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*

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 relationship between visceral fat depot and adiponectin level in OLETF rats.

METHODSTwenty male OLETF rats and 10 male Long-Evans Tokushima Otsuka (LETO) rats were subjected to regular oral glucose tolerance test (OGTT). The rats were sacrificed at the ages of 8, 32 and 40 weeks for measurements of the body weight, blood glucose, blood lipid level, blood insulin, and weight of the visceral fat.

RESULTSCompared with LETO rats, OLETF rats had significantly higher body weight and visceral fat with impaired glucose tolerance (P<0.05). OLETF rats also had higher blood insulin, TG, FFA and CHOL levels (P<0.05). The plasma adiponectin level was significantly lower in OLETF rats than in LETO rats at different ages (P<0.05). The adiponectin mRNA level in the adipose tissue of OLETF rats was comparable with that in LETO rats, but significantly decreased at 32 and 40 weeks of age (P<0.01).

CONCLUSIONPlasma adiponectin level is significantly correlated to insulin sensitivity and visceral fat depots in OLETF rats, but a lowered APN mRNA expression level is not the main reason for a decreased plasma adiponectin level in the early stage.

Adiponectin ; blood ; genetics ; metabolism ; Animals ; Insulin Resistance ; Intra-Abdominal Fat ; metabolism ; Male ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Inbred OLETF

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

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

OBJECTIVEThis meta-analysis was performed to summarize the association of the ADIPOQ rs2241766 and rs266729 polymorphisms with metabolic syndrome (MS) in the Chinese population.

METHODSWe searched for articles in MEDLINE via PubMed, EMBASE, HuGE Navigator, CNKI, and Wanfang databases and calculated odds ratios (ORs) with 95% confidence intervals (CIs) to determine the strength of associations in fixed- or random-effects models.

RESULTSWe included 21 articles in the meta-analysis: 17 reports of ADIPOQ rs2241766 with 3628 cases and 3000 controls and 8 of rs266729 with 2021 cases and 2226 controls. We found an increased risk of MS with the ADIPOQ rs2241766 polymorphism in some genetic models (allele model: OR=1.12, 95% CI: 1.03-1.21; dominant model: OR=1.15, 95% CI: 1.04-1.28; homozygote model: OR=1.22, 95% CI: 1.00-1.49) but no association with the ADIPOQ rs266729 polymorphism (allele model: OR=0.98, 95% CI: 0.82-1.17; dominant model: OR=0.90, 95% CI: 0.79-1.02; recessive model: OR=1.09, 95% CI: 0.85-1.39; homozygote model: OR=1.03, 95% CI: 0.80-1.33).

CONCLUSIONThe results of this meta-analysis suggest an association between the ADIPOQ rs2241766 polymorphism and MS in the Chinese population. G allele of ADIPOQ rs2241766 increases the risk of MS. Better designed studies with different ethnic populations and larger sample sizes are needed for assessing the relationship between ADIPOQ rs2241766 and rs266729 polymorphisms and MS in the future.

Adiponectin ; genetics ; metabolism ; China ; epidemiology ; Genetic Predisposition to Disease ; Genotype ; Humans ; Metabolic Syndrome ; epidemiology ; genetics ; Polymorphism, Genetic ; Risk Factors

BACKGROUNDThe synovial fluid concentrations of adiponectin are significantly higher in patients with rheumatoid arthritis (RA) than in patients with osteoarthritis (OA). Accumulating evidence suggests that adiponectin may be an inducer of inflammation in arthritis, but the mechanism remains unclear. The objectives of this study were to compare the expression levels of adiponectin receptors in rheumatoid arthritis synovial fibroblasts (RASF) and osteoarthritis synovial fibroblasts (OASF), evaluate the roles of adiponectin receptors in adiponectin-induced prostaglandin E(2) (PGE(2)) production, and then investigate the effects of a nonsteroidal anti-inflammatory drug (NSAID) and a cyclooxygenase (COX)-2-selective inhibitor on adiponectin-induced PGE(2) release.

METHODSThe expressions of adiponectin receptor 1 (AdipoR1) and AdipoR2 mRNA and protein in synovial fibroblasts from seven patients with RA and eight patients with OA undergoing total knee replacement were evaluated by real-time polymerase chain reaction, immunofluorescence microscopy and Western blotting analysis. Adiponectin-induced PGE(2) production was detected by enzyme-linked immunosorbent assay. RNA interference against the AdipoR1 and AdipoR2 genes was performed to investigate the effects of the adiponectin receptors on adiponectin-induced PGE(2) production in both RASF and OASF.

RESULTSAdipoR1 and AdipoR2 mRNA and protein were expressed by both RASF and OASF. Compared with OASF, RASF exhibited higher levels of AdipoR1, but there was no significant difference for AdipoR2. Adiponectin induced the production of PGE(2) by the synovial fibroblasts in a concentration-dependent manner, and this was more obvious in RASF. RNA interference showed that the difference may be mediated by the diverse distribution of AdipoR1. The adiponectin-induced PGE(2) production was efficiently relieved by the NSAID and COX-2-selective inhibitor.

CONCLUSIONThe present findings suggest that AdipoR1 may mediate the difference in adiponectin-induced PGE(2) production in RASF and OASF.

Adiponectin ; pharmacology ; Arthritis, Rheumatoid ; metabolism ; Blotting, Western ; Cells, Cultured ; Dinoprostone ; metabolism ; Female ; Fibroblasts ; drug effects ; metabolism ; Humans ; Immunoassay ; Male ; Microscopy, Fluorescence ; Middle Aged ; Osteoarthritis ; metabolism ; RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; Receptors, Adiponectin ; genetics ; metabolism ; Synovial Membrane ; cytology

PURPOSE: Obesity is a risk factor for asthma and type II diabetes. Peroxisome proliferator-activated receptor (PPAR)-gamma has been suggested to regulate inflammatory responses in diabetes and asthma. We investigated whether PPAR-alpha, PPAR-gamma, adiponectin receptors (AdipoR1, AdipoR2), leptin, and tumor necrosis factor (TNF)-alpha are expressed in rat lung tissues and whether the expression differs between obese Otsuka Long-Evans Tokushima Fatty (OLETF) and lean Long Evans Tokushima Otsuka (LETO) rats. MATERIALS AND METHODS: Obese and lean rats were given with a high fat diet or a 30% restricted diet for 32 weeks, and their blood glucose levels and weights were monitored. After 32 weeks, mRNA levels of PPAR-alpha, PPAR-gamma, AdipoR1, AdipoR2, leptin, and TNF-alpha in lung tissues were measured using real time PCR. RESULTS: PPAR-alpha, PPAR-gamma, AdipoR1, AdipoR2, leptin, and TNF-alpha were expressed in both obese and lean rat lung tissues. Increased serum glucose levels on intraperitoneal glucose tolerance testing and a higher weight gain at 32 weeks were observed in OLETF control rats compared to OLETF diet restricted rats. PPAR-gamma expression was markedly elevated in obese control and diet restricted rats compared to lean rats, although PPAR-gamma expression in obese rats was not affected by diet restriction. Leptin was highly expressed in OLETF rats compared to LETO rats. TNF-alpha expression was enhanced in OLETF control rats compared LETO diet restricted rats, and decreased by diet restriction. PPAR-alpha, AdipoR1, and AdipoR2 expression were not significantly different between obese and lean rats. CONCLUSION: PPAR-gamma was highly expressed in the lung tissues of obese rats and may be a novel treatment target for regulating lung inflammation associated with obesity.
Animals ; Body Weight ; Glucose Tolerance Test ; Leptin/genetics/metabolism ; Lung/*metabolism ; Male ; Obesity/genetics/*metabolism ; PPAR gamma/genetics/*metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Long-Evans ; Receptors, Adiponectin/genetics/metabolism ; Tumor Necrosis Factor-alpha/genetics/metabolism

PURPOSE: Although some CDH13 single nucleotide polymorphisms (SNPs) have been shown to be determinants of blood adiponectin levels, the clinical implications of CDH13 variants are not yet completely understood. The purpose of this study was to evaluate the effects of SNPs of CDH13 on metabolic and vascular phenotypes. MATERIALS AND METHODS: We included 238 hypertensive subjects and 260 age- and sex-matched controls. Seven tagging-SNPs were identified in the CDH13 gene by whole gene sequencing. The association between these SNP variants and the risk of hypertension, metabolic traits, and carotid intima-media thickness (IMT) was examined. RESULTS: Minor allele carriers of rs12444338 had a lower risk of hypertension, but the association turned out just marginal after adjusting confoudners. Blood glucose levels were higher in the minor allele carriers of c.1407C>T (p=0.01), whereas low-density lipoprotein-cholesterol levels were greater in those of rs6565105 (p=0.02). The minor allele of rs1048612 was associated with a higher body mass index (p=0.01). In addition, the mean carotid IMT was significantly associated with rs12444338 (p=0.02) and rs1048612 (p=0.02). CONCLUSION: These results provide evidence that CDH13 variants are associated with metabolic traits and carotid atherosclerosis in Koreans. This study shows the multifaceted effects of CDH13 variants on cardiometabolic risk.
Adiponectin/genetics ; Asian Continental Ancestry Group ; Atherosclerosis/epidemiology/genetics ; Blood Glucose/metabolism ; Cadherins/*genetics ; Cholesterol/blood ; Female ; Humans ; Hypertension/epidemiology/genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics

OBJECTIVETo construct and express the recombinant human adiponectin (gAd) global domain.

METHODSgAd complementary DNA (cDNA) was obtained from human fat tissue by RT-PCR. The PCR product was cloned into the vector pMD18-T and the prokaryotic expression vector pET32a(+). The recombinant vector was identified by digestion with double restriction endonucleases SalI and EcoRI, PCR and sequence analysis. The recombinant plasmid containing gAd gene was transformed into E. coli BL21 (DE3), and the expression of the fusion protein His-gAd was induced by IPTG.

RESULTSThe gAd cDNA of 412 bp was obtained from the total RNA of the fat tissue and verified by sequence analysis.

CONCLUSIONThe recombinant plasmid could stably express the 34-kD fusion protein His-gAd in the engineered bacteria in the form of inclusion bodies.

Adiponectin ; biosynthesis ; genetics ; Adult ; Cloning, Molecular ; DNA, Complementary ; genetics ; Escherichia coli ; genetics ; Female ; Genetic Vectors ; genetics ; Humans ; Prokaryotic Cells ; cytology ; metabolism ; Recombinant Proteins ; biosynthesis