scholarly journals Inositols in Insulin Signaling and Glucose Metabolism

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Arturo Bevilacqua ◽  
Mariano Bizzarri
Keyword(s):  
Glucose Metabolism ◽  
Insulin Signaling ◽  
De Novo ◽  
Endocrine System ◽  
Negative Effects ◽  
Hormonal Stimulation ◽  
Insulin Resistant ◽  
Beneficial Effects ◽  
Intermediate Metabolites ◽  
The Subject

In the past decades, both the importance of inositol for human health and the complex interaction between glucose and inositol have been the subject of increasing consideration. Glucose has been shown to interfere with cellular transmembrane transport of inositol, inhibiting, among others, its intestinal absorption. Moreover, intracellular glucose is required for de novo biosynthesis of inositol through the inositol-3-phosphate synthase 1 pathway, while a few glucose-related metabolites, like sorbitol, reduce intracellular levels of inositol. Furthermore, inositol, via its major isomersmyo-inositol and D-chiro-inositol, and probably some of its phosphate intermediate metabolites and correlated enzymes (like inositol hexakisphosphate kinase) participate in both insulin signaling and glucose metabolism by influencing distinct pathways. Indeed, clinical data support the beneficial effects exerted by inositol by reducing glycaemia levels and hyperinsulinemia and buffering negative effects of sustained insulin stimulation upon the adipose tissue and the endocrine system. Due to these multiple effects, myoIns has become a reliable treatment option, as opposed to hormonal stimulation, for insulin-resistant PCOS patients.

Astaxanthin prevents loss of insulin signaling and improves glucose metabolism in liver of insulin resistant mice

2012 ◽  
Vol 90 (11) ◽  
pp. 1544-1552 ◽  
Author(s):  
Saravanan Bhuvaneswari ◽  
Carani Venkatraman Anuradha
Keyword(s):  
Glucose Metabolism ◽  
Body Mass ◽  
Insulin Signaling ◽  
Serine Phosphorylation ◽  
Insulin Resistant ◽  
Extracellular Signal ◽  
High Fructose ◽  
Normal Chow ◽  
Serine Kinases ◽  
Irs Proteins

This study investigates the effects of astaxanthin (ASX) on insulin signaling and glucose metabolism in the liver of mice fed a high fat and high fructose diet (HFFD). Adult male Mus musculus mice of body mass 25–30 g were fed either normal chow or the HFFD. After 15 days, mice in each group were subdivided among 2 smaller groups and treated with ASX (2 mg·(kg body mass)–1) in olive oil for 45 days. At the end of 60 days, HFFD-fed mice displayed insulin resistance while ASX-treated HFFD animals showed marked improvement in insulin sensitivity parameters. ASX treatment normalized the activities of hexokinase, pyruvate kinase, glucose-6-phosphatase, fructose-1,6-bisphosphatase, glycogen phosphorylase, and increased glycogen reserves in the liver. Liver tissue from ASX-treated HFFD-fed animals showed increased tyrosine phosphorylation and decreased serine phosphorylation of insulin receptor substrates (IRS)-1 and -2. ASX increased IRS 1/2 and phosphatidylinositol 3-kinase (PI3K) association and serine phosphorylation of Akt. In addition, ASX decreased HFFD-induced serine kinases (c-jun N-terminal kinase-1 and extracellular signal-regulated kinase-1). The results suggest that ASX treatment promotes the IRS–PI3K–Akt pathway of insulin signaling by decreasing serine phosphorylation of IRS proteins, and improves glucose metabolism by modulating metabolic enzymes.

Fucosylated Chondroitin Sulfate From Sea Cucumber Improves Glucose Metabolism and Activates Insulin Signaling in the Liver of Insulin-Resistant Mice

2014 ◽  
Vol 17 (7) ◽  
pp. 749-757 ◽  
Author(s):  
Shi-Wei Hu ◽  
Ying-Ying Tian ◽  
Yao-Guang Chang ◽  
Zhao-Jie Li ◽  
Chang-Hu Xue ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Chondroitin Sulfate ◽  
Insulin Signaling ◽  
Sea Cucumber ◽  
Insulin Resistant

scholarly journals Up-Regulating the Hemeoxygenase System Enhances Insulin Sensitivity and Improves Glucose Metabolism in Insulin-Resistant Diabetes in Goto-Kakizaki Rats

Endocrinology ◽  
2009 ◽  
Vol 150 (6) ◽  
pp. 2627-2636 ◽  
Author(s):  
Joseph Fomusi Ndisang ◽  
Ashok Jadhav
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Insulin Signaling ◽  
Gastrocnemius Muscle ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Antidiabetic Effect ◽  
Insulin Resistant

Insulin-mediated signal transduction is positively correlated to adiponectin, adenosine monophosphate-activated protein kinase (AMPK), and glucose-transporter-4 (GLUT4) but negatively to oxidative/inflammatory mediators such as nuclear factor-κB, activating-protein (AP)-1, AP-2, and c-Jun-N-terminal-kinase. Although hemeoxygenase (HO) suppresses oxidative insults, its effects on insulin-sensitizing agents like AMPK and GLUT4 remains unclear and were investigated using Goto-Kakizaki rats (GK), a nonobese insulin-resistant type-2 diabetic model. HO was induced with hemin or inhibited with chromium mesoporphyrin (CrMP). The application of hemin to GK rats evoked a 3-month antidiabetic effect, whereas the HO-inhibitor, CrMP, exacerbated hyperglycemia and nullified insulin-signaling/glucose metabolism. Interestingly, the antidiabetic was accompanied by a paradoxical increase of insulin alongside the potentiation of insulin-sensitizing agents such as adiponectin, AMPK, and GLUT4 in the gastrocnemius muscle. Furthermore, hemin enhanced mediators/regulators of insulin signaling like cGMP and cAMP and suppressed oxidative insults by up-regulating HO-1, HO activity, superoxide dismutase, catalase, and the total antioxidant capacity in the gastrocnemius muscle. Accordingly, oxidative markers/mediators including nuclear factor-κB, AP-1, AP-2, c-Jun-N-terminal-kinase, and 8-isoprostane were abated, whereas CrMP annulled the cytoprotective and antidiabetic effects of hemin. Correspondingly, ip glucose tolerance, insulin tolerance, and homeostasis model assessment insulin resistance analyses revealed improved glucose tolerance, reduced insulin intolerance, enhanced insulin sensitivity, and reduced insulin resistance in hemin-treated GK rats. In contrast, CrMP, abolished the insulin-sensitizing effects and restored and/or exacerbated insulin resistance. Our study unveils a 3-month enduring antidiabetic effect of hemin and unmasks the synergistic interaction among the HO system, adiponectin, AMPK, and GLUT4 that could be explored to enhance insulin signaling and improve glucose metabolism in insulin-resistant diabetes.

Invited Review: Exercise training-induced changes in insulin signaling in skeletal muscle

2002 ◽  
Vol 93 (2) ◽  
pp. 773-781 ◽  
Author(s):  
Juleen R. Zierath
Keyword(s):  
Skeletal Muscle ◽  
Signal Transduction ◽  
Protein Kinase ◽  
Glucose Metabolism ◽  
Exercise Training ◽  
Molecular Mechanism ◽  
Insulin Signaling ◽  
Insulin Signal Transduction ◽  
Insulin Signal ◽  
Insulin Resistant

This review will provide insight on the current understanding of the intracellular signaling mechanisms by which exercise training increases glucose metabolism and gene expression in skeletal muscle. Participation in regular exercise programs can have important clinical implications, leading to improved health in insulin-resistant persons. Evidence is emerging that insulin signal transduction at the level of insulin receptor substrates 1 and 2, as well as phosphatidylinositol 3-kinase, is enhanced in skeletal muscle after exercise training. This is clinically relevant because insulin signaling is impaired in skeletal muscle from insulin-resistant Type 2 diabetic and obese humans. The molecular mechanism for enhanced insulin-stimulated glucose uptake after exercise training may be partly related to increased expression and activity of key proteins known to regulate glucose metabolism in skeletal muscle. Exercise also leads to an insulin-independent increase in glucose transport, mediated in part by AMP-activated protein kinase. Changes in protein expression may be related to increased signal transduction through the mitogen-activated protein kinase signaling cascades, a pathway known to regulate transcriptional activity. Understanding the molecular mechanism for the activation of insulin signal transduction pathways after exercise training may provide novel entry points for new strategies to enhance glucose metabolism and for improved health in the general population.

Beneficial Effects of a Polyphenol-Rich Supplement from Strawberry and Cranberry on Glucose Metabolism in Free-Living Insulin-Resistant Men and Women

2014 ◽  
Vol 38 (5) ◽  
pp. S68-S69
Author(s):  
Martine Paquette ◽  
S John Weisnagel ◽  
Yves Desjardins ◽  
Julie Marois ◽  
André Marette ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Free Living ◽  
Men And Women ◽  
Insulin Resistant ◽  
Beneficial Effects

scholarly journals The Zinc Transporter Zip7 Is Downregulated in Skeletal Muscle of Insulin-Resistant Cells and in Mice Fed a High-Fat Diet

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 663 ◽  
Author(s):  
Shaghayegh Norouzi ◽  
John Adulcikas ◽  
Darren Henstridge ◽  
Sabrina Sonda ◽  
Sukhwinder Sohal ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Cell Signaling ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
Muscle Cells ◽  
Zinc Transporter ◽  
Skeletal Muscle Cells ◽  
High Fat ◽  
Insulin Resistant

Background: The zinc transporter Zip7 modulates zinc flux and controls cell signaling molecules associated with glucose metabolism in skeletal muscle. The present study evaluated the role of Zip7 in cell signaling pathways involved in insulin-resistant skeletal muscle and mice fed a high-fat diet. Methods: Insulin-resistant skeletal muscle cells were prepared by treatment with an inhibitor of the insulin receptor, HNMPA-(AM)3 or palmitate, and Zip7 was analyzed along with pAkt, pTyrosine and Glut4. Similarly, mice fed normal chow (NC) or a high-fat diet (HFD) were also analyzed for protein expression of Glut4 and Zip7. An overexpression system for Zip7 was utilized to determine the action of this zinc transporter on several genes implicated in insulin signaling and glucose control. Results: We identified that Zip7 is upregulated by glucose in normal skeletal muscle cells and downregulated in insulin-resistant skeletal muscle. We also observed (as expected) a decrease in pAkt and Glut4 in the insulin-resistant skeletal muscle cells. The overexpression of Zip7 in skeletal muscle cells led to the modulation of key genes involved in the insulin signaling axis and glucose metabolism including Akt3, Dok2, Fos, Hras, Kras, Nos2, Pck2, and Pparg. In an in vivo mouse model, we identified a reduction in Glut4 and Zip7 in the skeletal muscle of mice fed a HFD compared to NC controls. Conclusions: These data suggest that Zip7 plays a role in skeletal muscle insulin signaling and is downregulated in an insulin-resistant, and HFD state. Understanding the molecular mechanisms of Zip7 action will provide novel opportunities to target this transporter therapeutically for the treatment of insulin resistance and type 2 diabetes.

scholarly journals Pioglitazone does not improve insulin signaling in mice with GH over-expression

2013 ◽  
Vol 219 (2) ◽  
pp. 109-117 ◽  
Author(s):  
Adam Gesing ◽  
Andrzej Bartke ◽  
Michal M Masternak
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Mammalian Target Of Rapamycin ◽  
Sensitivity Index ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Over Expression ◽  
Insulin Resistant ◽  
Beneficial Effects

Type 2 diabetes and obesity are very serious health problems in both developed and developing countries. An increased level of GH is known to promote insulin resistance. Transgenic (Tg) mice over-expressing bovine GH are short-living and characterized, among other traits, by hyperinsulinemia and increased insulin resistance in comparison with normal (N) mice. Pioglitazone (PIO) is a member of the thiazolidinediones – a group of insulin-sensitizing drugs that are selective agonists of peroxisome proliferator-activated receptor gamma (PPARγ). The aim of the study was to analyze the effects of PIO on the insulin-signaling pathway in Tg and N mice. Plasma levels of insulin and glucose as well as hepatic levels of proteins involved in insulin signaling were analyzed by ELISA or western blot methods. Treatment with PIO decreased plasma level of glucose in N mice only. Similarly, PIO increased insulin sensitivity (expressed as the relative insulin sensitivity index; RISI) only in N mice. In the liver, PIO decreased the phosphorylation of insulin receptor substrate-1 (IRS1) at a serine residue (Ser307-pS-IRS1), which inhibits insulin action, and had a tendency to increase tyrosine phosphorylation of IRS2 (Tyr-pY-IRS2) only in N mice but did not affect either of these parameters in Tg mice. Levels of total and phosphorylated mammalian target of rapamycin were increased in Tg mice. Moreover, the level of AKT2 was decreased by PIO in N mice only. In conclusion, the lack of improvement of insulin sensitivity in insulin-resistant Tg mice during PIO treatment indicates that chronically elevated GH levels can inhibit the beneficial effects of PIO on insulin signaling.

Diabetes and Heart Failure: Is it Hyperglycemia or Hyperinsulinemia?

2020 ◽  
Vol 18 (2) ◽  
pp. 148-157 ◽  
Author(s):  
Triantafyllos Didangelos ◽  
Konstantinos Kantartzis
Keyword(s):  
Heart Failure ◽  
Insulin Treatment ◽  
Close Association ◽  
Adverse Outcomes ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Appropriate Treatment ◽  
Increased Risk ◽  
Treatment Of Diabetes

The cardiac effects of exogenously administered insulin for the treatment of diabetes (DM) have recently attracted much attention. In particular, it has been questioned whether insulin is the appropriate treatment for patients with type 2 diabetes mellitus and heart failure. While several old and some new studies suggested that insulin treatment has beneficial effects on the heart, recent observational studies indicate associations of insulin treatment with an increased risk of developing or worsening of pre-existing heart failure and higher mortality rates. However, there is actually little evidence that the associations of insulin administration with any adverse outcomes are causal. On the other hand, insulin clearly causes weight gain and may also cause serious episodes of hypoglycemia. Moreover, excess of insulin (hyperinsulinemia), as often seen with the use of injected insulin, seems to predispose to inflammation, hypertension, dyslipidemia, atherosclerosis, heart failure, and arrhythmias. Nevertheless, it should be stressed that most of the data concerning the effects of insulin on cardiac function derive from in vitro studies with isolated animal hearts. Therefore, the relevance of the findings of such studies for humans should be considered with caution. In the present review, we summarize the existing data about the potential positive and negative effects of insulin on the heart and attempt to answer the question whether any adverse effects of insulin or the consequences of hyperglycemia are more important and may provide a better explanation of the close association of DM with heart failure.

scholarly journals Can Ultrasound Therapy Be an Environmental-Friendly Alternative to Non-Steroidal Anti-Inflammatory Drugs in Knee Osteoarthritis Treatment?

Materials ◽  
2021 ◽  
Vol 14 (11) ◽  
pp. 2715
Author(s):  
Rodica Ana Ungur ◽  
Viorela Mihaela Ciortea ◽  
Laszlo Irsay ◽  
Alina Deniza Ciubean ◽  
Bogdana Adriana Năsui ◽  
...  
Keyword(s):  
Ultrasound Therapy ◽  
Negative Effects ◽  
Beneficial Effects ◽  
Knee Oa ◽  
Environmental Friendly ◽  
Chemical Pollutants ◽  
Osteoarthritis Treatment ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
And Function

The non-steroidal anti-inflammatory drugs (NSAIDs) are the most used drugs in knee OA (osteoarthritis) treatment. Despite their efficiency in pain and inflammation alleviation, NSAIDs accumulate in the environment as chemical pollutants and have numerous genetic, morphologic, and functional negative effects on plants and animals. Ultrasound (US) therapy can improve pain, inflammation, and function in knee OA, without impact on environment, and with supplementary metabolic beneficial effects on cartilage compared to NSAIDs. These features recommend US therapy as alternative for NSAIDs use in knee OA treatment.

scholarly journals CeO2 Nanoparticle-Containing Polymers for Biomedical Applications: A Review

Polymers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 924
Author(s):  
Alexander B. Shcherbakov ◽  
Vladimir V. Reukov ◽  
Alexander V. Yakimansky ◽  
Elena L. Krasnopeeva ◽  
Olga S. Ivanova ◽  
...  
Keyword(s):  
Biomedical Applications ◽  
Metal Oxide Nanoparticles ◽  
Polymeric Materials ◽  
Negative Effects ◽  
New Horizons ◽  
Beneficial Effects ◽  
Advanced Composite ◽  
Unique Material ◽  
Biomedical Polymers ◽  
Biomedical Potential

The development of advanced composite biomaterials combining the versatility and biodegradability of polymers and the unique characteristics of metal oxide nanoparticles unveils new horizons in emerging biomedical applications, including tissue regeneration, drug delivery and gene therapy, theranostics and medical imaging. Nanocrystalline cerium(IV) oxide, or nanoceria, stands out from a crowd of other metal oxides as being a truly unique material, showing great potential in biomedicine due to its low systemic toxicity and numerous beneficial effects on living systems. The combination of nanoceria with new generations of biomedical polymers, such as PolyHEMA (poly(2-hydroxyethyl methacrylate)-based hydrogels, electrospun nanofibrous polycaprolactone or natural-based chitosan or cellulose, helps to expand the prospective area of applications by facilitating their bioavailability and averting potential negative effects. This review describes recent advances in biomedical polymeric material practices, highlights up-to-the-minute cerium oxide nanoparticle applications, as well as polymer-nanoceria composites, and aims to address the question: how can nanoceria enhance the biomedical potential of modern polymeric materials?

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