scholarly journals Exercise-Induced Muscle Damage Impairs Insulin Signaling Pathway Associated With IRS-1 Oxidative Modification

2012 ◽  
pp. 81-88 ◽  
Author(s):  
W. AOI ◽  
Y. NAITO ◽  
H. TOKUDA ◽  
Y. TANIMURA ◽  
T. OYA-ITO ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glucose Uptake ◽  
Signaling Pathway ◽  
Muscle Damage ◽  
Insulin Signaling ◽  
Acute Exercise ◽  
Insulin Signaling Pathway ◽  
Oxidative Modification ◽  
Whole Body ◽  
Strenuous Exercise

Strenuous exercise induces delayed-onset muscle damage including oxidative damage of cellular components. Oxidative stress to muscle cells impairs glucose uptake via disturbance of insulin signaling pathway. We investigated glucose uptake and insulin signaling in relation to oxidative protein modification in muscle after acute strenuous exercise. ICR mice were divided into sedentary and exercise groups. Mice in the exercise group performed downhill running exercise at 30 m/min for 30 min. At 24 hr after exercise, metabolic performance and insulin-signaling proteins in muscle tissues were examined. In whole body indirect calorimetry, carbohydrate utilization was decreased in the exercised mice along with reduction of the respiratory exchange ratio compared to the rested control mice. Insulin-stimulated uptake of 2-deoxy-[3H]glucose in damaged muscle was decreased after acute exercise. Tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and phosphatidyl-3-kinase/Akt signaling were impaired by exercise, leading to inhibition of the membrane translocation of glucose transporter 4. We also found that acute exercise caused 4-hydroxy-nonenal modification of IRS-1 along with elevation of oxidative stress in muscle tissue. Impairment of insulin-induced glucose uptake into damaged muscle after strenuous exercise would be related to disturbance of insulin signal transduction by oxidative modification of IRS-1.

Effects of collagen peptides from skate (Raja kenojei) skin on improvements of the insulin signaling pathway via attenuation of oxidative stress and inflammation

2020 ◽  
Vol 11 (3) ◽  
pp. 2017-2025 ◽  
Author(s):  
Minji Woo ◽  
Bo Gyeong Seol ◽  
Keon-Hee Kang ◽  
Yung Hyun Choi ◽  
Eun Ju Cho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Insulin Signaling Pathway ◽  
Antioxidative Status ◽  
Collagen Peptides ◽  
Hepatic Insulin Signaling

It has been well established that hepatic insulin signaling is significantly affected by the antioxidative status of the liver.

scholarly journals Sphingomyelinase has an insulin-like effect on glucose transporter translocation in adipocytes

1998 ◽  
Vol 274 (5) ◽  
pp. R1446-R1453 ◽  
Author(s):  
T. S. David ◽  
P. A. Ortiz ◽  
T. R. Smith ◽  
J. Turinsky
Keyword(s):  
Plasma Membrane ◽  
Insulin Receptor ◽  
Glucose Uptake ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Insulin Signaling Pathway ◽  
Glut 1 ◽  
Glut 4 ◽  
Glut 4 Translocation

Rat epididymal adipocytes were incubated with 0, 0.1, and 1 mU sphingomyelinase/ml for 30 or 60 min, and glucose uptake and GLUT-1 and GLUT-4 translocation were assessed. Adipocytes exposed to 1 mU sphingomyelinase/ml exhibited a 173% increase in glucose uptake. Sphingomyelinase had no effect on the abundance of GLUT-1 in the plasma membrane of adipocytes. In contrast, 1 mU sphingomyelinase/ml increased plasma membrane content of GLUT-4 by 120% and produced a simultaneous decrease in GLUT-4 abundance in the low-density microsomal fraction. Sphingomyelinase had no effect on tyrosine phosphorylation of either the insulin receptor β-subunit or the insulin receptor substrate-1, a signaling molecule in the insulin signaling pathway. It is concluded that the incubation of adipocytes with sphingomyelinase results in insulin-like translocation of GLUT-4 to the plasma membrane and that this translocation does not occur via the activation of the initial components of the insulin signaling pathway.

scholarly journals Modulation of Renal Insulin Signaling Pathway and Antioxidant Enzymes with Diabetes: Effects of Resveratrol

2018 ◽  
Author(s):  
Gökhan Sadi ◽  
Gamze Şahin ◽  
Aykut Bostancı
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Diabetic Rats ◽  
Insulin Signaling Pathway ◽  
Inflammatory Agent ◽  
Male Wistar Rats ◽  
The Relationship ◽  
Control State

Diabetes mellitus, a disease arising by the deficiency of insulin hormone or its inability of usage, affects carbohydrate, lipid and protein metabolism, and destruct variety of the tissues. A strong antioxidant and anti-inflammatory agent; resveratrol has a high potential to prevent or treat the pathogenesis of diseases. This study was conducted to reveal the relationship between diabetes-induced oxidative stress and tissue inflammation with changes in antioxidant enzymes (cat, sod, gpx, and gst) and the components of insulin signaling pathway (insulin Rβ, irs-1, pi3k, akt, mtor) in kidney tissues. Additionally, the effects of resveratrol on these parameters were evaluated. Male Wistar rats were randomly divided into four groups; (1) control/vehicle; (2) control/20 mg/kg resveratrol; (3) diabetic/vehicle; (4) diabetic/20 mg/kg resveratrol. Results demonstrated down-regulation of antioxidant enzymes in the kidney tissues of diabetic rats and this situation was devoted partially to the reduced expression of nfκb. Moreover, the components of renal insulin signaling elements were up-regulated in diabetic rats, and resveratrol treatment decreased this sensitization towards the control state. In conclusion, resveratrol improved diabetes-induced renal oxidative stress and inflammation partly due to healing action on renal antioxidant enzymes and insulin signaling pathway components.

scholarly journals Modulation of Renal Insulin Signaling Pathway and Antioxidant Enzymes with Streptozotocin-Induced Diabetes: Effects of Resveratrol

Medicina ◽  
2018 ◽  
Vol 55 (1) ◽  
pp. 3 ◽  
Author(s):  
Gökhan Sadi ◽  
Gamze Şahin ◽  
Aykut Bostanci
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Antioxidant Enzymes ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Diabetic Rats ◽  
Insulin Signaling Pathway ◽  
Enzymatic Antioxidants ◽  
Gene And Protein Expression ◽  
Male Wistar Rats

Background and objectives: Diabetes mellitus is a disease of insulin deficiency or its inability of usage by the target tissues leading to impairment of carbohydrate, lipid, and protein metabolisms. Resveratrol, having robust anti-inflammatory and anti-oxidant properties, has a high potential to treat or prevent the pathogenesis of diseases. This study was conducted to reveal the relationship between diabetes-induced oxidative stress and tissue inflammation with changes in main enzymatic antioxidants (cat, sod, gpx, and gst) and the components of the insulin signaling pathway (insulin Rβ, irs-1, pi3k, akt, mtor) in kidney tissues. Additionally, the effects of resveratrol on these parameters were evaluated. Materials and Methods: Male Wistar rats were randomly divided into four groups; (1) control/vehicle; (2) control/20 mg/kg resveratrol; (3) diabetic/vehicle; (4) diabetic/20 mg/kg resveratrol. Gene and protein expressions of antioxidant enzymes and insulin signaling elements were evaluated in renal tissues. Results: Downregulation of antioxidant enzymes’ gene expression in the kidney tissues of diabetic rats was demonstrated and this situation was devoted partially to the reduced gene expression of nfκb. Moreover, the components of renal insulin signaling elements were upregulated at both gene and protein expression levels in diabetic rats, and resveratrol treatment decreased this sensitization towards the control state. Conclusion: Resveratrol partially improved diabetes-induced renal oxidative stress and inflammation due to healing action on renal antioxidant enzymes and insulin signaling pathway components.

scholarly journals Glucose regulates the histone acetylation of gene promoters in decidualizing stromal cells

Reproduction ◽  
2019 ◽  
Vol 157 (5) ◽  
pp. 457-464 ◽  
Author(s):  
Kosuke Jozaki ◽  
Isao Tamura ◽  
Haruka Takagi ◽  
Yuichiro Shirafuta ◽  
Yumiko Mihara ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Stromal Cells ◽  
Insulin Signaling Pathway ◽  
Gene Promoters ◽  
Promoter Regions ◽  
Endometrial Stromal Cells ◽  
Expression Levels ◽  
Low Glucose

Decidualization stimuli activate the insulin signaling pathway and increase the glucose uptake in human endometrial stromal cells (ESCs). The inductions of prolactin (PRL) and IGF-binding protein-1 (IGFBP1), specific markers of decidualization, were inhibited by incubating ESCs under low glucose concentrations. These results suggested that decidualization stimuli activate the insulin signaling pathway, which contributes to decidualization through the increase of glucose uptake. Here, we investigated the mechanisms by which glucose regulates decidualization. ESCs were incubated with cAMP to induce decidualization. We examined whether low glucose affects the expression levels of transcription factors that induce decidualization. Forkhead box O1 (FOXO1) expression was significantly suppressed under low glucose conditions. Knockdown of FOXO1 by siRNA inhibited the expression levels of PRL and IGFBP1 during decidualization. Taken together, our results showed that low glucose inhibits decidualization by decreasing FOXO1 expression. We also examined the levels of histone H3K27 acetylation (H3K27ac), which is related to active transcription, of the promoter regions of FOXO1, PRL and IGFBP1 by ChIP assay. The H3K27ac levels of these promoter regions were increased by decidualization under normal glucose conditions, but not under low glucose conditions. Thus, our results show that glucose is indispensable for decidualization by activating the histone modification status of the promoters of PRL, IGFBP1 and FOXO1.

scholarly journals MicroRNA-506 modulates insulin resistance in human adipocytes by targeting S6K1 and altering the IRS1/PI3K/AKT insulin signaling pathway

2021 ◽  
Author(s):  
Feng-Yu Zhong ◽  
Jing Li ◽  
Yu-Mei Wang ◽  
Yao Chen ◽  
Jia Song ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Uptake ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Underlying Mechanism ◽  
Insulin Signaling Pathway ◽  
Akt Pathway ◽  
Public Health Issue ◽  
Pathway Activation ◽  
Candidate Target

AbstractThe incidence of obesity has increased rapidly, becoming a worldwide public health issue that involves insulin resistance. A growing number of recent studies have demonstrated that microRNAs play a significant role in controlling the insulin signaling network. For example, miR-506-3p expression has been demonstrated to correlate with insulin sensitivity; however, the underlying mechanism remains unknown. In this study, we found that miR-506-3p enhanced glucose uptake by 2-deoxy-D-glucose uptake assays and regulated the protein expression of key genes involved in the PI3K/AKT insulin signaling pathway including IRS1, PI3K, AKT, and GlUT4. We next predicted ribosomal protein S6 kinase B1 (S6K1) to be a candidate target of miR-506-3p by bioinformatics analysis and confirmed using dual-luciferase assays that miR-506-3p regulated S6K1 expression by binding to its 3′-UTR. Moreover, modulating S6K1 expression counteracted the effects of miR-506-3p on glucose uptake and PI3K/AKT pathway activation. In conclusion, miR-506-3p altered IR in adipocytes by regulating S6K1-mediated PI3K/AKT pathway activation. Taken together, these findings provide novel insights and potential targets for IR therapy.

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