Adiponectin receptor 1 (AdipoR1) and Adiponectin receptor 2 (AdipoR2) can bind to adiponectin (AdipoQ) secreted by adipose tissue to participate in various physiological functions of the body. In order to explore the role of AdipoR1 and AdipoR2 in amphibians infected by Aeromonas hydrophila (Ah), the genes adipor1 and adipor2 of Rana dybowskii were cloned by reverse transcription-polymerase chain reaction (RT-PCR) and analyzed by bioinformatics. The tissue expression difference of adipor1 and adipor2 was analyzed by real-time fluorescence quantitative polymerase chain reaction (qRT-PCR), and an inflammatory model of R. dybowskii infected by Ah was constructed. The histopathological changes were observed by hematoxylin-eosin staining (HE staining); the expression profiles of adipor1 and adipor2 after infection were dynamically detected by qRT-PCR and Western blotting. The results show that AdipoR1 and AdipoR2 are cell membrane proteins with seven transmembrane domains. Phylogenetic tree also shows that AdipoR1 and AdipoR2 cluster with the amphibians in the same branch. qRT-PCR and Western blotting results show that adipor1 and adipor2 were up-regulated at different levels of transcription and translation upon Ah infection, but the response time and level were different. It is speculated that AdipoR1 and AdipoR2 participate in the process of bacterial immune response, providing a basis for further exploring the biological functions of AdipoR1 and AdipoR2 in amphibians.
Animals ; Receptors, Adiponectin/metabolism* ; Phylogeny ; Adiponectin/metabolism* ; Cloning, Molecular ; Ranidae/genetics*

BACKGROUND: Adiponectin is an adipokine that regulates lipid and glucose metabolism and has been shown to have anti-inflammatory and anti-atherogenic effects. It also plays an important role in the development of cardiovascular disease (CVD). METHODS: This study evaluated the association between adiponectin 45T/G polymorphism and cardiovascular complication in type 2 diabetes in Koreans. RESULTS: The present study included 758 patients with type 2 diabetes. The distribution of the adiponectin 45T/G polymorphism was 3.56% (n = 27) for GG, 42.35% (n = 321) for TG, and 54.09% (n = 410) for TT in patients with type 2 diabetes. The prevalence of CVD was significantly higher in subjects with the GG + TG genotype compared to those with the TT genotype (17.5% vs. 9.8%, P = 0.002). The G allele was associated with a higher risk of CVD (P = 0.002). CONCLUSION: Our findings suggest that the adiponectin 45T/G polymorphism is associated with diabetic cardiovascular complication in type 2 diabetes.
Adipokines ; Adiponectin* ; Alleles ; Cardiovascular Diseases ; Genotype ; Glucose ; Humans ; Metabolism ; Prevalence

OBJECTIVETo investigate the expression of adiponectin and its receptors (AdipoRs) in the retina of normal mice and mice with type 1 diabetes mellitus (T1DM).

METHODSC57BL/6 mice were randomly divided into control group and streptozotocin-induced T1DM group. Two months after the modeling, the total protein and adiponectin protein expression in the retina and choroid were measured using BCA method and enzyme-linked immunosorbent assay, respectively. Quantitative RT-PCR was performed to detect the mRNA expressions of AdipoRs in the retina and choroid, and Western blotting was employed to examine the protein expressions of AdipoRs in the retina.

RESULTSAdiponectin and AdipoRs proteins were expressed in the retina and choroid in normal mice. The expressions of adiponectin and AdipoR1 were up-regulated in the retina of mice with T1DM while AdipoR2 expression exhibited no significant changes.

CONCLUSIONAdiponectin and AdipoR1 may play an important role in the evolvement of type 1 diabetic retinopathy.

Adiponectin ; metabolism ; Animals ; Diabetes Mellitus, Experimental ; metabolism ; Diabetes Mellitus, Type 1 ; metabolism ; Diabetic Retinopathy ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Adiponectin ; metabolism ; Retina ; metabolism

OBJECTIVETo explore the changes in the mRNA expression of adiponectin (Adp), adiponectin receptors(AdpR), and leptin in different adipose tissues of Wannanhua pigs at different stages of development, and their sexual dimorphism.

METHODSFive Wannanhua boars and five Wannanhua gilts were sampled at birth, 30, 45, 90, and 180 days of age respectively. The delta delta Ct relative quantification real-time PCR was used to detect the transcription levels of Adp, AdpR1, AdpR2, and leptin mRNAs in subcutaneous (SC) and perirenal (PR) adipose tissues, and beta-actin were used as internal standards.

RESULTSThe expression level of Adp, AdpR1, AdpR2, and leptin mRNA in SC and PR adipose tissue were changed with age significantly (P < 0.01). In general, Adp mRNA expression in SC adipose tissue was significantly lower than that in PR adipose tissue (P < 0.05), while AdpR1, AdpR2, and leptin mRNA expression in SC adipose tissue were significantly higher than those in PR adipose tissue (P < 0.05 or P < 0.01). Although the sexual dimorphism were found in apart genes or apart days of age, Adp, AdpR1, AdpR2, and leptin mRNA expression both in SC adipose tissue and PR adipose tissue had no significant differences between Wannanhua gilts and boars in general. Significant positive correlation was found between Adp and AdpR1, AdpR2 (P < 0.05 or P < 0.01), and significant negative correlation was found between Adp and leptin (P < 0.05) in SC adipose tissue and PR adipose tissue respectively (P < 0.05).

CONCLUSIONThe expression of Adp, AdpR1, AdpR2, and leptin mRNA in adipose tissue of Wannanhua pigs followed specific developmental patterns and tissue specificity. Adp correlated with its receptors.

Actins ; metabolism ; Adiponectin ; metabolism ; Adipose Tissue ; growth & development ; metabolism ; Animals ; Female ; Leptin ; metabolism ; Male ; RNA, Messenger ; genetics ; Receptors, Adiponectin ; metabolism ; Swine

OBJECTIVETo investigate the effects of GW4064, a farnesoid X receptor (FXR) agonist, on adiponectin and its receptors during the differentiation of 3T3-L1 preadipocytes and on adiponectin receptors in HepG2 cells.

METHODSThe mRNA expressions of FXR, PPARγ2, adiponectin, AdipoR1, and AdipoR2 and the protein levels of adiponectin on days 0, 2, 4, 6, and 8 during the differentiation of 3T3-L1 preadipocytes treated with GW4064 were detected by fluorescent real-time PCR and ELISA, respectively. The mRNA expressions of AdipoR1 and AdipoR2 in HepG2 cells were also examined at 0, 12, 24, and 48 h after GW4064 treatment.

RESULTSThe mRNA expressions of FXR, PPARγ2, adiponectin, and AdipoR2 in 3T3-L1 preadipocytes and AdipoR2 in HepG2 cells treated with GW4064 was significantly increased compared with the control group (all P<0.05). The protein level of adiponectin was also significantly increased after GW4064 treatment. The expression of AdipoR1 in either 3T3-L1 preadipocytes or HepG2 cells showed no significant changes after GW4064 treatment.

CONCLUSIONGW4064 can up-regulate the expressions of FXR, PPARγ2, adiponectin, AdipoR2 in 3T3-L1 preadipocytes and AdipoR2 in HepG2 cells. As adiponectin and its receptors are two important factors in the treatment of non-alcoholic fatty liver disease, FXR agonist may potentially produce therapeutic effect on non-alcoholic fatty liver disease and can regulate adipocytes via up-regulating PPARγ during adipocyte differentiation.

3T3-L1 Cells ; Adiponectin ; metabolism ; Animals ; Cell Differentiation ; drug effects ; Hep G2 Cells ; Humans ; Isoxazoles ; pharmacology ; Mice ; PPAR gamma ; metabolism ; Receptors, Adiponectin ; metabolism ; Receptors, Cytoplasmic and Nuclear ; agonists

OBJECTIVE: To investigate the effect of adiponectin on the osteoblast differentiation and its signal transduction. METHODS: Adipopnectin receptor (AdipoR) was detected by immunoblot analysis. Alkaline phosphatase (ALP) activity was measured by enzyme-linked immunosorbent assay. Osteocalcin was measured by a specific radioimmunoassay kit, and the extent of mineralized matrix was determined. RNA interference was used to down-regulate the expression of AdipoR1 in human osteoblasts, and the effect of adiponectin on osteoblast differentiation was investigated. RESULTS: Only AdipoR1 protein was detected in human osteoblasts. Adiponectin could promote osteoblast differentiation, and result in a dose-dependent increase in ALP activity, osteocalcin secretion, and an increase in mineralized nodules. Suppression of AdipoR1 with siRNA could abolish the adiponectin induced ALP expression. Adiponectin could induce the activation of p38 and JNK, but not ERK1/2 in osteoblasts, and the pretreatment of osteoblasts with the p38 inhibitor (SB203580) could block the adiponectin-induced ALP activity. CONCLUSION Adiponectin can induce human osteoblast differentiation via AdipoR1/p38 pathway.
Adiponectin ; pharmacology ; Alkaline Phosphatase ; metabolism ; Cell Differentiation ; drug effects ; Cells, Cultured ; Humans ; Osteoblasts ; cytology ; metabolism ; Osteocalcin ; analysis ; RNA, Small Interfering ; genetics ; Receptors, Adiponectin ; biosynthesis ; Signal Transduction

OBJECTIVETo preliminarily investigate the expression and clinical significance of leptin and adiponectin in esophageal squamous cell carcinoma (ESCC).

METHODSThe expression of leptin and adiponectin in ESCC and normal esophageal mucosal tissue was detected by immunohistochemical staining with tissue microarray. The correlation between leptin, adiponectin and clinicalpathological features was statistically analyzed.

RESULTSThe expression of leptin was significantly upregulated in the ESCC than in the normal esophageal mucosa tissue [65.6% (80/122) versus 27.5% (11/40), P < 0.001]. Expression of leptin was significantly correlated with lymph node involvement and advanced tumor stage (P = 0.009 and P = 0.043, respectively). Expression of adiponectin was significantly down-regulated in ESCC compared with that in normal esophageal mucosal tissue [22.1% (27/122) versus 47.5% (19/40), P = 0.002]. Expression of adiponectin was significantly correlated with lymph node involvement (P = 0.020). Correlation analysis showed a positive correlation between the expression of leptin and lymph node metastasis and TNM stage (r = 0.235 and r = 0.183, respectively), and a negative correlation between the expression of adiponectin and lymph node metastasis (r = -0.229). There was no significant correlation between the expressions of leptin and adiponectin (P > 0.05), and between the body mass index and the expression of leptin and adiponectin, and lymph node metastasis (P > 0.05 for all).

CONCLUSIONSAn imbalanced expression of adipocytokines exits in ESCC. The expression of leptin and adiponectin is correlated with lymph node metastasis and/or tumor stage. Therefore, imbalanced expression of leptin and adiponectin may have a potential role in the carcinogenesis and disease progression of ESCC.

Adiponectin ; metabolism ; Carcinoma, Squamous Cell ; metabolism ; Down-Regulation ; Esophageal Neoplasms ; metabolism ; Leptin ; metabolism ; Lymphatic Metastasis ; Neoplasm Staging ; Up-Regulation

OBJECTIVES: Weight gain and glucose intolerance are the most common symptoms of metabolic syndrome. Certain patients complain of weight-change and hyperglycemia after receiving antidepressants. Our study evaluated the effects of antidepressants on serum glucose and energy metabolism. METHODS: Subjects were 32 Otsuka Long-Evans Tokushima Fatty (OLETF) and 35 wild-type Long-Evans Tokushima Otsuka (LETO) rats. From age 11 weeks, the rats were divided into 4 subgroups within each strain. We administered the designated antidepressant-amitriptyline, fluoxetine, or mirtazapine-to these subgroups, allocating the fourth as the control. After exactly 4 weeks' medication, we sacrificed the animals and checked their weight, glucose, insulin, leptin, adiponectin, and expression of adiponectin receptor mRNA. RESULTS: Fluoxetine subgroups in both strains gained the least weight. The glucose, triglyceride, and cholesterol levels of all OLETF antidepressant subgroups did not differ from the controls. Adiponectins in amitriptyline- and mirtazapine-subgroups were higher than control. All antidepressant subgroups showed elevated expressions of adiponectin receptor mRNA in fat, muscle, and the pancreas. CONCLUSION: Amitriptyline and mirtazapine seem to regulate adiponectin and expression of adiponectin receptor mRNA. Even though the underlying mechanisms were different, we conclude none of the antidepressants would have negative influences on energy metabolism in diabetogenic animals.
Adiponectin ; Amitriptyline ; Animals ; Antidepressive Agents ; Cholesterol ; Energy Metabolism ; Fluoxetine ; Glucose ; Glucose Intolerance ; Humans ; Hyperglycemia ; Insulin ; Leptin ; Mianserin ; Muscles ; Pancreas ; Rats ; Receptors, Adiponectin ; RNA, Messenger ; Sprains and Strains ; Weight Gain

Adiponectin ; blood ; Aged ; Fatty Liver ; blood ; metabolism ; Female ; Humans ; Insulin Resistance ; Male ; Middle Aged

Mutation and reduction of mitochondrial DNA (mtDNA) have been suggested as factors in the pathogenesis of several metabolic diseases. Recently, we demonstrated that C1qTNF-related protein-6 (CTRP6) is involved in fatty acid metabolism in muscle cells. In this study, we showed that expression of CTRP6 was up-regulated in mtDNA-depleted C2C12 cells, which displayed a marked decrease in cellular mtDNA and ATP content. Replacement of mtDNA normalized the expression level of CTRP6 similar to that in normal C2C12 cells, indicating that CTRP6 expression was up-regulated by mtDNA depletion. However, CTRP6 promoter activity remained unchanged in mtDNA-depleted cells. We also found that mtDNA depletion inhibited decay of CTRP6 mRNA. Taken together, mtDNA depletion induces an increase in CTRP6 expression by increasing mRNA stability.
Adiponectin/*genetics/metabolism ; Animals ; Cell Line ; DNA, Mitochondrial/*metabolism ; Mice ; Promoter Regions, Genetic ; RNA Stability ; RNA, Messenger/*metabolism ; Up-Regulation