Structure, Signalling and Physiologic Role of Adiponectin-Dietary and Exercise- Related Variations
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Since its discovery in 1995 adiponectin has garnered considerable interest from the academic, clinical and biotech communities due to its proposed salutary anti-inflammatory, anti-diabetic, anti-atherogenic and cardioprotective properties. As a result our appreciation of adiponectin's structure and the importance of post-translational modifications (PTMs) in adiponectin production are now relatively advanced. So too, following the identification of a variety of adiponectin receptors, binding proteins and downstream signalling networks, is our understanding of adiponectin's intracellular signalling pathways that are implicated in mediating adiponectin's pleiotropic effects. Adiponectin's ability to moderate inflammation, which is recognised as a key protagonist in many modern diseases, may be the key to many of its beneficial effects. Recent insights indicate that adiponectin modulates cellular inflammation by affecting sphingolipid metabolism, with the adiponectin receptors displaying intrinsic ceramidase activity. In the current review we will summarise the molecular details of adiponectin, discuss key players and recent insights into adiponectin signalling and consider the physiologic role(s) of adiponectin. We will also review studies into the effects of diet or exercise on circulating adiponectin levels focusing largely on reports from human trials.Keywords:
Adiponectin receptor 1
To observe the effect of moxibustion on serum adiponectin content, and expression of adiponectin and adiponectin receptor in adipose tissue in Alzheimer's disease (AD) rats, so as to explore its mechanism underlying improvement of AD.Fifty male SD rats were randomly divided into control, model, Shenque (CV8), Zusanli (ST36) and CV8＋ST36 groups (n＝10 in each group). The AD model was established by intraperitoneal injection of D-galactose (400 mg•kg－1•d－1) for 5 weeks and scopolamine hydrobromide (3 mg •kg－1•d－1) for 2 weeks. Moxibustion was applied to CV8, ST36 and CV8＋ST36 respectively for 3 moxa-cones every time, once daily for 5 weeks. Morris water maze tests were used to assess the rats' learning-memory ability. The contents of serum adiponectin were assayed using ELISA, and the expression of adiponectin and adiponectin receptor in the adipose tissue was detected by quantitative real-time PCR and Western blot, separately.Following modeling, the average escape latency of Morris water maze tests was significantly prolonged (P<0.05), the content of serum adiponectin and the expression level of adiponectin mRNA in adipose tissue were significantly decreased (P<0.01), the expression of adiponectin receptor protein significantly decreased in the model group relevant to the control group (P<0.01). After the intervention, the average escape latency was significantly shortened (P<0.05), the decreased serum adiponectin content and adiponectin mRNA expression, and the decreased adiponectin receptor protein expression in adipose tissue were all reversed in the 3 treatment groups (P<0.01，P<0.05). No significant differences were found among the three moxibustion groups in the above indexes (P>0.05).Moxibustion at CV8, ST36 and CV8＋ST36 is effective in up-regulating serum adiponectin content，adiponectin mRNA expression and adiponectin receptor protein expression in adipose tissue, which may provide evidence for clinical election of acupoints.
Zusanli
Adiponectin receptor 1
Moxibustion
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Abstract Although obesity is a risk factor for colorectal cancer, the underlying mechanism is not clear. Adiponectin is an adipokine that binds to 2 types of receptors, AdipoR1 and AdipoR2. The plasma concentrations of adiponectin are reduced in obese individuals and adiponectin has been reported to have anticarcinogenic properties. Furthermore, AdipoR1 and AdipoR2 have been reported to be expressed in several malignancies. However, little is known about the expression of AdipoR1 and AdipoR2 in colorectal cancer and its clinicopathological implications. In addition, the relationship between adiponectin and colorectal cancer has not yet been determined. Here, we sought to investigate adiponectin and adiponectin receptors in relation to colorectal cancer. AdipoR1 and AdipoR2 immunostaining was detected in 72 and 68% of human colorectal cancer tissue, respectively. AdipoR1 and AdipoR2 expression levels were inversely related to T stage. The lowest AdipoR1 and AdipoR2 expression were detected in poorly differentiated adenocarcinoma. RT‐PCR also showed the expression of AdipoR1 and AdipoR2 in HCT116 and SW620. MTT assay and TUNEL assay demonstrated the tendency of growth inhibition and apoptosis induction in both cell lines after full‐length adiponectin treatment although statistically insignificant. Microarray analysis revealed several gene responses to full‐length adiponectin, including upregulation of ENDOGL1 and MT1G . In conclusion, AdipoR1 and AdipoR2 may be intimately related to the progression of colorectal cancer. Further studies may be warranted to assess adiponectin and its receptors as a novel target for inhibition of colorectal cancer growth.
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瞄准：决定传播并且在有脂肝疾病或肝肝硬化的啮齿类动物的肝的 adiponectin 并且在 mRNA 水平上在 mRNA 和蛋白质水平和 AdipoR2 上调查 adiponectin 受体 AdipoR1 的表示。方法：胖美联储老鼠在老鼠为脂肝疾病和胆汁管结扎被用作一个模型调查硬变肝。AdipoR1 和 AdipoR2 mRNA 的表示被实时 RT-PCR 决定。AdipoR1 蛋白质被免疫污点分析。Adiponectin 被 ELISA 测量。结果：全身的 adiponectin 在胖美联储的老鼠被减少，但是在胆汁管结扎(BDL ) 以后在老鼠被提高。当时，肝的 adiponectin 蛋白质在 steatotic 肝然而并非在 BDL 老鼠的肝是更低的与控制相比。Adiponectin mRNA 也没在老鼠肝在人的肝样品或主要人的 hepatocytes 被检测，但是 recombinant adiponectin 被孤立的 hepatocytes in-vitro 收起。AdipoR1 mRNA 和 AdipoR1 蛋白质层次在控制的肝织物是类似的，而 AdipoR2 mRNA 被导致，脂肪喂动物。AdipoR2 mRNA 和 AdipoR1 mRNA 和蛋白质在 BDL 老鼠的肝被压制。结论：而传播 adiponectin 在肝硬化的一个老鼠模型被提高，类似的调查结果在人被描述了，我们的研究在脂肝疾病的一个老鼠模型显示出减少的传播 adiponectin。adiponectin 受体的减少的肝的表示仅仅在肝肝硬化被发现。
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Calorie restriction and endurance exercise are known robust lifestyle modifications that delay the onset of type 2 diabetes and metabolic syndrome, however, its protective mechanism needs to be elucidated.To investigate the role of adiponectin in lifestyle modifications, male Sprague-Dawley rats were divided into groups of caloric restriction, exercise, and control for a 6-month intervention. Tissue and serum adiponectin levels, tissue expression of SIRT1, AMP-activated protein kinase (AMPK)α phosphorylation and AdipoR1, and insulin sensitivity were determined. All effects of adiponectin found in vivo were confirmed by L6 myoblast cells cultured with serum from a rat that received an intervention or by L6 cells with an AdipoR1 knockdown.Circulating adiponectin levels increased twofold to threefold in those rats in the caloric restriction and aerobic exercise groups, and adiponectin expression increased significantly not only in adipose tissue but also in skeletal muscle. The enhancement of SIRT1, AdipoR1 expression, and AMPKα phosphorylation in the skeletal muscle of the rats that underwent an intervention was simulated in the L6 myoblast cells cultured with serum from the intervention rats. The transferable effects of adiponectin in the serum were confirmed by blunting these effects in L6 myoblast cells upon knockdown of AdipoR1 or neutralizing the serum with an anti-adiponectin antibody. Adiponectin also exhibited a dose-dependent induction of its own receptor. The induction of AdipoR1 and SIRT1 expression and AMPKα phosphorylation by adiponectin was blunted when AMPKα, SIRT1, or AdipoR1, respectively, were knocked down.An elevated muscle-derived adiponectin can be attributed to lifestyle modifications. Adiponectin, which triggers the adiponectin receptor1 (AdipoR1) and its downstream targets AMPKα and SIRT1, was involved in the lifestyle modifications and control of type 2 diabetes.
Adiponectin receptor 1
AMP-Activated Protein Kinase
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Adiponectin is inversely related to BMI, positively correlates with insulin sensitivity, and has anti-atherogenic effects. In recent years, adiponectin has been well studied in the field of oncology. Adiponectin has been shown to have antiproliferative effects on gastric cancer, and adiponectin expression is inversely correlated with clinical staging of the disease. However, no studies have reported the correlation between serum adiponectin and receptor expression with disease progression.In this study, we evaluated expression levels of 2 adiponectin receptors--AdipoR1 and AdipoR2--and attempted to correlate their expression with prognosis in gastric cancer patients. AdipoR1 and AdipoR2 expression in gastric cancer cell lines (MKN45, TMK-1, NUGC3, and NUGC4) was evaluated by western blotting analysis, and the antiproliferative potential of adiponectin was examined in vitro. Serum adiponectin levels were evaluated in 100 gastric cancer patients, and the expression of AdipoR1 and AdipoR2 was assessed by immunohistochemical staining.MKN45 and NUGC3 expressed higher levels of AdipoR1 compared to NUGC4, even though there was no significance in AdipoR2 expression. The antiproliferative effect of adiponectin was confirmed in MKN45 and NUGC3 at 10 μg/ml. No significant associations were observed between serum adiponectin levels and clinicopathological characteristics, but lymphatic metastasis and peritoneal dissemination were significantly higher in the negative AdipoR1 immunostaining group (24/32, p = 0.013 and 9/32, p = 0.042, respectively) compared to the positive AdipoR1 group (lymphatic metastasis, 33/68; peritoneal dissemination, 8/68). On the other hand, AdipoR2 expression was only associated with histopathological type (p = 0.001). In survival analysis, the AdipoR1 positive staining group had significantly longer survival rates than the negative staining group (p = 0.01). However, multivariate analysis indicated that AdipoR1 was not an independent prognostic factor on patient's survival on gastric cancer.In gastric cancer, adiponectin has the possibility to be involved in cell growth suppression via AdipoR1. The presence of AdipoR1 could be a novel anticancer therapeutic target in gastric cancer.
Adiponectin receptor 1
Immunostaining
Lymphovascular invasion
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Objective To study the expression of adiponectin and adiponectin receptors mRNA in rats fed diets with different fatty acid ratios.Method Seventy two male Wistar rats were randomly divided into control group and 5 experimental groups(A～E).The experimental group were fed diets with saturated fatty acids(SFA)/monounsaturated fatty acid(MUFA)/polyunsaturated fatty acid ratio(PUFA)(S/M/P) 1:1,7:1.2,1:1:1,2:1:1,1:2:1 and 1:1:2.The adipose tissue adiponectin(ADPN),skeletal muscle adiponectin receptor 1(AdipoR1) and liver adiponectin receptor 2(AdipoR2) mRNA expression levels were determined after 12 w.Result The mRNA levels of adiponectin in both adipose tissues of group 1:1.7:1.2 and 1:1:1 were significantly lower as compared with the control group(P0.05),as well as the mRNA level of adiponectin in subcutaneous adipose tissues of group 2:1:1.The mRNA levels of adiponectin in other experimental groups were significantly higher as compared with the control(P0.05),the highest in group 1:1:2(P0.001).There was no significant difference in AdipoR mRNA levels between the control group and other groups.Conclusion The adiponectin mRNA level in adipose tissue was decreased in rats fed high-fat diet.Unsaturated fatty acid increased adiponectin mRNA level,more conspicuous in PUFA than MUFA.
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Objective:The purpose of the present experiment is to observe the change of adiponectin receptor 1 in aorta.Methods:8-week-old ApoE deficient mice were randomly assigned to two groups:ApoE deficient mice control group(C);aerobic exercise-trained group(E).The mice were fed by high fat diet.Mice in the aerobic exercise-trained groups ran on a treadmill for a total of 14 weeks.At the end of experiment,atherosclerotic was observed.Adiponectin mRNA in adipose tissue and serum adiponectin was tested.Adiponectin receptor 1 protein in aortic was detected.Results:The results showed that vascular of E group was significantly better than C group;Adiponectin-mRNA in the adipose tissue,serum Adiponectin and adiponectin receptor 1 protein of E group were significantly higher than that of the C group.Conclusion:It suggests that 14 weeks aerobic exercise can significantly increase adiponectin-mRNA in the adipose tissue,serum adiponectin as well as adiponectin receptor 1 protein.Aerobic exercise is likely to be one of the factors to anti-atherogenesis.
Adiponectin receptor 1
Aerobic Exercise
Apolipoprotein E
Treadmill
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Background: The adipokine adiponectin has direct beneficial effects on cardiomyocytes. However, obesity and ageing are characterized by an adiponectin deficit. Recently, a family of adiponectin paralogs, comprising 15 members so far, was discovered and designated as C1q/tumor necrosis factor-alpha-related proteins (CTRPs). While the protective adiponectin actions are well recognized, questions remain unanswered concerning the role of the CTRPs.
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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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Physical exercise
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Obesity and osteoarthritis (OA) are well-known comorbidities and their precise molecular interactions are still unidentified. Adiponectin, a major adipokine, known to have an anti-inflammatory effect in atherosclerosis or Type 2 Diabetes Mellitus (T2DM), has also been postulated to be pro-inflammatory in OA. This dual role of adiponectin is still not explained. The precise mechanism by which adiponectin affects cartilage and chondrocytes remains to be elucidated. In the present observational study chondrocytes from 30 patients with OA (18 females and 12 males) undergoing total knee replacement (TKR) were isolated. Expression of adiponectin receptors 1 and 2 (ADIPOR1 and ADIPOR2) was examined both at gene and protein levels in chondrocytes. The difference in adiponectin receptor expression between lean and obese patients with OA and the role of adiponectin in regulating pro-inflammatory genes (MCP-1, IL-6, and VCAM-1, MMP-1, MMP-2, and TIMP-1) has been investigated. We found that ADIPOR1 represented the most abundant adiponectin receptor in primary OA chondrocytes. ADIPOR1 and ADIPOR2 genes and ADIPOR1 protein were differently expressed in OA chondrocytes obtained from obese compared with lean patients with OA. Adiponectin induced gene expression of MCP-1, IL-6, and MMP-1 in all OA patients' chondrocytes. In contrast, VCAM-1 and MMP-2 were differently regulated by adiponectin depending on the patient's body mass index. This study suggests that adiponectin and ADIPOR1 may have important roles in the pathogenesis of cartilage degeneration in OA of obese subjects.
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