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Christos S. Mantzoros - One of the best experts on this subject based on the ideXlab platform.
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variants of the Adiponectin and Adiponectin Receptor 1 genes and posttransplantation diabetes mellitus in renal allograft recipients
The Journal of Clinical Endocrinology and Metabolism, 2012Co-Authors: Eun Seok Kang, Faidon Magkos, Beom Seok Kim, Rihong Zhai, Yu Seun Kim, David C Christiani, Hyun Chul Lee, Christos S. MantzorosAbstract:Context: Posttransplantation diabetes mellitus (PTDM) is a major metabolic complication in renal transplant recipients. Adiponectin (ADIPOQ) and Adiponectin Receptor-1 (ADIPOR1) gene polymorphisms have been associated with type 2 diabetes. However, it is unknown whether these polymorphisms are also risk factors for PTDM. Objective: We investigated the association between PTDM and single-nucleotide polymorphisms of ADIPOQ and ADIPOR1 in a cohort of renal allograft recipients. Design, Setting, and Participants: Five hundred seventy-five patients (367 men and 208 women) who received kidney transplants between 1989 and 2007, without a history of diabetes and with a pretransplant fasting glucose concentration less than 5.5 mmol/liter. Patients were followed up for a median 10 yr. Genotypes included single-nucleotide polymorphisms of the following: ADIPOQ rs266729, rs822395, rs822396, rs2241766, and rs1501299 and ADIPOR1 rs2232853, rs12733285, and rs1342387. Results: TT-homozygotes in ADIPOQ rs1501299 [hazard r...
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variants of the Adiponectin adipoq and Adiponectin Receptor 1 adipor1 genes and colorectal cancer risk
JAMA, 2008Co-Authors: Virginia G Kaklamani, Christos S. Mantzoros, Maureen Sadim, Kenneth Offit, Habibul Ahsan, Boris Pasche, Kari B Wisinski, Cassandra Gulden, John A BaronAbstract:Context Current epidemiological evidence suggests an association between obesity, hyperinsulinemia, and colorectal cancer risk. Adiponectin is a hormone secreted by the adipose tissue, and serum levels are inversely correlated with obesity and hyperinsulinemia. While there is evidence of an association between circulating Adiponectin levels and colorectal cancer risk, no association between genes of the Adiponectin pathway and colorectal cancer have been reported to date. Objective To determine the association of 10 haplotype-tagging single-nucleotide polymorphisms (SNPs) of the Adiponectin (ADIPOQ) and Adiponectin Receptor 1 (ADIPOR1) genes with colorectal cancer risk. Design, Setting, and Patients Two case-control studies including patients with a diagnosis of colorectal cancer and controls were recruited between 2000 and 2007. Case-control study 1 included a total of 441 patients with a diagnosis of colorectal cancer and 658 controls; both groups were of Ashkenazi Jewish ancestry and from New York, New York. Case-control study 2 included 199 patients with a diagnosis of colorectal cancer and 199 controls from Chicago, Illinois, matched 1:1 for sex, age, and ethnicity. Main Outcome Measures ADIPOQ and ADIPOR1 SNP frequency among cases and controls. Results In study 1, after adjustment for age, sex, and SNPs from the same gene, 3 ADIPOQ SNPs and 1 ADIPOR1 SNP were associated with colorectal cancer risk: rs266729 (adjusted odds ratio [AOR], 0.72; 95% confidence interval [CI], 0.55-0.95) and rs822396 (AOR, 0.37; 95% CI, 0.14-1.00) were associated with decreased risk whereas rs822395 (AOR, 1.76; 95% CI, 1.09-2.84) and rs1342387 (AOR, 1.79; 95% CI, 1.18-2.72) were associated with increased risk. In study 2, after adjustment for age, sex, race, and SNPs from the same gene, the ADIPOQ SNP rs266729 was associated with a decreased colorectal cancer risk of similar magnitude as in study 1 (AOR, 0.52; 95% CI, 0.34-0.78). Combined analysis of both studies shows an association of rs266729 with decreased colorectal cancer risk (AOR, 0.73; 95% CI, 0.53-0.99). Conclusion The SNP rs266729, which tags the 5′ flanking region of the ADIPOQ gene, is associated with decreased colorectal cancer risk.
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variants of the Adiponectin and Adiponectin Receptor 1 genes and breast cancer risk
Cancer Research, 2008Co-Authors: Virginia G Kaklamani, Alex Hsi, Maureen Sadim, Kenneth Offit, Carole Oddoux, Harry Ostrer, Habibul Ahsan, Boris Pasche, Christos S. MantzorosAbstract:Breast cancer risk is higher among obese women and women with diabetes. Adiponectin is a protein exclusively secreted by adipose tissue, circulating levels of which have been associated with breast cancer risk. Whether genetic variants within the Adiponectin pathway are associated with breast cancer risk is unknown. To explore the association of genetic variants of the Adiponectin ( ADIPOQ ) and Adiponectin Receptor 1 ( ADIPOR1 ) genes with breast cancer risk, we conducted a case control study of female patients with breast cancer and healthy female controls from New York City recruited between 1999 and 2004. We genotyped 733 hospital-based breast cancer cases and 839 controls for 10 haplotype-tagging single nucleotide polymorphisms (SNP) of ADIPOQ and ADIPOR1 . Two ADIPOQ SNPs (rs2241766 and rs1501299), which have been associated with circulating levels of Adiponectin, were associated with breast cancer risk [rs1501299*GG: odd ratios (OR), 1.80; 95% confidence interval (95% CI), 1.14–2.85; rs2241766*TG: OR, 0.61; 95% CI, 0.46–0.80]. One ADIPOR1 SNP (rs7539542), which modulates expression of Adiponectin Receptor 1 mRNA, was also associated with breast cancer risk (OR, 0.51; 95% CI, 0.28–0.92). Based on the known function of rs2241766 and rs1501299, we categorized individuals by Adiponectin signaling status and found that, when compared with high signalers, intermediate signalers had a 4.16-fold increase in breast cancer risk (95% CI, 0.49–35.19), and low signalers had a 6.56-fold increase in breast cancer risk (95% CI, 0.78–54.89; P trend = 0.001). This is the first report of an association between functionally relevant variants of the Adiponectin pathway and breast cancer risk. The results warrant further studies of the Adiponectin pathway in breast cancer. [Cancer Res 2008;68(9):3178–83]
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Adiponectin Receptor expression is elevated in colorectal carcinomas but not in gastrointestinal stromal tumors.
Endocrine-related cancer, 2008Co-Authors: Catherine J. Williams, Nicholas Mitsiades, Elias Sozopoulos, Alex Hsi, Alicja Wolk, Artemissia-phoebe Nifli, Sofia Tseleni-balafouta, Christos S. MantzorosAbstract:Circulating Adiponectin is inversely associated with colorectal carcinoma. However, Adiponectin Receptor expression has not been examined in normal gastrointestinal tissue, colorectal malignancies, or gastrointestinal stromal tumors (GISTs). We collected 40 colorectal carcinomas and 12 non-tumor colorectal tissue specimens from patients with colorectal cancer, as well as 45 tumor and 13 non-tumor specimens from patients with GIST. Expression and localization of Adiponectin Receptors (AdipoR1 and AdipoR2) were assessed using immunohistochemistry. We also confirmed expression of Adiponectin Receptors using rtPCR in matched normal and colorectal cancer specimens obtained from five patients. Finally, we detected Adiponectin Receptors and assessed Adiponectin signaling in three colon cancer cell lines. Adiponectin Receptor expression, assessed by either rtPCR or immunohistochemistry, was present in normal tissue and was significantly lower than in colorectal carcinomas. Among carcinomas, 95% displayed positive or strongly positive expression of AdipoR1 and 88% of AdipoR2, versus 8% and 0%, respectively, for non-tumor specimens (P
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Adiponectin Receptor expression is elevated in colorectal carcinomas but not in gastrointestinal stromal tumors
Endocrine-related Cancer, 2008Co-Authors: Catherine J. Williams, Nicholas Mitsiades, Elias Sozopoulos, Alex Hsi, Alicja Wolk, Artemissia-phoebe Nifli, Sofia Tselenibalafouta, Christos S. MantzorosAbstract:Circulating Adiponectin is inversely associated with colorectal carcinoma. However, Adiponectin Receptor expression has not been examined in normal gastrointestinal tissue, colorectal malignancies, or gastrointestinal stromal tumors (GISTs). We collected 40 colorectal carcinomas and 12 non-tumor colorectal tissue specimens from patients with colorectal cancer, as well as 45 tumor and 13 non-tumor specimens from patients with GIST. Expression and localization of Adiponectin Receptors (AdipoR1 and AdipoR2) were assessed using immunohistochemistry. We also confirmed expression of Adiponectin Receptors using rtPCR in matched normal and colorectal cancer specimens obtained from five patients. Finally, we detected Adiponectin Receptors and assessed Adiponectin signaling in three colon cancer cell lines. Adiponectin Receptor expression, assessed by either rtPCR or immunohistochemistry, was present in normal tissue and was significantly lower than in colorectal carcinomas. Among carcinomas, 95% displayed positive or strongly positive expression of AdipoR1 and 88% of AdipoR2, versus 8% and 0%, respectively, for non-tumor specimens (P<0.0001). AdipoR1 expression assessed by rtPCR was 1.6-fold higher in tumor than in non-tumor tissue (P<0.05). In addition, we found that Adiponectin at physiological concentrations can activate in vitro intracellular signaling pathways in three colon cancer cell lines, expressing both Adiponectin Receptors 1 and 2. No significant differences in expression of Adiponectin Receptors in tumor versus non-tumor GI specimens were detected among patients with GIST. Colon cancer cell lines express Adiponectin Receptors, through which Adiponectin activates in vitro intracellular signaling pathways. Adiponectin Receptors are also detected in normal GI tissue and their expression is elevated in colorectal carcinomas, but not in GIST.
Yasushi Kawakami - One of the best experts on this subject based on the ideXlab platform.
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Effects of Short-Term Exercise on Adiponectin and Adiponectin Receptor Levels in Rats
Journal of atherosclerosis and thrombosis, 2007Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Yasushi Kawakami, Kazumasa IsobeAbstract: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.
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beta-adrenoceptor agonists downregulate Adiponectin, but upregulate Adiponectin Receptor 2 and tumor necrosis factor-alpha expression in adipocytes.
European journal of pharmacology, 2007Co-Authors: Kazumasa Isobe, Qin Zeng, Kazuhiro Takekoshi, Kazumi Suzukawa, Yasushi KawakamiAbstract: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.
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Effects of exercise on Adiponectin and Adiponectin Receptor levels in rats.
Life sciences, 2006Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Kazumasa Isobe, N. Ohkoshi, Hajime Ohmori, Yasushi KawakamiAbstract: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
Kazumasa Isobe - One of the best experts on this subject based on the ideXlab platform.
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Effects of Short-Term Exercise on Adiponectin and Adiponectin Receptor Levels in Rats
Journal of atherosclerosis and thrombosis, 2007Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Yasushi Kawakami, Kazumasa IsobeAbstract: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.
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beta-adrenoceptor agonists downregulate Adiponectin, but upregulate Adiponectin Receptor 2 and tumor necrosis factor-alpha expression in adipocytes.
European journal of pharmacology, 2007Co-Authors: Kazumasa Isobe, Qin Zeng, Kazuhiro Takekoshi, Kazumi Suzukawa, Yasushi KawakamiAbstract: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.
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Effects of exercise on Adiponectin and Adiponectin Receptor levels in rats.
Life sciences, 2006Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Kazumasa Isobe, N. Ohkoshi, Hajime Ohmori, Yasushi KawakamiAbstract: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.
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Effects of Short-Term Exercise on Adiponectin and Adiponectin Receptor Levels in Rats
Journal of atherosclerosis and thrombosis, 2007Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Yasushi Kawakami, Kazumasa IsobeAbstract: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.
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beta-adrenoceptor agonists downregulate Adiponectin, but upregulate Adiponectin Receptor 2 and tumor necrosis factor-alpha expression in adipocytes.
European journal of pharmacology, 2007Co-Authors: Kazumasa Isobe, Qin Zeng, Kazuhiro Takekoshi, Kazumi Suzukawa, Yasushi KawakamiAbstract: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.
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Effects of exercise on Adiponectin and Adiponectin Receptor levels in rats.
Life sciences, 2006Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Kazumasa Isobe, N. Ohkoshi, Hajime Ohmori, Yasushi KawakamiAbstract: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.
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Effects of Short-Term Exercise on Adiponectin and Adiponectin Receptor Levels in Rats
Journal of atherosclerosis and thrombosis, 2007Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Yasushi Kawakami, Kazumasa IsobeAbstract: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.
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beta-adrenoceptor agonists downregulate Adiponectin, but upregulate Adiponectin Receptor 2 and tumor necrosis factor-alpha expression in adipocytes.
European journal of pharmacology, 2007Co-Authors: Kazumasa Isobe, Qin Zeng, Kazuhiro Takekoshi, Kazumi Suzukawa, Yasushi KawakamiAbstract: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.
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Effects of exercise on Adiponectin and Adiponectin Receptor levels in rats.
Life sciences, 2006Co-Authors: Qin Zeng, Kazuhiro Takekoshi, Kazumasa Isobe, N. Ohkoshi, Hajime Ohmori, Yasushi KawakamiAbstract: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
