Adiponectin Receptor - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

Adiponectin Receptor

The Experts below are selected from a list of 7782 Experts worldwide ranked by ideXlab platform

Adiponectin Receptor – Free Register to Access Experts & Abstracts

Christos S. Mantzoros – One of the best experts on this subject based on the ideXlab platform.

Yasushi Kawakami – One of the best experts on this subject based on the ideXlab platform.

Kazumasa Isobe – One of the best experts on this subject based on the ideXlab platform.

  • Effects of Short-Term Exercise on Adiponectin and Adiponectin Receptor Levels in Rats
    Journal of atherosclerosis and thrombosis, 2007
    Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Yasushi Kawakami, Kazumasa Isobe
    Abstract:

    Aim: Adiponectin reportedly reduces insulin resistance. Exercise has also been shown to lessen insulin resistance, although it is not well known whether exercise increases levels of Adiponectin and/or its Receptors nor whether it effects are dependent on exercise intensity and/or period. We previously reported that blood Adiponectin levels increased by 150% in animals that exercised at a rate of 30 m/min for 60 minutes, 2 days per week, and Adiponectin Receptor 1 (AdipoR1) mRNA levels in muscle increased up to 4 times in response to exercise at a rate of 25 m/min for 30 min, 5 days per week for 12 weeks.Methods: In light of this information, we examined the effects of short-term exercise on Adiponectin, and Adiponectin Receptor levels in rats, using ELISA and real-time PCR. Results: Our data showed that Adiponectin mRNA levels in adipose tissue increased by 280% in rats exercised at a rate of 30 m/min for 60 minutes for 2 weeks and correlated with the exercise time periods. No effects of short-term exercise on Adiponectin Receptor 1 mRNA in muscle were observed. Conclusion: Thus, long-term exercise may be required to regulate Adiponectin Receptor 1 mRNA expression in muscle and Adiponectin mRNA expression in adipose tissue.

  • beta-adrenoceptor agonists downregulate Adiponectin, but upregulate Adiponectin Receptor 2 and tumor necrosis factor-alpha expression in adipocytes.
    European journal of pharmacology, 2007
    Co-Authors: Kazumasa Isobe, Qin Zeng, Kazuhiro Takekoshi, Kazumi Suzukawa, Yasushi Kawakami
    Abstract:

    Recently, the insulin-sensitizing adipokine Adiponectin and the insulin resistance-inducing adipokine tumor necrosis factor-alpha (TNF-alpha) were reported to inhibit each other’s production in adipocytes. We investigated the effects of two beta(3)-adrenoceptor agonists, 5-[(2R)-2-[[(2R)-2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]-1,3-benzodioxole-2,2-dicarboxylate (CL-316,243) and (+/-)-(R(*),R(*))-[4-[2-[[2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]phenoxy]acetic acid (BRL37344), on the gene expression of Adiponectin, two Adiponectin Receptors, and TNF-alpha in adipose tissues of C57BL/6J mice. CL-316,243 and BRL37344 downregulated Adiponectin, but upregulated Adiponectin Receptor 2 (not Receptor 1) in epididymal or/and subcutaneous white adipose tissues and in brown adipose tissue. TNF-alpha expression was upregulated only in epididymal adipose tissue. To further explore these effects, we treated differentiated 3T3-L1 adipocytes with the non-selective beta-adrenoceptor agonist isoproterenol. As a result, Adiponectin Receptor 2 (but not Receptor 1) gene expression and TNF-alpha protein expression increased, but gene expression and secretion of Adiponectin decreased. The upregulation of Adiponectin Receptor 2 by isoproterenol is most likely via beta(2),beta(3)-adrenoceptors, adenylyl cyclases, and protein kinase A (PKA). However, the accompanying activation of AMP-activated protein kinase (AMPK) may inhibit this upregulation. Our results suggest that upregulation of TNF-alpha and downregulation of Adiponectin by beta-adrenoceptor activation may contribute to the pathogenesis of catecholamine-induced insulin resistance, and that upregulation of Adiponectin Receptor 2 may be a feedback result of reduced Adiponectin.

  • Effects of exercise on Adiponectin and Adiponectin Receptor levels in rats.
    Life sciences, 2006
    Co-Authors: Qin Zeng, Kazumasa Isobe, Kazuhiro Takekoshi, N. Ohkoshi, Hajime Ohmori, Yasushi Kawakami
    Abstract:

    Adiponectin reportedly reduces insulin-resistance. Exercise has also been shown to lessen insulin-resistance, though it is not known whether exercise increases levels of Adiponectin and/or its Receptors or whether its effects are dependent on exercise intensity and/or frequency. Catecholamine levels have been shown to increase during exercise and to fluctuate based on exercise intensity and duration. In light of this information, we examined the effects of exercise on catecholamine, Adiponectin, and Adiponectin Receptor levels in rats. Our data showed that blood Adiponectin levels increased by 150% in animals that exercised at a rate of 30 m/min for 60 min 2 days per week, but not 5 days, per week; no such increase was observed in rats that exercised at a rate of 25 m/min for 30 min. The effects of exercise on Adiponectin Receptor mRNA were variable, with Adiponectin Receptor 1 (AdipoR1) levels in muscle increasing up to 4 times while Adiponectin Receptor 2 (AdipoR2) levels in liver fell to below half in response to exercise at a rate of 25 m/min for 30 min 5 days per week. We also observed that urinary epinephrine levels and plasma lipids were elevated by exercise at a rate of 25 m/min for 30 min 2 days per week. Exercise frequency at a rate of 25 m/min for 30 min correlated with AdipoR1 and AdipoR2 mRNA expression in the muscle and liver, respectively (r=0.640, p

Qin Zeng – One of the best experts on this subject based on the ideXlab platform.

  • Effects of Short-Term Exercise on Adiponectin and Adiponectin Receptor Levels in Rats
    Journal of atherosclerosis and thrombosis, 2007
    Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Yasushi Kawakami, Kazumasa Isobe
    Abstract:

    Aim: Adiponectin reportedly reduces insulin resistance. Exercise has also been shown to lessen insulin resistance, although it is not well known whether exercise increases levels of Adiponectin and/or its Receptors nor whether it effects are dependent on exercise intensity and/or period. We previously reported that blood Adiponectin levels increased by 150% in animals that exercised at a rate of 30 m/min for 60 minutes, 2 days per week, and Adiponectin Receptor 1 (AdipoR1) mRNA levels in muscle increased up to 4 times in response to exercise at a rate of 25 m/min for 30 min, 5 days per week for 12 weeks.Methods: In light of this information, we examined the effects of short-term exercise on Adiponectin, and Adiponectin Receptor levels in rats, using ELISA and real-time PCR. Results: Our data showed that Adiponectin mRNA levels in adipose tissue increased by 280% in rats exercised at a rate of 30 m/min for 60 minutes for 2 weeks and correlated with the exercise time periods. No effects of short-term exercise on Adiponectin Receptor 1 mRNA in muscle were observed. Conclusion: Thus, long-term exercise may be required to regulate Adiponectin Receptor 1 mRNA expression in muscle and Adiponectin mRNA expression in adipose tissue.

  • beta-adrenoceptor agonists downregulate Adiponectin, but upregulate Adiponectin Receptor 2 and tumor necrosis factor-alpha expression in adipocytes.
    European journal of pharmacology, 2007
    Co-Authors: Kazumasa Isobe, Qin Zeng, Kazuhiro Takekoshi, Kazumi Suzukawa, Yasushi Kawakami
    Abstract:

    Recently, the insulin-sensitizing adipokine Adiponectin and the insulin resistance-inducing adipokine tumor necrosis factor-alpha (TNF-alpha) were reported to inhibit each other’s production in adipocytes. We investigated the effects of two beta(3)-adrenoceptor agonists, 5-[(2R)-2-[[(2R)-2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]-1,3-benzodioxole-2,2-dicarboxylate (CL-316,243) and (+/-)-(R(*),R(*))-[4-[2-[[2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]phenoxy]acetic acid (BRL37344), on the gene expression of Adiponectin, two Adiponectin Receptors, and TNF-alpha in adipose tissues of C57BL/6J mice. CL-316,243 and BRL37344 downregulated Adiponectin, but upregulated Adiponectin Receptor 2 (not Receptor 1) in epididymal or/and subcutaneous white adipose tissues and in brown adipose tissue. TNF-alpha expression was upregulated only in epididymal adipose tissue. To further explore these effects, we treated differentiated 3T3-L1 adipocytes with the non-selective beta-adrenoceptor agonist isoproterenol. As a result, Adiponectin Receptor 2 (but not Receptor 1) gene expression and TNF-alpha protein expression increased, but gene expression and secretion of Adiponectin decreased. The upregulation of Adiponectin Receptor 2 by isoproterenol is most likely via beta(2),beta(3)-adrenoceptors, adenylyl cyclases, and protein kinase A (PKA). However, the accompanying activation of AMP-activated protein kinase (AMPK) may inhibit this upregulation. Our results suggest that upregulation of TNF-alpha and downregulation of Adiponectin by beta-adrenoceptor activation may contribute to the pathogenesis of catecholamine-induced insulin resistance, and that upregulation of Adiponectin Receptor 2 may be a feedback result of reduced Adiponectin.

  • Effects of exercise on Adiponectin and Adiponectin Receptor levels in rats.
    Life sciences, 2006
    Co-Authors: Qin Zeng, Kazumasa Isobe, Kazuhiro Takekoshi, N. Ohkoshi, Hajime Ohmori, Yasushi Kawakami
    Abstract:

    Adiponectin reportedly reduces insulin-resistance. Exercise has also been shown to lessen insulin-resistance, though it is not known whether exercise increases levels of Adiponectin and/or its Receptors or whether its effects are dependent on exercise intensity and/or frequency. Catecholamine levels have been shown to increase during exercise and to fluctuate based on exercise intensity and duration. In light of this information, we examined the effects of exercise on catecholamine, Adiponectin, and Adiponectin Receptor levels in rats. Our data showed that blood Adiponectin levels increased by 150% in animals that exercised at a rate of 30 m/min for 60 min 2 days per week, but not 5 days, per week; no such increase was observed in rats that exercised at a rate of 25 m/min for 30 min. The effects of exercise on Adiponectin Receptor mRNA were variable, with Adiponectin Receptor 1 (AdipoR1) levels in muscle increasing up to 4 times while Adiponectin Receptor 2 (AdipoR2) levels in liver fell to below half in response to exercise at a rate of 25 m/min for 30 min 5 days per week. We also observed that urinary epinephrine levels and plasma lipids were elevated by exercise at a rate of 25 m/min for 30 min 2 days per week. Exercise frequency at a rate of 25 m/min for 30 min correlated with AdipoR1 and AdipoR2 mRNA expression in the muscle and liver, respectively (r=0.640, p

Kazuhiro Takekoshi – One of the best experts on this subject based on the ideXlab platform.

  • Effects of Short-Term Exercise on Adiponectin and Adiponectin Receptor Levels in Rats
    Journal of atherosclerosis and thrombosis, 2007
    Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Yasushi Kawakami, Kazumasa Isobe
    Abstract:

    Aim: Adiponectin reportedly reduces insulin resistance. Exercise has also been shown to lessen insulin resistance, although it is not well known whether exercise increases levels of Adiponectin and/or its Receptors nor whether it effects are dependent on exercise intensity and/or period. We previously reported that blood Adiponectin levels increased by 150% in animals that exercised at a rate of 30 m/min for 60 minutes, 2 days per week, and Adiponectin Receptor 1 (AdipoR1) mRNA levels in muscle increased up to 4 times in response to exercise at a rate of 25 m/min for 30 min, 5 days per week for 12 weeks.Methods: In light of this information, we examined the effects of short-term exercise on Adiponectin, and Adiponectin Receptor levels in rats, using ELISA and real-time PCR. Results: Our data showed that Adiponectin mRNA levels in adipose tissue increased by 280% in rats exercised at a rate of 30 m/min for 60 minutes for 2 weeks and correlated with the exercise time periods. No effects of short-term exercise on Adiponectin Receptor 1 mRNA in muscle were observed. Conclusion: Thus, long-term exercise may be required to regulate Adiponectin Receptor 1 mRNA expression in muscle and Adiponectin mRNA expression in adipose tissue.

  • beta-adrenoceptor agonists downregulate Adiponectin, but upregulate Adiponectin Receptor 2 and tumor necrosis factor-alpha expression in adipocytes.
    European journal of pharmacology, 2007
    Co-Authors: Kazumasa Isobe, Qin Zeng, Kazuhiro Takekoshi, Kazumi Suzukawa, Yasushi Kawakami
    Abstract:

    Recently, the insulin-sensitizing adipokine Adiponectin and the insulin resistance-inducing adipokine tumor necrosis factor-alpha (TNF-alpha) were reported to inhibit each other’s production in adipocytes. We investigated the effects of two beta(3)-adrenoceptor agonists, 5-[(2R)-2-[[(2R)-2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]-1,3-benzodioxole-2,2-dicarboxylate (CL-316,243) and (+/-)-(R(*),R(*))-[4-[2-[[2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]phenoxy]acetic acid (BRL37344), on the gene expression of Adiponectin, two Adiponectin Receptors, and TNF-alpha in adipose tissues of C57BL/6J mice. CL-316,243 and BRL37344 downregulated Adiponectin, but upregulated Adiponectin Receptor 2 (not Receptor 1) in epididymal or/and subcutaneous white adipose tissues and in brown adipose tissue. TNF-alpha expression was upregulated only in epididymal adipose tissue. To further explore these effects, we treated differentiated 3T3-L1 adipocytes with the non-selective beta-adrenoceptor agonist isoproterenol. As a result, Adiponectin Receptor 2 (but not Receptor 1) gene expression and TNF-alpha protein expression increased, but gene expression and secretion of Adiponectin decreased. The upregulation of Adiponectin Receptor 2 by isoproterenol is most likely via beta(2),beta(3)-adrenoceptors, adenylyl cyclases, and protein kinase A (PKA). However, the accompanying activation of AMP-activated protein kinase (AMPK) may inhibit this upregulation. Our results suggest that upregulation of TNF-alpha and downregulation of Adiponectin by beta-adrenoceptor activation may contribute to the pathogenesis of catecholamine-induced insulin resistance, and that upregulation of Adiponectin Receptor 2 may be a feedback result of reduced Adiponectin.

  • Effects of exercise on Adiponectin and Adiponectin Receptor levels in rats.
    Life sciences, 2006
    Co-Authors: Qin Zeng, Kazumasa Isobe, Kazuhiro Takekoshi, N. Ohkoshi, Hajime Ohmori, Yasushi Kawakami
    Abstract:

    Adiponectin reportedly reduces insulin-resistance. Exercise has also been shown to lessen insulin-resistance, though it is not known whether exercise increases levels of Adiponectin and/or its Receptors or whether its effects are dependent on exercise intensity and/or frequency. Catecholamine levels have been shown to increase during exercise and to fluctuate based on exercise intensity and duration. In light of this information, we examined the effects of exercise on catecholamine, Adiponectin, and Adiponectin Receptor levels in rats. Our data showed that blood Adiponectin levels increased by 150% in animals that exercised at a rate of 30 m/min for 60 min 2 days per week, but not 5 days, per week; no such increase was observed in rats that exercised at a rate of 25 m/min for 30 min. The effects of exercise on Adiponectin Receptor mRNA were variable, with Adiponectin Receptor 1 (AdipoR1) levels in muscle increasing up to 4 times while Adiponectin Receptor 2 (AdipoR2) levels in liver fell to below half in response to exercise at a rate of 25 m/min for 30 min 5 days per week. We also observed that urinary epinephrine levels and plasma lipids were elevated by exercise at a rate of 25 m/min for 30 min 2 days per week. Exercise frequency at a rate of 25 m/min for 30 min correlated with AdipoR1 and AdipoR2 mRNA expression in the muscle and liver, respectively (r=0.640, p