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Hitoshi Ashida - One of the best experts on this subject based on the ideXlab platform.
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Green Tea Ameliorates Hyperglycemia by Promoting the Translocation of Glucose Transporter 4 in the Skeletal Muscle of Diabetic Rodents
International journal of molecular sciences, 2019Co-Authors: Manabu Ueda-wakagi, Yoko Yamashita, Hironobu Nagayasu, Hitoshi AshidaAbstract:It is known that green tea helps prevent obesity and diabetes mellitus. In this study, we aimed to determine whether green tea ameliorates hyperglycemia and the mechanism involved in diabetic rodents. Green tea consumption reduced blood Glucose and ameliorated Glucose intolerance, which was assessed using an oral Glucose tolerance test in both streptozotocin-induced type 1 diabetic rats and type 2 diabetic KK-Ay mice. Green tea also reduced the plasma fructosamine and glycated hemoglobin concentrations in both models. Furthermore, it increased Glucose uptake into the skeletal muscle of both model animals, which was accompanied by greater translocation of Glucose Transporter 4 (GLUT4). Moreover, epigallocatechin gallate (EGCG), the principal catechin in green tea, also ameliorated Glucose intolerance in high-fat diet-induced obese and diabetic mice. These results suggest that green tea can ameliorate hyperglycemia in diabetic rodents by stimulating GLUT4-mediated Glucose uptake in skeletal muscle, and that EGCG is one of the effective compounds that mediate this effect.
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rutin potentiates insulin receptor kinase to enhance insulin dependent Glucose Transporter 4 translocation
Molecular Nutrition & Food Research, 2014Co-Authors: Chia-yu Hsu, Hung-yuan Shih, Yi-chen Chia, Chia-hung Lee, Hitoshi Ashida, Yiu-kay Lai, Ching-feng WengAbstract:cope We investigated whether rutin, a flavonoid isolated from Toona sinensis Roem, has the ability to enhance insulin-dependent receptor kinase (IRK) activity and Glucose Transporter 4 (GLUT4) translocation in differentiated myotubes. We also tested the effects of rutin treatment in insulin-resistant mice using an oral Glucose tolerance test (OGTT). Methods and results Rutin potentiated insulin receptor kinase (IRK) phosphorylation when IRK autophosphorylation was triggered by insulin in differentiated myotubes. Co-treatment of cells with rutin and insulin attenuated S961-mediated inhibition of insulin-dependent GLUT4 translocation. In S961-treated C57BL/6 mice, an in vivo model of insulin resistance and type 2 diabetes, rutin treatment showed a normoglycemic effect in the OGTT. Conclusion This study shows evidence that rutin may serve as a potential agent for glycemic control through enhancement of IRK activity, thereby inducing the insulin signaling pathway causing increased GLUT4 translocation and increased Glucose uptake.
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Rutin potentiates insulin receptor kinase to enhance insulin‐dependent Glucose Transporter 4 translocation
Molecular nutrition & food research, 2014Co-Authors: Chia-yu Hsu, Hung-yuan Shih, Yi-chen Chia, Chia-hung Lee, Hitoshi Ashida, Yiu-kay Lai, Ching-feng WengAbstract:cope We investigated whether rutin, a flavonoid isolated from Toona sinensis Roem, has the ability to enhance insulin-dependent receptor kinase (IRK) activity and Glucose Transporter 4 (GLUT4) translocation in differentiated myotubes. We also tested the effects of rutin treatment in insulin-resistant mice using an oral Glucose tolerance test (OGTT). Methods and results Rutin potentiated insulin receptor kinase (IRK) phosphorylation when IRK autophosphorylation was triggered by insulin in differentiated myotubes. Co-treatment of cells with rutin and insulin attenuated S961-mediated inhibition of insulin-dependent GLUT4 translocation. In S961-treated C57BL/6 mice, an in vivo model of insulin resistance and type 2 diabetes, rutin treatment showed a normoglycemic effect in the OGTT. Conclusion This study shows evidence that rutin may serve as a potential agent for glycemic control through enhancement of IRK activity, thereby inducing the insulin signaling pathway causing increased GLUT4 translocation and increased Glucose uptake.
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Fermented tea improves Glucose intolerance in mice by enhancing translocation of Glucose Transporter 4 in skeletal muscle.
Journal of agricultural and food chemistry, 2012Co-Authors: Yoko Yamashita, Lihua Wang, Zhang Tinshun, Toshiyuki Nakamura, Hitoshi AshidaAbstract:The antihyperglycemic effects of tea are well documented. However, the effects of fermented tea on the translocation of Glucose Transporter 4 (GLUT4), the major Glucose Transporter for Glucose uptake in the postprandial period, in skeletal muscle and the underlying molecular mechanisms are not fully understood. This study investigated the translocation of GLUT4 and its related signaling pathways in skeletal muscle of male ICR mice given fermented tea. Intake of oolong, black, or pu-erh tea for 7 days enhanced GLUT4 translocation to the plasma membrane of skeletal muscle. Each type of fermented tea stimulated the phosphorylation of phosphoinositide 3-kinase (PI3K), Akt/protein kinase B, and AMP-activated protein kinase (AMPK). Fermented tea also increased the protein expression of insulin receptor. These results strongly suggest that fermented tea activates both PI3K/Akt- and AMPK-dependent signaling pathways to induce GLUT4 translocation and increases the expression of insulin receptor to improve Glucose ...
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cardamonin stimulates Glucose uptake through translocation of Glucose Transporter 4 in l6 myotubes
Phytotherapy Research, 2011Co-Authors: Norio Yamamoto, Kyuichi Kawabata, Keisuke Sawada, Manabu Ueda, Itsuko Fukuda, Kengo Kawasaki, Akira Murakami, Hitoshi AshidaAbstract:Glucose Transporter-4 (GLUT4) is a transmembrane protein that plays a major role in insulin-mediated Glucose transport in muscle and adipocytes. For Glucose transport to occur, the GLUT4 protein needs to be translocated from the intracellular pool to the plasma membrane, and certain compounds may enhance this process. The present study investigated the promotion of Glucose uptake in differentiated L6 myotubes by cardamonin, isolated from Alpinia katsumadai. Cardamonin increased translocation of GLUT4 to the plasma membrane in L6 cells, but did not activate protein kinase C ζ/λ, Akt, or AMP-activated protein-kinase, all of which are known to regulate GLUT4 translocation. The Glucose-uptake-promoting activity of cardamonin was not lowered by treatment with a phosphatidylinositol 3'-kinase inhibitor. These results suggest that cardamonin is a promising active compound for maintaining Glucose homeostasis, and that it acts via an unknown mechanism that does not involve activation of the downstream insulin signal and AMP-activated protein kinase.
Kejian Pang - One of the best experts on this subject based on the ideXlab platform.
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New flavonoids from the roots of Sophora davidii (Franch.) Skeels and their Glucose Transporter 4 translocation activities.
Bioorganic chemistry, 2020Co-Authors: Tongxi Zhou, Ping Zhao, Xinzhou Yang, Ho-young Choi, Ji Hao, Huiqi Huang, Kejian PangAbstract:Five new flavanones, davidones A-E (1-5), one new isoflavonoid, cyclolicoisoflavones A3 (8), together with seven known compounds were isolated from the petroleum ether and the ethyl acetate fractions of the roots of Sophora davidii (Franch.) Skeels. The structures of new compounds were established by 1D and 2D NMR and MS data. The absolute configuration of 1-5 was assigned by NMR calculations and comparing its experimental and calculated ECD spectra. Flavanones were the main active principles responsible for the Glucose Transporter 4 (GLUT-4) translocation activities of SD-PE and SD-EtOAc. Compounds 1-7 and acacetin (12) promoted GLUT-4 translocation by the range of 1.35-3.00 folds, respectively.
Xinzhou Yang - One of the best experts on this subject based on the ideXlab platform.
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Chemical Constituents from Roots of Sophora davidii (Franch.) Skeels and Their Glucose Transporter 4 Translocation Activities.
Molecules (Basel Switzerland), 2021Co-Authors: Tongxi Zhou, Xinzhou Yang, Ho-young ChoiAbstract:Sophora davidii (Franch.) Skeels is a multi-purpose traditional medicine that has long been used for the treatment of various diseases. To discover the potential bioactive composition of S. davidii, a chemical investigation was thus performed. In this research, two new stilbene oligomers, Davidiol E–F (1–2), one new 4-aryl-substituted isoflavan Davidinin A (3), and one new 2-arylbenzofuran dimer, Shandougenine C (4), as well as six known compounds (5–10) were obtained from the ethyl acetate fraction of Sophora davidii (Franch.) Skeels. The structures of new compounds were established by extensive 1D and 2D nuclear magnetic resonance (NMR) spectra with mass spectroscopy data. The absolute configuration of 1–3 was assigned by comparing its experimental and calculated electronic circular dichroism (ECD) spectra. Compounds 1–10 promoted Glucose Transporter 4 (GLUT-4) translocations by the range of 1.28–2.60 folds, respectively. Compound 9 showed the most potent Glucose Transporter 4 translocations with 1.60 fold enhancement. The result attained in this study indicated that the separation and characterization of these compounds plays an important role in the research and development of new anti-diabetic drugs and pharmaceutical industry.
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New flavonoids from the roots of Sophora davidii (Franch.) Skeels and their Glucose Transporter 4 translocation activities.
Bioorganic chemistry, 2020Co-Authors: Tongxi Zhou, Ping Zhao, Xinzhou Yang, Ho-young Choi, Ji Hao, Huiqi Huang, Kejian PangAbstract:Five new flavanones, davidones A-E (1-5), one new isoflavonoid, cyclolicoisoflavones A3 (8), together with seven known compounds were isolated from the petroleum ether and the ethyl acetate fractions of the roots of Sophora davidii (Franch.) Skeels. The structures of new compounds were established by 1D and 2D NMR and MS data. The absolute configuration of 1-5 was assigned by NMR calculations and comparing its experimental and calculated ECD spectra. Flavanones were the main active principles responsible for the Glucose Transporter 4 (GLUT-4) translocation activities of SD-PE and SD-EtOAc. Compounds 1-7 and acacetin (12) promoted GLUT-4 translocation by the range of 1.35-3.00 folds, respectively.
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Chemical constituents from Eucalyptus citriodora Hook leaves and their Glucose Transporter 4 translocation activities.
Bioorganic & medicinal chemistry letters, 2014Co-Authors: Chao Wang, Jing Yang, Ping Zhao, Qi Zhou, Zhinan Mei, Guangzhong Yang, Xinzhou Yang, Yunjiang FengAbstract:Bioassay-guided phytochemical investigation of the EtOAc fraction from the leaves of a Chinese medicinal herb, Eucalyptus citriodora Hook, resulted in the isolation of a new compound rhodomyrtosone E (1), along with 12 known compounds (2-13). The structure of the new compound was established by 1D and 2D NMR, MS data and X-ray crystallographic analysis. Betulinic acid (2) and corosolic acid (5) increased Glucose Transporter 4 (GLUT-4) translocation by 2.38 and 1.78-fold, respectively.
Amira Klip - One of the best experts on this subject based on the ideXlab platform.
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Endocytosis, Recycling, and Regulated Exocytosis of Glucose Transporter 4
Biochemistry, 2011Co-Authors: Kevin P. Foley, Shlomit Boguslavsky, Amira KlipAbstract:Glucose Transporter 4 (GLUT4) is responsible for the uptake of Glucose into muscle and adipose tissues. Under resting conditions, GLUT4 is dynamically retained through idle cycling among selective intracellular compartments, from whence it undergoes slow recycling to the plasma membrane (PM). This dynamic retention can be released by command from intracellular signals elicited by insulin and other stimuli, which result in 2-10-fold increases in the surface level of GLUT4. Insulin-derived signals promote translocation of GLUT4 to the PM from a specialized compartment termed GLUT4 storage vesicles (GSV). Much effort has been devoted to the characterization of the intracellular compartments and dynamics of GLUT4 cycling and to the signals by which GLUT4 is sorted into, and recruited from, GSV. This review summarizes our understanding of intracellular GLUT4 traffic during its internalization from the membrane, its slow, constitutive recycling, and its regulated exocytosis in response to insulin. In spite of specific differences in GLUT4 dynamic behavior in adipose and muscle cells, the generalities of its endocytic and exocytic itineraries are consistent and an array of regulatory proteins that regulate each vesicular traffic event emerges from these cell systems.
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regulation of Glucose Transporter 4 traffic by energy deprivation from mitochondrial compromise
Acta Physiologica, 2009Co-Authors: Amira Klip, Jonathan D Schertzer, Phillip J Bilan, F Thong, Costin N AntonescuAbstract:Skeletal muscle is the major store and consumer of fatty acids and Glucose. Glucose enters muscle through Glucose Transporter 4 (GLUT4). Upon insufficient oxygen availability or energy compromise, aerobic metabolism of Glucose and fatty aids cannot proceed, and muscle cells rely on anaerobic metabolism of Glucose to restore cellular energy status. An increase in Glucose uptake into muscle is a key response to stimuli requiring rapid energy supply. This chapter analyses the mechanisms of the adaptive regulation of Glucose transport that rescue muscle cells from mitochondrial uncoupling. Under these conditions, the initial drop in ATP recovers rapidly, through a compensatory increase in Glucose uptake. This adaptive response involves AMPK activation by the initial ATP drop, which elevates cell surface GLUT4 and Glucose uptake. The gain in surface GLUT4 involves different signals and routes of intracellular traffic compared with those engaged by insulin. The hormone increases GLUT4 exocytosis through phosphatidylinositol 3-kinase and Akt, whereas energy stress retards GLUT4 endocytosis through AMPK and calcium inputs. Given that energy stress is a component of muscle contraction, and that contraction activates AMPK and raises cytosolic calcium, we hypothesize that the increase in Glucose uptake during contraction may also involve a reduction in GLUT4 endocytosis.
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The many ways to regulate Glucose Transporter 4.
Applied physiology nutrition and metabolism = Physiologie appliquee nutrition et metabolisme, 2009Co-Authors: Amira KlipAbstract:Glucose uptake into skeletal muscle is primarily mediated by Glucose Transporter 4 (GLUT4). The number of GLUT4 polypeptides at the surface of muscle cells rises rapidly in response to insulin, contraction, depolarization, or energy deprivation. However, distinct mechanisms underlie the gain in surface GLUT4 in each case. Insulin promotes its exocytosis to the membrane, regulating vesicle movement, tethering, docking, and fusion. In contrast, muscle contraction, depolarization, and energy demand reduce GLUT4 endocytosis. The signals involved in each case also differ. Insulin utilizes Akt, Rabs, and selective actin remodelling, whereas depolarization and energy deprivation engage AMP-activated protein kinase and Ca2+-dependent signals. GLUT4 internalizes via 2 major routes that involve dynamin, but only one requires clathrin. The clathrin-independent route is slowed down by energy deprivation, and is regulated by AMP-activated protein kinase. In addition to regulation of the exocytic and endocytic movement...
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Clathrin-dependent and independent endocytosis of Glucose Transporter 4 (GLUT4) in myoblasts: regulation by mitochondrial uncoupling.
Traffic (Copenhagen Denmark), 2008Co-Authors: Costin N Antonescu, Mònica Díaz, Guiseppe Femia, Josep V. Planas, Amira KlipAbstract:In myocytes and adipocytes, insulin increases Glucose Transporter 4 (GLUT4) exocytosis by promoting GLUT4 vesicle docking/fusion with the membrane. Less is known about the mechanism and regulation of GLUT4 endocytosis, particularly in myocytes. Here, we show that GLUT4 internalization in L6 myoblasts was inhibited in part by hypertonicity or clathrin heavy chain knockdown and in part by cholesterol depletion. Both strategies had additive effects, abolishing GLUT4 endocytosis. GLUT4 internalization was abrogated by expressing dominant-negative dynamin-2 but unaffected by inhibiting caveolar-dependent endocytosis through syntaxin-6 knockdown or caveolin mutants (which reduced lactosylceramide endocytosis). Insulin did not affect GLUT4 internalization rate or sensitivity to clathrin or cholesterol depletion. In contrast, the mitochondrial uncoupler dinitrophenol (DNP), which like insulin increases surface GLUT4, reduced GLUT4 (but not transferrin) internalization, an effect additive to that of depleting clathrin but not cholesterol. Trout GLUT4 (a natural variant of GLUT4 bearing different endocytic motifs) exogenously expressed in mammalian L6 cells internalized only through the cholesterol-dependent route that also included the non-clathrin-dependent cargo interleukin-2 receptor β, and DNP reduced internalization of both proteins. These results suggest that in muscle cells, GLUT4 internalizes simultaneously through clathrin-mediated endocytosis and a caveolae-independent but cholesterol- and dynamin-dependent route. Manipulating GLUT4 endocytosis to maintain surface GLUT4 may bypass insulin resistance.
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Selective regulation of the perinuclear distribution of Glucose Transporter 4 (GLUT4) by insulin signals in muscle cells.
European journal of cell biology, 2008Co-Authors: Chandrasagar B. Dugani, Varinder K. Randhawa, Alex Won-pang Cheng, Nish Patel, Amira KlipAbstract:Abstract Insulin regulates Glucose Transporter 4 (GLUT4) availability at the surface of muscle and adipose cells. In L6 myoblasts, stably expressed GLUT4myc is detected mostly in a perinuclear region. In unstimulated cells, about half of perinuclear GLUT4myc colocalizes with the transferrin receptor (TfR). Insulin stimulation selectively decreased the perinuclear colocalization of GLUT4myc with TfR determined by 3D-reconstruction of fluorescence images. Perinuclear GLUT4myc adopted two main distributions defined morphometrically as ‘conical’ and ‘concentric’. Insulin rapidly reduced the proportion of cells with conical in favor of concentric perinuclear GLUT4myc distributions in association with the gain in surface GLUT4myc. Upon removal of insulin, the GLUT4myc perinuclear distribution and surface levels reversed in parallel. In contrast, hypertonicity (which like insulin elevates surface GLUT4myc) did not elicit perinuclear GLUT4myc redistribution. Insulin also caused redistribution of perinuclear vesicle-associated membrane protein-2 (VAMP2), without alteration of perinuclear TfR and VAMP3. Inhibitory mutants of phosphatidylinositol-3 kinase (Δp85) or Akt substrate AS160 (AS160-4P) prevented insulin-mediated perinuclear GLUT4myc redistribution. Tetanus toxin expression did not prevent the perinuclear GLUT4myc redistribution, suggesting that redistribution is independent of GLUT4myc fusion with the plasma membrane. We propose that insulin causes selective, dynamic relocalization of perinuclear GLUT4myc and VAMP2 and perinuclear GLUT4myc redistribution is a direct target of insulin-derived signals.
Tongxi Zhou - One of the best experts on this subject based on the ideXlab platform.
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Chemical Constituents from Roots of Sophora davidii (Franch.) Skeels and Their Glucose Transporter 4 Translocation Activities.
Molecules (Basel Switzerland), 2021Co-Authors: Tongxi Zhou, Xinzhou Yang, Ho-young ChoiAbstract:Sophora davidii (Franch.) Skeels is a multi-purpose traditional medicine that has long been used for the treatment of various diseases. To discover the potential bioactive composition of S. davidii, a chemical investigation was thus performed. In this research, two new stilbene oligomers, Davidiol E–F (1–2), one new 4-aryl-substituted isoflavan Davidinin A (3), and one new 2-arylbenzofuran dimer, Shandougenine C (4), as well as six known compounds (5–10) were obtained from the ethyl acetate fraction of Sophora davidii (Franch.) Skeels. The structures of new compounds were established by extensive 1D and 2D nuclear magnetic resonance (NMR) spectra with mass spectroscopy data. The absolute configuration of 1–3 was assigned by comparing its experimental and calculated electronic circular dichroism (ECD) spectra. Compounds 1–10 promoted Glucose Transporter 4 (GLUT-4) translocations by the range of 1.28–2.60 folds, respectively. Compound 9 showed the most potent Glucose Transporter 4 translocations with 1.60 fold enhancement. The result attained in this study indicated that the separation and characterization of these compounds plays an important role in the research and development of new anti-diabetic drugs and pharmaceutical industry.
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New flavonoids from the roots of Sophora davidii (Franch.) Skeels and their Glucose Transporter 4 translocation activities.
Bioorganic chemistry, 2020Co-Authors: Tongxi Zhou, Ping Zhao, Xinzhou Yang, Ho-young Choi, Ji Hao, Huiqi Huang, Kejian PangAbstract:Five new flavanones, davidones A-E (1-5), one new isoflavonoid, cyclolicoisoflavones A3 (8), together with seven known compounds were isolated from the petroleum ether and the ethyl acetate fractions of the roots of Sophora davidii (Franch.) Skeels. The structures of new compounds were established by 1D and 2D NMR and MS data. The absolute configuration of 1-5 was assigned by NMR calculations and comparing its experimental and calculated ECD spectra. Flavanones were the main active principles responsible for the Glucose Transporter 4 (GLUT-4) translocation activities of SD-PE and SD-EtOAc. Compounds 1-7 and acacetin (12) promoted GLUT-4 translocation by the range of 1.35-3.00 folds, respectively.