The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Toshimasa Yamauchi - One of the best experts on this subject based on the ideXlab platform.
-
structure and function analysis of Adiponectin Receptors toward development of novel antidiabetic agents promoting healthy longevity
Endocrine Journal, 2018Co-Authors: Miki Okadaiwabu, Takashi Kadowaki, Toshimasa Yamauchi, Masato IwabuAbstract:Plasma Adiponectin levels and expression of its Receptors, AdipoRs are decreased in obesity, which cause insulin resistance and diabetes. AdipoR-deficient mice exhibit insulin resistance and impaired glucose tolerance. Moreover, newly identified AdipoR agonists not only improve insulin resistance but prolong lifespan shortened by obesity via AdipoR. Furthermore, efforts to promote structure-based drug discovery research at our laboratory have led to the first ever successful crystallization of AdipoR as well as to clarification of their structures. Structural analysis of AdipoRs as key molecules in lifestyle-related diseases is thus expected to lead not only to the acceleration of structure-based drug discovery but to the elucidation of novel aspects of the AdipoR structures and functions in the years to come. Finally, with the development of novel AdipoR-targeted antidiabetic agents also capable of prolonging lifespan, the attainment of healthy longevity may finally be brought within reach.
-
Adiponectin Adiponectin receptor in disease and aging
npj Aging and Mechanisms of Disease, 2015Co-Authors: Masato Iwabu, Toshimasa Yamauchi, Miki Okadaiwabu, Takashi KadowakiAbstract:Adipocytes are not merely organs for energy conservation but endocrine organs secreting a wide array of physiologically active substances, i.e., adipokines. Of these adipokines, Adiponectin is known to exert anti-diabetic and anti-atherosclerotic effects via Adiponectin Receptors (AdipoR)s, AdipoR1 and AdipoR2. Adiponectin has also recently been shown to regulate longevity signaling thus prolonging lifespan. Therefore, the strategy for activating Adiponectin/AdipoR signaling pathways are expected to provide a solid basis for the prevention and treatment of obesity-related diseases such as the metabolic syndrome, type 2 diabetes and cardiovascular disease, as well as for ensuring healthy longevity in humans.
-
Adiponectin Receptors a review of their structure function and how they work
Best Practice & Research Clinical Endocrinology & Metabolism, 2014Co-Authors: Toshimasa Yamauchi, Masato Iwabu, Miki Okadaiwabu, Takashi KadowakiAbstract:The discovery of Adiponectin and subsequently the Receptors it acts upon have lead to a great surge forward in the understanding of the development of insulin resistance and obesity-linked diseases. Adiponectin is a hormone that is derived from adipose tissue and is reduced in obesity-linked diseases including insulin resistance/type 2 diabetes and atherosclerosis. Adiponectin exerts its effects by binding to Adiponectin Receptors, two of which, AdipoR1 and AdipoR2, have been cloned. This has enabled researchers to carry out detailed studies elucidating the role played by these Receptors and the metabolic pathways that are involved following their activation. Such studies have clearly shown that the stimulation of these Receptors is associated with glucose homeostasis and ongoing research into their role will clarify the underlying molecular mechanisms of Adiponectin. Such knowledge can then be used to provide therapeutic targets aimed at managing obesity-linked diseases including type 2 diabetes and metabolic syndrome.
-
Adiponectin receptor as a key player in healthy longevity and obesity related diseases
Cell Metabolism, 2013Co-Authors: Toshimasa Yamauchi, Takashi KadowakiAbstract:Adiponectin is a fat-derived hormone whose reduction plays central roles in obesity-linked diseases including insulin resistance/type 2 diabetes and atherosclerosis. The cloning of Adiponectin Receptors AdipoR1 and AdipoR2 has stimulated Adiponectin research, revealing pivotal roles for AdipoRs in pleiotropic Adiponectin actions, as well as some postreceptor signaling mechanisms. Adiponectin signaling has thus become one of the major research fields in metabolism and clinical medicine. Studies on AdipoRs will further our understanding of the role of Adiponectin in obesity-linked diseases and shortened life span and may guide the design of antidiabetic and antiaging drugs with AdipoR as a target.
-
Expression levels of Adiponectin Receptors are decreased in human endometrial adenocarcinoma tissues.
International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists, 2012Co-Authors: Naoko Yamauchi, Takashi Kadowaki, Toshimasa Yamauchi, Yutaka Takazawa, Daichi Maeda, Takashi Hibiya, Mariko Tanaka, Masato Iwabu, Miki Okada-iwabu, Masashi FukayamaAbstract:Adiponectin is a cytokine secreted by adipocytes, whose plasma levels are decreased in obesity. Adiponectin has insulin-sensitizing, antiatherogenic, and antidiabetogenic effects. It has been shown that Adiponectin may also exert antineoplastic activity through suppression of tumor proliferation and neoangiogenesis and through induction of apoptosis. Recently, low Adiponectin serum concentration has been found in obesity-related malignancies, including endometrial cancer. In addition, the expression of Adiponectin Receptors (AdipoR1 and AdipoR2) has been documented in several human cancer tissues, but the expression has previously not been assessed in human endometrial cancer tissues. In this study, we analyzed the immunohistochemical expression of AdipoR1 and AdipoR2 in a series of surgically resected human endometrioid adenocarcinoma tissues from a total of 141 cases. Decreased AdipoR1 or AdipoR2 expression was significantly associated with histological higher grade (P=0.0026 and 0.0004, respectively). Decreased expression of AdipoR1 was associated with myometrial invasion and lymph node metastasis of endometrioid adenocarcinoma (P=0.0039 and P=0.0069, respectively). AdipoR1 and AdipoR2 immunoexpression was significantly associated with the expression of the progesterone receptor, although it was not significantly correlated with the expression of the estrogen receptor, Ki-67 or p53. Our present study raises the possibility that decreased expression of Adiponectin Receptors is implicated in the development, invasion, and metastasis of human endometrioid adenocarcinoma. Our findings, moreover, indicate that Adiponectin Receptors could be considered as therapeutic targets for endometrioid adenocarcinoma. In Adiponectin receptor-positive endometrioid adenocarcinoma, we think Adiponectin-based anticancer therapy is useful; however, in histological high-grade endometrioid adenocarcinoma, in which the expression levels of Adiponectin Receptors are relatively low, Adiponectin therapy supported by Adiponectin receptor induction is needed.
Zhixin Guo - One of the best experts on this subject based on the ideXlab platform.
-
Effect of rosiglitazone on the expression of cardiac Adiponectin Receptors and NADPH oxidase in type 2 diabetic rats
European Journal of Pharmacology, 2012Co-Authors: Zhixin Guo, Zhihong Qin, Rong Zhang, Yan YinAbstract:Abstract This study investigated the effect of rosiglitazone on the expression of cardiac Adiponectin Receptors and NADPH oxidase in type 2 diabetic rats. Thirty-six male Wistar rats were randomly divided into control (C, n = 10), diabetic (D, n = 13) and diabetic treated with rosiglitazone (DT, n = 13). Type 2 diabetes was induced by high-fat and high-sugar diet and intraperitoneal injection of a low dose of streptozotocin (STZ). Eleven rats in diabetic untreated group and twelve rats in diabetic treated group were successfully induced to be diabetes. After induction of diabetes, rosiglitazone (3 mg/kg/day) was administrated to diabetic treated rats by gavage for 12 weeks. Twelve weeks later, the heart function was detected. Plasma and myocardial Adiponectin levels were detected by enzyme linked immunosorbent assay (ELISA). The cardiac mRNA expression of Adiponectin Receptors 1 and 2, and monocyte chemoattractant protein-1 (MCP-1) was assayed by reverse transcript-polymerase chain reaction (RT-PCR). The cardiac mRNA expression of p22phox and NOX4 was assayed by real-time fluorescence quantitative PCR. The cardiac protein expression of phosphor-AMPK-α (Thr172) and glucose transporter 4 (GLUT4) was determined by Western blotting. The protein expression of Adiponectin Receptors 1 and 2, and connective tissue growth factor (CTGF)were determined by immunohistochemistrial staining. The ratio of heart weight to body weight was significantly increased in diabetic rats compared to control. Heart function, plasma and myocardial Adiponectin levels, the protein and mRNA expression of myocardial Adiponectin Receptors 1 and 2, myocardial phosphorylation of AMPK-α (Thr172) and the protein expression of myocardial GLUT4 were significantly decreased in diabetic rats compared to control (P
-
cardiac expression of Adiponectin and its Receptors in streptozotocin induced diabetic rats
Metabolism-clinical and Experimental, 2007Co-Authors: Zhixin Guo, Zhengyuan Xia, Violet G Yuen, John H McneillAbstract:Adiponectin can improve both glucose metabolism and insulin resistance via the adenosine monophosphate–activated protein kinase (AMPK) signaling pathway. Activated AMPK phosphorylates a variety of intracellular proteins, including acetyl coenzyme A carboxylase (ACC) that is involved in fatty acid oxidation. Adenosine monophosphate–activated protein kinase increases glucose transport by stimulating the translocation of glucose transporter 4 (GLUT4) to the sarcolemma in the heart. Adiponectin exerts its effect through Adiponectin Receptors, which are predominantly expressed in the liver and skeletal muscle. It is unknown whether the cardiac expression of Adiponectin and its Receptors is changed in diabetic rats. In the present study, we investigated the protein expression of Adiponectin and its Receptors in streptozotocin (STZ)–induced diabetic rat hearts. We also explored whether the levels of AMPK, ACC, and GLUT4 will be altered with the changed Adiponectin and its Receptors in STZ diabetic rat hearts. Plasma and cardiac Adiponectin levels were measured by radioimmunoassay. Plasma and cardiac interleukin 6 and plasma tumor necrosis factor α (TNF-α) were assayed by enzyme-linked immunosorbent assay. Cardiac Adiponectin Receptors, AMPK-α, ACC, GLUT4, and TNF-α were analyzed by Western blot in control and STZ diabetic rats. The plasma Adiponectin level was decreased, but the cardiac protein expression of Adiponectin receptor 1 was increased in diabetic rats. There was no difference in the cardiac Adiponectin level and the cardiac Adiponectin receptor 2 protein expression between control and diabetic rats. The phosphorylation of AMPK-α and protein expression of GLUT4 were decreased, but the phosphorylation of ACC was unchanged in diabetic rat hearts. Plasma and cardiac levels of interleukin 6 and TNF-α were increased in diabetic rats. In conclusion, STZ-induced diabetes up-regulates Adiponectin Receptors in the heart. Despite an increase in cardiac Adiponectin receptor 1 expression, there is an increased cardiac inflammatory response and a decreased GLUT4 protein expression associated with a reduction in circulating Adiponectin.
-
Effect of N-acetylcysteine on plasma Adiponectin and renal Adiponectin Receptors in streptozotocin-induced diabetic rats.
European journal of pharmacology, 2006Co-Authors: Zhixin Guo, Zhihua ZhaoAbstract:This study investigated the effect of N-acetylcysteine on plasma Adiponectin, renal Adiponectin Receptors, lipid metabolism and oxidative stress in streptozotocin-induced diabetic rats. Metabolic parameters, plasma Adiponectin level, renal protein expression of Adiponectin Receptors were analyzed in controls and diabetic rats treated with or without N-acetylcysteine in drinking water for 8 weeks. Plasma lipid, creatinine and free 5-F(2t)-isoprostane levels, urine protein excretion rate, mesangial matrix expansion index, and protein expression of renal connective tissue growth factor (CTGF) were increased in diabetic rats. The decreased plasma Adiponectin levels and renal protein expression of Adiponectin receptor 1 were accompanied by the decreased renal phosphorylation of adenosine monophosphate (AMP)-activated protein kinase (AMPK)-alpha (Thr172) and protein expression of phospho-acetyl coenzyme A carboxylase (ACC) (Ser79) which led to the increased renal triglyceride levels in diabetic rats. There was no difference in the protein expression of renal Adiponectin receptor 2 between control and diabetic rats. N-acetylcysteine treatment attenuated the increased oxidative stress, plasma and renal lipids, urine protein excretion rate, mesangial matrix expansion index, and protein expression of renal CTGF, but did not affect plasma Adiponectin levels, renal protein expression of Adiponectin receptor 1, phosphorylation of AMPK-alpha (Thr172) and renal protein expression of phospho-ACC (Ser79) in diabetic rats. These results suggested that the decreased plasma Adiponectin and renal Adiponectin receptor 1 result in the increased renal triglyceride that stimulates renal CTGF expression leading to the renal hypertrophy and the deteriorated renal function in the diabetic rats. N-acetylcysteine treatment attenuates the increased oxidative stress, but has no effect on the decreased plasma Adiponectin and renal Adiponectin receptor 1 in diabetic rats, indicating that oxidative stress may not contribute to the decreased plasma Adiponectin and renal Adiponectin receptor 1 protein expression in diabetic rats.
Takashi Kadowaki - One of the best experts on this subject based on the ideXlab platform.
-
structure and function analysis of Adiponectin Receptors toward development of novel antidiabetic agents promoting healthy longevity
Endocrine Journal, 2018Co-Authors: Miki Okadaiwabu, Takashi Kadowaki, Toshimasa Yamauchi, Masato IwabuAbstract:Plasma Adiponectin levels and expression of its Receptors, AdipoRs are decreased in obesity, which cause insulin resistance and diabetes. AdipoR-deficient mice exhibit insulin resistance and impaired glucose tolerance. Moreover, newly identified AdipoR agonists not only improve insulin resistance but prolong lifespan shortened by obesity via AdipoR. Furthermore, efforts to promote structure-based drug discovery research at our laboratory have led to the first ever successful crystallization of AdipoR as well as to clarification of their structures. Structural analysis of AdipoRs as key molecules in lifestyle-related diseases is thus expected to lead not only to the acceleration of structure-based drug discovery but to the elucidation of novel aspects of the AdipoR structures and functions in the years to come. Finally, with the development of novel AdipoR-targeted antidiabetic agents also capable of prolonging lifespan, the attainment of healthy longevity may finally be brought within reach.
-
Adiponectin Adiponectin receptor in disease and aging
npj Aging and Mechanisms of Disease, 2015Co-Authors: Masato Iwabu, Toshimasa Yamauchi, Miki Okadaiwabu, Takashi KadowakiAbstract:Adipocytes are not merely organs for energy conservation but endocrine organs secreting a wide array of physiologically active substances, i.e., adipokines. Of these adipokines, Adiponectin is known to exert anti-diabetic and anti-atherosclerotic effects via Adiponectin Receptors (AdipoR)s, AdipoR1 and AdipoR2. Adiponectin has also recently been shown to regulate longevity signaling thus prolonging lifespan. Therefore, the strategy for activating Adiponectin/AdipoR signaling pathways are expected to provide a solid basis for the prevention and treatment of obesity-related diseases such as the metabolic syndrome, type 2 diabetes and cardiovascular disease, as well as for ensuring healthy longevity in humans.
-
Adiponectin Receptors a review of their structure function and how they work
Best Practice & Research Clinical Endocrinology & Metabolism, 2014Co-Authors: Toshimasa Yamauchi, Masato Iwabu, Miki Okadaiwabu, Takashi KadowakiAbstract:The discovery of Adiponectin and subsequently the Receptors it acts upon have lead to a great surge forward in the understanding of the development of insulin resistance and obesity-linked diseases. Adiponectin is a hormone that is derived from adipose tissue and is reduced in obesity-linked diseases including insulin resistance/type 2 diabetes and atherosclerosis. Adiponectin exerts its effects by binding to Adiponectin Receptors, two of which, AdipoR1 and AdipoR2, have been cloned. This has enabled researchers to carry out detailed studies elucidating the role played by these Receptors and the metabolic pathways that are involved following their activation. Such studies have clearly shown that the stimulation of these Receptors is associated with glucose homeostasis and ongoing research into their role will clarify the underlying molecular mechanisms of Adiponectin. Such knowledge can then be used to provide therapeutic targets aimed at managing obesity-linked diseases including type 2 diabetes and metabolic syndrome.
-
Adiponectin receptor as a key player in healthy longevity and obesity related diseases
Cell Metabolism, 2013Co-Authors: Toshimasa Yamauchi, Takashi KadowakiAbstract:Adiponectin is a fat-derived hormone whose reduction plays central roles in obesity-linked diseases including insulin resistance/type 2 diabetes and atherosclerosis. The cloning of Adiponectin Receptors AdipoR1 and AdipoR2 has stimulated Adiponectin research, revealing pivotal roles for AdipoRs in pleiotropic Adiponectin actions, as well as some postreceptor signaling mechanisms. Adiponectin signaling has thus become one of the major research fields in metabolism and clinical medicine. Studies on AdipoRs will further our understanding of the role of Adiponectin in obesity-linked diseases and shortened life span and may guide the design of antidiabetic and antiaging drugs with AdipoR as a target.
-
Expression levels of Adiponectin Receptors are decreased in human endometrial adenocarcinoma tissues.
International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists, 2012Co-Authors: Naoko Yamauchi, Takashi Kadowaki, Toshimasa Yamauchi, Yutaka Takazawa, Daichi Maeda, Takashi Hibiya, Mariko Tanaka, Masato Iwabu, Miki Okada-iwabu, Masashi FukayamaAbstract:Adiponectin is a cytokine secreted by adipocytes, whose plasma levels are decreased in obesity. Adiponectin has insulin-sensitizing, antiatherogenic, and antidiabetogenic effects. It has been shown that Adiponectin may also exert antineoplastic activity through suppression of tumor proliferation and neoangiogenesis and through induction of apoptosis. Recently, low Adiponectin serum concentration has been found in obesity-related malignancies, including endometrial cancer. In addition, the expression of Adiponectin Receptors (AdipoR1 and AdipoR2) has been documented in several human cancer tissues, but the expression has previously not been assessed in human endometrial cancer tissues. In this study, we analyzed the immunohistochemical expression of AdipoR1 and AdipoR2 in a series of surgically resected human endometrioid adenocarcinoma tissues from a total of 141 cases. Decreased AdipoR1 or AdipoR2 expression was significantly associated with histological higher grade (P=0.0026 and 0.0004, respectively). Decreased expression of AdipoR1 was associated with myometrial invasion and lymph node metastasis of endometrioid adenocarcinoma (P=0.0039 and P=0.0069, respectively). AdipoR1 and AdipoR2 immunoexpression was significantly associated with the expression of the progesterone receptor, although it was not significantly correlated with the expression of the estrogen receptor, Ki-67 or p53. Our present study raises the possibility that decreased expression of Adiponectin Receptors is implicated in the development, invasion, and metastasis of human endometrioid adenocarcinoma. Our findings, moreover, indicate that Adiponectin Receptors could be considered as therapeutic targets for endometrioid adenocarcinoma. In Adiponectin receptor-positive endometrioid adenocarcinoma, we think Adiponectin-based anticancer therapy is useful; however, in histological high-grade endometrioid adenocarcinoma, in which the expression levels of Adiponectin Receptors are relatively low, Adiponectin therapy supported by Adiponectin receptor induction is needed.
Christos S. Mantzoros - One of the best experts on this subject based on the ideXlab platform.
-
serum Adiponectin levels and tissue expression of Adiponectin Receptors are associated with risk stage and grade of colorectal cancer
Metabolism-clinical and Experimental, 2011Co-Authors: Spyros P Gialamas, Christos S. Mantzoros, Sofia Tselenibalafouta, Eleni Petridou, Themistoklis N Spyridopoulos, Ioannis L Matsoukis, A Kondipafiti, George C ZografosAbstract:Adiponectin has been associated with colorectal cancer (CRC) risk. This study aims to investigate the association of both Adiponectin and tissue expression of its Receptors with CRC risk as well as clinicopathological characteristics, notably stage and grade. Determination of serum Adiponectin and immunohistochemical expression of Adiponectin Receptors in adenocarcinoma/normal colorectal tissue was performed in samples from 104 newly diagnosed CRC patients and 208 age- and sex-matched controls. Multiple logistic regression odds ratios and 95% confidence intervals for CRC risk were derived, controlling for a series of covariates. Serum Adiponectin was negatively associated with CRC risk (odds ratio, 0.72; confidence interval, 0.53-0.99) and also with tumor grade (P = .05). Expression of both Adiponectin Receptors was stronger in adenocarcinoma vs normal tissue (P = .001). AdipoR1 expression was negatively associated with nodal stage (P = .03); AdipoR2 expression was positively associated with tumor, node, metastasis stage (P = .01). Established positive associations with red meat consumption and diabetes, and negative associations with physical exercise and plant food consumption were confirmed along with a more than 60% higher risk associated with central obesity. Adiponectin levels and tissue expression of hormonal Receptors seem to be associated not only with CRC risk but also with components of clinicopathological characteristics; given power limitations, these results should be interpreted with caution. The exact nature of the association and the underlying pathophysiological mechanisms need to be further examined in large prospective studies assessing Adiponectin and its Receptors as novel targets for exploring CRC growth.
-
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.
-
serum Adiponectin concentrations and tissue expression of Adiponectin Receptors are reduced in patients with prostate cancer a case control study
Cancer Epidemiology Biomarkers & Prevention, 2007Co-Authors: Konstantinos Michalakis, Catherine J. Williams, Nicholas Mitsiades, Jennifer Blakeman, Sofia Balafoutatselenis, Aris Giannopoulos, Christos S. MantzorosAbstract:Purpose: Adiponectin, an adipocyte-secreted hormone with insulin-sensitizing effects, has been inversely associated with several hormonally dependent malignancies, including breast, endometrial, and colorectal cancer. Few studies have examined serum Adiponectin in relation to prostate cancer, and expression of Adiponectin Receptors has previously not been assessed in prostate tumors. Experimental Design: We collected plasma samples and covariate data in the context of a case-control study of 300 Greek men, including 75 prostate cancer cases, 75 patients with benign prostatic hyperplasia (BPH), and 150 healthy controls. Prostate tissue samples were taken from 72 cases and 27 noncases and examined for relative expression of Adiponectin Receptors AdipoR1 and AdipoR2 using immunohistochemistry. Results: Prostate cancer patients had significantly lower plasma Adiponectin concentrations as compared with men with BPH and healthy controls (7.4 ± 5.0 versus 11.5 ± 6.4 and 12.8 ± 8.0 ng/mL, respectively). Men in the top two quartiles of Adiponectin had a 71% to 73% reduced risk of prostate cancer as compared with men in the lowest quartile after adjusting for age, body mass index, and additional potential confounders. We found no similar relationship between Adiponectin and risk of BPH. Results from immunohistochemistry experiments show weaker expression of Adiponectin Receptors AdipoR1 and AdipoR2 in cancerous versus healthy prostate tissue. Conclusions: Higher serum Adiponectin is associated with a marked reduction in risk of prostate cancer, but not BPH, independently of other risk factors. Malignant prostate tissue samples have reduced expression of Adiponectin Receptors as compared with benign prostate tissue. These results support a role for Adiponectin in the pathogenesis of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(2):308–13)
Bjorn Richelsen - One of the best experts on this subject based on the ideXlab platform.
-
diet induced weight loss and exercise alone and in combination enhance the expression of Adiponectin Receptors in adipose tissue and skeletal muscle but only diet induced weight loss enhanced circulating Adiponectin
The Journal of Clinical Endocrinology and Metabolism, 2010Co-Authors: Tore Christiansen, Steen B Pedersen, Jens M Bruun, Soren K Paulsen, Thorkil Ploug, Bjorn RichelsenAbstract:Objective: The aim of the study was to investigate the effect of weight loss and exercise independently and in combination on circulating levels of Adiponectin including low molecular weight, medium molecular weight, and high molecular weight Adiponectin and expression of Adiponectin and Adiponectin Receptors (AdipoR) in adipose tissue (AT) and skeletal muscle (SM). Design and Methods: Seventy-nine obese males and females were randomized into the following: 1) exercise only (12 wk of exercise without diet restriction); 2) hypocaloric diet [8 wk of very low energy diet (600 kcal/d) followed by 4 wk with a weight maintenance diet]; and 3) hypocaloric diet and exercise (DEX; 8 wk very low energy diet 800 kcal/d followed by 4 wk weight maintenance diet combined with exercise throughout the 12 wk). Blood samples and biopsies from sc abdominal AT and SM were collected at baseline and after 12 wk. The molecular subforms of Adiponectin in serum were determined by Western blot. Results: The mRNA expression of Adip...
-
Adiponectin Receptors in human adipose tissue effects of obesity weight loss and fat depots
Obesity, 2006Co-Authors: Maria Rasmussen, Aina S Lihn, Steen B Pedersen, Jens M Bruun, Mads Rasmussen, Bjorn RichelsenAbstract:RASMUSSEN, MARIA S., AINA S. LIHN, STEEN B. PEDERSEN, JENS M. BRUUN, MADS RASMUSSEN, AND BJORN RICHELSEN. Adiponectin Receptors in human adipose tissue: effects of obesity, weight loss, and fat depots. Obesity. 2006;14:28–35. Objective: To investigate the presence and regulatory properties of the Adiponectin Receptors, AdipoR1 and AdipoR2, in human adipose tissue (AT) and in isolated human adipocytes. Research Methods and Procedures: The effect of obesity, weight loss, and gender on expression of AdipoR1 and AdipoR2 was investigated in subcutaneous AT. The influence of fat distribution on these Receptors was investigated in paired samples of subcutaneous and omental AT. Gene expression of these Receptors was quantified by reverse transcriptase-polymerase chain reaction. Results: AdipoR1 mRNA levels were 10-fold higher than adipoR2 in both AT fragments and in isolated adipocytes. AdipoR1 expression was lower in AT from obese subjects (p 0.05) compared with that from normal-weight subjects, and AdipoR1 displayed a negative correlation with BMI (r 0.53, p 0.01). In obese subjects, weight loss (12 kg) increased AdipoR1 expression by 80% in AT (p 0.01). Concerning regional differences, AdipoR1 showed significantly lower expression in omental AT than in subcutaneous AT (p 0.01). No gender difference was observed in the expression of these Receptors. In human preadipocyte cultures, AdipoR1 expression was not induced during the differentiation process, whereas AdipoR2 was induced by 5-fold (p 0.05). Discussion: AdipoR1 is highly expressed in human AT, indicating that Adiponectin may have biological effects in AT in an autocrine/paracrine manner. AdipoR1 expression in AT is reduced in obese subjects and is increased after weight loss. Thus, it can be suggested that Adiponectin might have reduced biological effects in AT due to low levels of Adiponectin Receptors in obese subjects and in omental adipocytes, which may further aggravate the negative metabolic effect of low levels of Adiponectin characterizing the obese state.