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Ludwik K. Malendowicz - One of the best experts on this subject based on the ideXlab platform.

  • Effects of prolonged exendin-4 administration on entero-insular axis of normal and streptozotocin-induced diabetic rats.
    International journal of molecular medicine, 2003
    Co-Authors: Ludwik K. Malendowicz, Krzysztof W. Nowak, Carlo Macchi, Gastone G. Nussdorfer, Agnieszka Zyterska, Agnieszka Ziolkowska
    Abstract:

    The effects of the glucagon-like peptide 1 (GLP-1) receptor agonist exendin-4 (EX4) and antagonist EX4(9-39) EX4-A on entero-insular axis have been investigated in normoglycemic and streptozotocin (STZ)-induced diabetic rats. Rats were administered daily subcutaneous injections of 1 nmol/kg EX4 and/or EX4-A for 7 days, and were decapitated 3 h after the last injection. In STZ-untreated rats, EX4 reduced body-weight (BW) gain and raised glycemia, and the effects were prevented by EX4-A; conversely, EX4 did not alter plasma concentrations of Insulin, glucagon and leptin. STZ-treated rats displayed body and hematochemical alterations typical of experimental diabetes: decrease in BW and Insulin Blood Level, coupled with normal glucagon plasma concentration and marked hyperglycemia. In diabetic rats, both EX4 and EX4-A decreased BW gain, thereby suggesting a mechanism at least in part independent of GLP- I receptors. EX4 did not alter glucagon Blood Level, but decreased glycemia and raised Insulin and leptin plasma Levels. These effects were annulled by EX4-A, which indicates that they occur through the activation of GLP-1 receptors. Collectively, our findings add support to the view that EX4 can be considered an important therapeutical tool to improve glucose metabolism in diabetes.

  • Acute leptin action on Insulin Blood Level and liver Insulin receptor in the rat
    Life sciences, 1998
    Co-Authors: Krzysztof W. Nowak, Paweł Maćkowiak, Leszek Nogowski, Tomasz Szkudelski, Ludwik K. Malendowicz
    Abstract:

    Abstract Aim of the study was to investigate acute leptin effect on Insulin Blood Level and liver Insulin binding in the rat. The administration of leptin induced time and dose dependent decrease in the Insulin Level, which was statistically significant in comparison to the control animals 120 min after administration of higher dose of peptide (0.30 ± 0.05 vs 0.14 ± 0.01 nmol l , respectively). Simultaneously, we have shown the attenuation of liver sensitivity to Insulin 2 hours after higher leptin dose injection. This phenomenon was caused by the decrease of binding capacity of high affinity Insulin receptor sites (HAIR), which was statistically significant after higher leptin dose administration at both time points (0.54 ± 0.13 vs 0.26 ± 0.03 and 0.71 ± 0.12 vs 0.40 ± 0.05 pmol mg protein for 1 and 2 h, respectively). The present study provides evidence that leptin, in addition to its inhibitory effect on Insulin secretion, acts as a modulator of Insulin receptor, through the decrease of binding capacity. It seems legitimate to suggest that leptin-induced decrease of Insulin receptor binding capacity may be one of several causes of Insulin resistance.

Krzysztof W. Nowak - One of the best experts on this subject based on the ideXlab platform.

  • Effects of prolonged exendin-4 administration on entero-insular axis of normal and streptozotocin-induced diabetic rats.
    International journal of molecular medicine, 2003
    Co-Authors: Ludwik K. Malendowicz, Krzysztof W. Nowak, Carlo Macchi, Gastone G. Nussdorfer, Agnieszka Zyterska, Agnieszka Ziolkowska
    Abstract:

    The effects of the glucagon-like peptide 1 (GLP-1) receptor agonist exendin-4 (EX4) and antagonist EX4(9-39) EX4-A on entero-insular axis have been investigated in normoglycemic and streptozotocin (STZ)-induced diabetic rats. Rats were administered daily subcutaneous injections of 1 nmol/kg EX4 and/or EX4-A for 7 days, and were decapitated 3 h after the last injection. In STZ-untreated rats, EX4 reduced body-weight (BW) gain and raised glycemia, and the effects were prevented by EX4-A; conversely, EX4 did not alter plasma concentrations of Insulin, glucagon and leptin. STZ-treated rats displayed body and hematochemical alterations typical of experimental diabetes: decrease in BW and Insulin Blood Level, coupled with normal glucagon plasma concentration and marked hyperglycemia. In diabetic rats, both EX4 and EX4-A decreased BW gain, thereby suggesting a mechanism at least in part independent of GLP- I receptors. EX4 did not alter glucagon Blood Level, but decreased glycemia and raised Insulin and leptin plasma Levels. These effects were annulled by EX4-A, which indicates that they occur through the activation of GLP-1 receptors. Collectively, our findings add support to the view that EX4 can be considered an important therapeutical tool to improve glucose metabolism in diabetes.

  • Acute leptin action on Insulin Blood Level and liver Insulin receptor in the rat
    Life sciences, 1998
    Co-Authors: Krzysztof W. Nowak, Paweł Maćkowiak, Leszek Nogowski, Tomasz Szkudelski, Ludwik K. Malendowicz
    Abstract:

    Abstract Aim of the study was to investigate acute leptin effect on Insulin Blood Level and liver Insulin binding in the rat. The administration of leptin induced time and dose dependent decrease in the Insulin Level, which was statistically significant in comparison to the control animals 120 min after administration of higher dose of peptide (0.30 ± 0.05 vs 0.14 ± 0.01 nmol l , respectively). Simultaneously, we have shown the attenuation of liver sensitivity to Insulin 2 hours after higher leptin dose injection. This phenomenon was caused by the decrease of binding capacity of high affinity Insulin receptor sites (HAIR), which was statistically significant after higher leptin dose administration at both time points (0.54 ± 0.13 vs 0.26 ± 0.03 and 0.71 ± 0.12 vs 0.40 ± 0.05 pmol mg protein for 1 and 2 h, respectively). The present study provides evidence that leptin, in addition to its inhibitory effect on Insulin secretion, acts as a modulator of Insulin receptor, through the decrease of binding capacity. It seems legitimate to suggest that leptin-induced decrease of Insulin receptor binding capacity may be one of several causes of Insulin resistance.

Paweł Maćkowiak - One of the best experts on this subject based on the ideXlab platform.

  • Acute leptin action on Insulin Blood Level and liver Insulin receptor in the rat
    Life sciences, 1998
    Co-Authors: Krzysztof W. Nowak, Paweł Maćkowiak, Leszek Nogowski, Tomasz Szkudelski, Ludwik K. Malendowicz
    Abstract:

    Abstract Aim of the study was to investigate acute leptin effect on Insulin Blood Level and liver Insulin binding in the rat. The administration of leptin induced time and dose dependent decrease in the Insulin Level, which was statistically significant in comparison to the control animals 120 min after administration of higher dose of peptide (0.30 ± 0.05 vs 0.14 ± 0.01 nmol l , respectively). Simultaneously, we have shown the attenuation of liver sensitivity to Insulin 2 hours after higher leptin dose injection. This phenomenon was caused by the decrease of binding capacity of high affinity Insulin receptor sites (HAIR), which was statistically significant after higher leptin dose administration at both time points (0.54 ± 0.13 vs 0.26 ± 0.03 and 0.71 ± 0.12 vs 0.40 ± 0.05 pmol mg protein for 1 and 2 h, respectively). The present study provides evidence that leptin, in addition to its inhibitory effect on Insulin secretion, acts as a modulator of Insulin receptor, through the decrease of binding capacity. It seems legitimate to suggest that leptin-induced decrease of Insulin receptor binding capacity may be one of several causes of Insulin resistance.

Tomasz Szkudelski - One of the best experts on this subject based on the ideXlab platform.

  • Acute leptin action on Insulin Blood Level and liver Insulin receptor in the rat
    Life sciences, 1998
    Co-Authors: Krzysztof W. Nowak, Paweł Maćkowiak, Leszek Nogowski, Tomasz Szkudelski, Ludwik K. Malendowicz
    Abstract:

    Abstract Aim of the study was to investigate acute leptin effect on Insulin Blood Level and liver Insulin binding in the rat. The administration of leptin induced time and dose dependent decrease in the Insulin Level, which was statistically significant in comparison to the control animals 120 min after administration of higher dose of peptide (0.30 ± 0.05 vs 0.14 ± 0.01 nmol l , respectively). Simultaneously, we have shown the attenuation of liver sensitivity to Insulin 2 hours after higher leptin dose injection. This phenomenon was caused by the decrease of binding capacity of high affinity Insulin receptor sites (HAIR), which was statistically significant after higher leptin dose administration at both time points (0.54 ± 0.13 vs 0.26 ± 0.03 and 0.71 ± 0.12 vs 0.40 ± 0.05 pmol mg protein for 1 and 2 h, respectively). The present study provides evidence that leptin, in addition to its inhibitory effect on Insulin secretion, acts as a modulator of Insulin receptor, through the decrease of binding capacity. It seems legitimate to suggest that leptin-induced decrease of Insulin receptor binding capacity may be one of several causes of Insulin resistance.

Leszek Nogowski - One of the best experts on this subject based on the ideXlab platform.

  • Acute leptin action on Insulin Blood Level and liver Insulin receptor in the rat
    Life sciences, 1998
    Co-Authors: Krzysztof W. Nowak, Paweł Maćkowiak, Leszek Nogowski, Tomasz Szkudelski, Ludwik K. Malendowicz
    Abstract:

    Abstract Aim of the study was to investigate acute leptin effect on Insulin Blood Level and liver Insulin binding in the rat. The administration of leptin induced time and dose dependent decrease in the Insulin Level, which was statistically significant in comparison to the control animals 120 min after administration of higher dose of peptide (0.30 ± 0.05 vs 0.14 ± 0.01 nmol l , respectively). Simultaneously, we have shown the attenuation of liver sensitivity to Insulin 2 hours after higher leptin dose injection. This phenomenon was caused by the decrease of binding capacity of high affinity Insulin receptor sites (HAIR), which was statistically significant after higher leptin dose administration at both time points (0.54 ± 0.13 vs 0.26 ± 0.03 and 0.71 ± 0.12 vs 0.40 ± 0.05 pmol mg protein for 1 and 2 h, respectively). The present study provides evidence that leptin, in addition to its inhibitory effect on Insulin secretion, acts as a modulator of Insulin receptor, through the decrease of binding capacity. It seems legitimate to suggest that leptin-induced decrease of Insulin receptor binding capacity may be one of several causes of Insulin resistance.