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*

Rats were exposed to 1 or 10 μg/mL bisphenol A (BPA) in water during pregnancy and lactation. Offspring rats were given normal water and a standard diet from weaning to postnatal day (PND) 50. Perinatal exposure to BPA resulted in significantly increased body weight, visceral adipose tissue, abnormal serum lipids, and lower adiponectin (ADP) levels in both female and male offspring rats. Liver adipose triglyceride lipase (Atgl) mRNA levels and ADP protein in visceral adipose tissue were significantly decreased in BPA-exposed offspring rats. In both female or male offspring rats, obesity and dyslipidemia induced by perinatal exposure to BPA were associated with down regulation of Atgl mRNA in liver and ADP protein in visceral adipose tissue.
Adiponectin ; metabolism ; Adipose Tissue ; metabolism ; Animals ; Benzhydryl Compounds ; adverse effects ; metabolism ; Body Weight ; Dyslipidemias ; enzymology ; etiology ; metabolism ; physiopathology ; Female ; Humans ; Lipase ; genetics ; metabolism ; Lipids ; blood ; Male ; Obesity ; enzymology ; etiology ; metabolism ; physiopathology ; Phenols ; adverse effects ; metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; enzymology ; etiology ; metabolism ; physiopathology ; Rats ; Rats, Sprague-Dawley

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

This study was performed to evaluate the contribution of adiponectin to the production of interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-1 and MMP-13 in human endothelial cells and osteoblasts in arthritic joints. Cultured human umbilical vascular endothelial cells (HUVECs) and osteoblasts were stimulated with adiponectin (1 or 10 mug ml-1) or IL-1beta (0.1 ng ml-1) in the presence or absence of hypoxia for 24 h. The protein expression patterns were examined by analyzing culture supernatants using the enzyme-linked immunosorbent assay (ELISA). Adiponectin significantly stimulated the production of VEGF, MMP-1 and MMP-13 in osteoblasts but not in endothelial cells, whereas it significantly stimulated the production of IL-6 and IL-8 in both endothelial cells and osteoblasts. The increase in VEGF production induced by adiponectin was significantly greater than that induced by IL-1beta. The production of IL-6 and IL-8 in adiponectin-stimulated endothelial cells was approximately 10-fold higher than that in IL-1beta-stimulated endothelial cells; in osteoblasts, adiponectin-induced IL-6 and IL-8 secretion was approximately twofold higher than that induced by IL-1beta. In addition, IL-8 production in endothelial cells was approximately sevenfold higher than in osteoblasts. However, IL-6 levels were similar between the two cell types, suggesting that adiponectin may be involved in the production of IL-8 in endothelial cells, which may have an important role in neutrophil recruitment to arthritic joints. Furthermore, the increases in protein expression induced by adiponectin were differentially regulated by hypoxia. In conclusion, adiponectin has a more important role than does IL-1beta in the production of mediators that drive synovitis and joint destruction in endothelial cells and osteoblasts at physiological concentrations.
Adiponectin/pharmacology/*physiology ; Arthritis, Rheumatoid/metabolism ; Cell Hypoxia ; Cell Line ; Human Umbilical Vein Endothelial Cells/drug effects/*metabolism ; Humans ; Interleukin-6/genetics/*metabolism ; Interleukin-8/genetics/*metabolism ; Matrix Metalloproteinase 1/genetics/*metabolism ; Osteoblasts/drug effects/*metabolism ; Vascular Endothelial Growth Factor A/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 assess the association between a rs7903146(C/T) polymorphism of TCF7L2 gene and metabolic syndrome (MS), plasma lipoprotein, and plasma adiponectin (PA) in Chinese Korean and Han populations from Yanbian region.

METHODSPolymerase chain reaction and DNA sequencing were used to determine the genotype of rs7903146 in 310 Chinese Korean (190 in case group and 120 in control group) and 344 Chinese Han (255 in case group and 89 in control group). ELIAS was used to test serum insulin (INS) and PA.

RESULTSThe frequency of T allele was higher in ethnic Han compared with ethnic Koreans (0.022 vs. 0.008), lower than that of Europeans (0.279) and Africans (0.257), but similar to those of Beijing Chinese and Japanese. For ethnic Korean Chinese, the frequencies of TT and CT genotypes as well as the T allele in patients with EH were significantly higher than those of the control group (P< 0.01), which also showed an increasing trend for both MS and T2DM groups (P=0.09 and P=0.07, respectively). By contrast, for Chinese Han, the frequencies of genotypes and particular allele in patients with MS, T2DM and EH showed no significant difference from those of the control group. For T2DM, EH, and control groups, PA level of individuals with CT or TT genotypes was significantly higher compared with that of the CC genotype (P< 0.05). The TC and LDL-C levels were significantly higher in T2DM, MS and EH groups compared with those of the control group. The PA level was lower in MS group compared with the control group.

CONCLUSIONThe T allele of SNP rs7903146 of TCF7L2 gene may be a risk factor for EH in Chinese Korean population from Yanbian region. The T allele also affects the PA level; lower PA is a risk factor for MS. The rs7903146 polymorphism showed a racial and ethnic difference.

Adiponectin ; blood ; Base Sequence ; China ; ethnology ; Female ; Humans ; Male ; Metabolic Syndrome ; blood ; enzymology ; genetics ; Molecular Sequence Data ; Polymorphism, Single Nucleotide ; Transcription Factor 7-Like 2 Protein ; genetics ; metabolism

3T3-L1 adipocytes express the B-cell-activating factor (BAFF) and three different BAFF receptors (BAFF-Rs). Furthermore, BAFF expression is regulated by inflammatory modulators, such as tumor necrosis factor-alpha and rosiglitazone. Here we investigated the function of BAFF in 3T3-L1 adipocytes and RAW 264.7 macrophages. We examined adipokine expression in 3T3-L1 adipocytes treated with 10 ng ml-1 BAFF. We also examined inflammatory molecule expression in RAW 264.7 macrophages treated with 10 or 100 ng ml-1 BAFF. We examined BAFF expression in the coculture of 3T3-L1 adipocytes and RAW 264.7 macrophages, as well as in white adipose tissue (WAT) of diet-induced obese (DIO) mice. We found that BAFF decreases leptin and adiponectin expression, but increases the expression of proinflammatory adipokines monocyte chemotactic protein-1, interleukin-6 (IL-6), cyclooxygenase-2 (COX-2) and haptoglobin. Coculturing the two cell types resulted in increased BAFF mRNA and protein expression, as well as modulation of BAFF-R mRNA expression in both cell types. These data indicate that BAFF might mediate adipocyte and macrophage interaction. When RAW 264.7 macrophages were treated with BAFF, BAFF-R expression was modulated as in coculture, and nitric oxide synthase and IL-6 expression increased. BAFF expression also increased in WAT of DIO mice. We propose that BAFF can regulate adipokine expression and possibly mediate adipocyte and macrophage interaction.
3T3-L1 Cells ; Adipocytes/drug effects/*metabolism ; Adipokines/genetics/*metabolism ; Adiponectin/genetics/metabolism ; Animals ; B-Cell Activating Factor/*metabolism/pharmacology ; Chemokine CCL2/genetics/metabolism ; Coculture Techniques ; Gene Expression Regulation/drug effects ; Haptoglobins/genetics/metabolism ; Inflammation Mediators/metabolism ; Interleukin-6/genetics/metabolism ; Leptin/genetics/metabolism ; Macrophages/drug effects/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; RNA, Messenger/genetics/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

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

Mitochondrial dysfunction and endoplasmic reticulum (ER) stress are considered the key determinants of insulin resistance. Impaired mitochondrial function in obese animals was shown to induce the ER stress response, resulting in reduced adiponectin synthesis in adipocytes. The expression of inducible nitric oxide synthase (iNOS) is increased in adipose tissues in genetic and dietary models of obesity. In this study, we examined whether activation of iNOS is responsible for palmitate-induced mitochondrial dysfunction, ER stress, and decreased adiponectin synthesis in 3T3L1 adipocytes. As expected, palmitate increased the expression levels of iNOS and ER stress response markers, and decreased mitochondrial contents. Treatment with iNOS inhibitor increased adiponectin synthesis and reversed the palmitate-induced ER stress response. However, the iNOS inhibitor did not affect the palmitate-induced decrease in mitochondrial contents. Chemicals that inhibit mitochondrial function increased iNOS expression and the ER stress response, whereas measures that increase mitochondrial biogenesis (rosiglitazone and adenoviral overexpression of nuclear respiratory factor-1) reversed them. Inhibition of mitochondrial biogenesis prevented the rosiglitazone-induced decrease in iNOS expression and increase in adiponectin synthesis. These results suggest that palmitate-induced mitochondrial dysfunction is the primary event that leads to iNOS induction, ER stress, and decreased adiponectin synthesis in cultured adipocytes.
3T3-L1 Cells ; *Adipocytes/drug effects/metabolism ; Adiponectin/biosynthesis ; Adipose Tissue/metabolism ; Animals ; Endoplasmic Reticulum Stress/drug effects ; Insulin Resistance/genetics ; Mice ; Mitochondria/drug effects/*metabolism/pathology ; Mitochondrial Turnover/drug effects/genetics ; *Nitric Oxide Synthase Type II/genetics/metabolism ; Nuclear Respiratory Factor 1 ; Obesity/genetics/metabolism ; Palmitic Acid/pharmacology ; Thiazolidinediones/pharmacology