Imidazoline Receptors in Insulin Signaling Metabolic Regulation (Paperback)
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Imidazoline Receptors in Insulin Signaling Metabolic Regulation (2015)
DE PB NW
ISBN: 9783836475907 bzw. 3836475901, in Deutsch, VDM VERLAG 01/04/2015, Taschenbuch, neu.
Von Händler/Antiquariat, Books2Anywhere [190245], Swindon, United Kingdom.
New Book. Shipped from UK in 4 to 14 days. Established seller since 2000. This item is printed on demand.
New Book. Shipped from UK in 4 to 14 days. Established seller since 2000. This item is printed on demand.
2
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Imidazoline Receptors in Insulin Signaling and Metabolic Regulation (2008)
DE PB NW RP
ISBN: 9783836475907 bzw. 3836475901, in Deutsch, Vdm Verlag Apr 2008, Taschenbuch, neu, Nachdruck.
Von Händler/Antiquariat, AHA-BUCH GmbH [51283250], Einbeck, NDS, Germany.
This item is printed on demand - Print on Demand Titel. - IRAS is a gene candidate for the I1-imidazoline receptor. Antisense oligo-nucleotides were designed and transfected into PC12 cells. Antisense transfection reduced specific imidazoline radioligand binding to plasma membrane fractions with parallel drops in IRAS protein expression. Furthermore, transfection with antisense caused functional impairment of I1-imidazoline receptor signaling without affecting basal ERK level or ERK activation by growth factors. These findings strongly suggested that IRAS encodes an I1-imidazoline receptor or at least an important subunit of it. The mechanism of insulin sensitizing effect from imidazolines was studied in the SHROB rat. Akt activation was found to be severely impaired in isolated adipocytes from SHROB. Insulin induced glucose uptake in these cells from SHROB were also similarly resistant to insulin stimulation. Chronic treatment of SHROB with moxonidine partially restored both Akt activation and glucose uptake stimulated by insulin in isolated ab***l adipocytes without affecting basal Akt activation level. These results implicate adipose tissue as a locus of insulin resistance in this model of metabolic syndrome. 212 pp. Deutsch.
This item is printed on demand - Print on Demand Titel. - IRAS is a gene candidate for the I1-imidazoline receptor. Antisense oligo-nucleotides were designed and transfected into PC12 cells. Antisense transfection reduced specific imidazoline radioligand binding to plasma membrane fractions with parallel drops in IRAS protein expression. Furthermore, transfection with antisense caused functional impairment of I1-imidazoline receptor signaling without affecting basal ERK level or ERK activation by growth factors. These findings strongly suggested that IRAS encodes an I1-imidazoline receptor or at least an important subunit of it. The mechanism of insulin sensitizing effect from imidazolines was studied in the SHROB rat. Akt activation was found to be severely impaired in isolated adipocytes from SHROB. Insulin induced glucose uptake in these cells from SHROB were also similarly resistant to insulin stimulation. Chronic treatment of SHROB with moxonidine partially restored both Akt activation and glucose uptake stimulated by insulin in isolated ab***l adipocytes without affecting basal Akt activation level. These results implicate adipose tissue as a locus of insulin resistance in this model of metabolic syndrome. 212 pp. Deutsch.
3
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Imidazoline Receptors in Insulin Signaling and Metabolic Regulation (2013)
DE PB NW RP
ISBN: 9783836475907 bzw. 3836475901, in Deutsch, VDM Verlag Dr. Müller E.K. Nov 2013, Taschenbuch, neu, Nachdruck.
Von Händler/Antiquariat, AHA-BUCH GmbH [51283250], Einbeck, Germany.
This item is printed on demand - Print on Demand Titel. Neuware - IRAS is a gene candidate for the I1-imidazoline receptor. Antisense oligo-nucleotides were designed and transfected into PC12 cells. Antisense transfection reduced specific imidazoline radioligand binding to plasma membrane fractions with parallel drops in IRAS protein expression. Furthermore, transfection with antisense caused functional impairment of I1-imidazoline receptor signaling without affecting basal ERK level or ERK activation by growth factors. These findings strongly suggested that IRAS encodes an I1-imidazoline receptor or at least an important subunit of it. The mechanism of insulin sensitizing effect from imidazolines was studied in the SHROB rat. Akt activation was found to be severely impaired in isolated adipocytes from SHROB. Insulin induced glucose uptake in these cells from SHROB were also similarly resistant to insulin stimulation. Chronic treatment of SHROB with moxonidine partially restored both Akt activation and glucose uptake stimulated by insulin in isolated ab***l adipocytes without affecting basal Akt activation level. These results implicate adipose tissue as a locus of insulin resistance in this model of metabolic syndrome. 212 pp. Deutsch.
This item is printed on demand - Print on Demand Titel. Neuware - IRAS is a gene candidate for the I1-imidazoline receptor. Antisense oligo-nucleotides were designed and transfected into PC12 cells. Antisense transfection reduced specific imidazoline radioligand binding to plasma membrane fractions with parallel drops in IRAS protein expression. Furthermore, transfection with antisense caused functional impairment of I1-imidazoline receptor signaling without affecting basal ERK level or ERK activation by growth factors. These findings strongly suggested that IRAS encodes an I1-imidazoline receptor or at least an important subunit of it. The mechanism of insulin sensitizing effect from imidazolines was studied in the SHROB rat. Akt activation was found to be severely impaired in isolated adipocytes from SHROB. Insulin induced glucose uptake in these cells from SHROB were also similarly resistant to insulin stimulation. Chronic treatment of SHROB with moxonidine partially restored both Akt activation and glucose uptake stimulated by insulin in isolated ab***l adipocytes without affecting basal Akt activation level. These results implicate adipose tissue as a locus of insulin resistance in this model of metabolic syndrome. 212 pp. Deutsch.
4
Symbolbild
Imidazoline Receptors in Insulin Signaling and Metabolic Regulation (2008)
DE PB NW RP
ISBN: 9783836475907 bzw. 3836475901, in Deutsch, Taschenbuch, neu, Nachdruck.
Von Händler/Antiquariat, English-Book-Service - A Fine Choice [1048135], Waldshut-Tiengen, Germany.
This item is printed on demand for shipment within 3 working days.
This item is printed on demand for shipment within 3 working days.
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