989). Thus, in theory, an increase in GLUT4 expression with n-3PUFA supplementation may play a key role in improving tissue insulin sensitivity and thus endurance performance.