New advances of adiponectin in regulating obesity and related metabolic syndromes

Obesity and related metabolic syndromes have been recognized as important disease risks,in which the role of adipokines cannot be ignored.Adiponectin(ADP)is one of the key adipokines with various beneficial effects,including improving glucose and lipid metabolism,enhancing insulin sensitivity,reducing oxidative stress and inflammation,promoting ceramides degradation,and stimulating adipose tissue vascularity.Based on those,it can serve as a positive regulator in many metabolic syndromes,such as type 2 diabetes(T2D),cardiovascular diseases,non-alcoholic fatty liver disease(NAFLD),sarcopenia,neurodegenerative diseases,and certain cancers.Therefore,a promising therapeutic approach for treating various metabolic diseases may involve elevating ADP levels or activating ADP receptors.The modulation of ADP genes,multimerization,and secretion covers the main processes of ADP generation,providing a comprehensive orientation for the development of more appropriate therapeutic strategies.In order to have a deeper understanding of ADP,this paper will provide an all-encompassing review of ADP.

Study on the Correlation between Adiponectin and Bone Mineral Density in Postmenopausal Women from Guangxi Zhuang Autonomous Region

Objectives: To explore the relationship between adiponectin (APN) and bone mineral density in this Zhuang ethnic group, thus providing a basis underpinning the prevention and treatment of osteoporosis (OP). Methods: Zhuang women over 50 years old in Guangxi Zhuang Autonomous Region were included in the study. The broadband ultrasound attenuation (BUA) was adopted as the reference to calculate the T value. Quantitative ultrasonic bone density was measured on the right. Body composition measuring instrument was used to measure weight, fat, and muscle mass. Plasma APN level was detected by ELISA and blood lipids were detected by enzymatic method. Results: Plasma APN level was found with significant differences in the normal bone mineral density group, bone mineral density reduction group, and osteoporosis group (P β = −0.176, P = 0.001) when the partial correlation coefficient of APN is −0.210. Elevated APN was an independent risk factor for bone mineral density reduction (OR = 1.191, 95%CI: 1.004 - 1.407, P = 0.04) and OP (OR = 1.1337, 95%CI: 1.137 - 1.572, P Conclusion: Increased APN in postmenopausal women of Zhuang is an independent risk factor for OP. The application of APN in the OP screening and prevention of middle-aged and ageing Zhuang women still needs further research.

Growth hormone improves insulin resistance in visceral adipose tissue after duodenal-jejunal bypass by regulating adiponectin secretion

BACKGROUND The mechanism of improvement of type 2 diabetes after duodenal-jejunal bypass(DJB)surgery is not clear.AIM To study the morphological and functional changes in adipose tissue after DJB and explore the potential mechanisms contributing to postoperative insulin sensitivity improvement of adipose tissue in a diabetic male rat model.METHODS DJB and sham surgery was performed in a-high-fat-diet/streptozotocin-induced diabetic rat model.All adipose tissue was weighed and observed under microscope.Use inguinal fat to represent subcutaneous adipose tissue(SAT)and mesangial fat to represent visceral adipose tissue.RNA-sequencing was utilized to evaluate gene expression alterations adipocytes.The hematoxylin and eosin staining,reverse transcription-quantitative polymerase chain reaction,western blot,and enzyme-linked immunosorbent assay were used to study the changes.Insulin resistance was evaluated by immunofluorescence.RESULTS After DJB,whole body blood glucose metabolism and insulin sensitivity in adipose tissue improved.Fat cell volume in both visceral adipose tissue(VAT)and SAT increased.Compared to SAT,VAT showed more significantly functional alterations after DJB and KEGG analysis indicated growth hormone(GH)pathway and downstream adiponectin secretion were involved in metabolic regulation.The circulating GH and adiponectin levels and GH receptor and adiponectin levels in VAT increased.Cytological experiment showed that GH stimulated adiponectin secretion and improve insulin sensitivity.CONCLUSION GH improves insulin resistance in VAT in male diabetic rats after receiving DJB,possibly by increasing adiponectin secretion.

Exercise preconditioning alleviates ischemia-induced memory deficits by increasing circulating adiponectin

Cerebral ischemia is a major health risk that requires preventive approaches in addition to drug therapy.Physical exercise enhances neurogenesis and synaptogenesis,and has been widely used for functional rehabilitation after stroke.In this study,we determined whether exercise training before disease onset can alleviate the severity of cerebral ischemia.We also examined the role of exercise-induced circulating factors in these effects.Adult mice were subjected to 14 days of treadmill exercise training before surgery for middle cerebral artery occlusion.We found that this exercise pre-conditioning strategy effectively attenuated brain infarct area,inhibited gliogenesis,protected synaptic proteins,and improved novel object and spatial memory function.Further analysis showed that circulating adiponectin plays a critical role in these preventive effects of exercise.Agonist activation of adiponectin receptors by Adipo Ron mimicked the effects of exercise,while inhibiting receptor activation abolished the exercise effects.In summary,our results suggest a crucial role of circulating adiponectin in the effects of exercise pre-conditioning in protecting against cerebral ischemia and supporting the health benefits of exercise.

Boiogito Increases the Synthesis and Secretion of Adiponectin by Promoting Differentiation in Cultured Human Adipocytes

Boiogito (BOT) ameliorates insulin resistance and diabetes in several animal models;however, the underlying mechanisms for these in vivo effects remain unclear. Thiazolidine derivatives, which are peroxisome proliferator-activated receptor γ (PPARγ) agonists for the treatment of type II diabetes, promote adiponectin production by inducing adipocyte differentiation, thereby reducing insulin resistance. This study aimed to evaluate the effect of BOT on adipocyte differentiation using cultured human visceral preadipocytes (HVPAds) compared with the thiazolidine derivative troglitazone (TRG). We investigated the effects of BOT (0.125 - 1 mg/mL) and TRG (10 μM) on the differentiation of adipocytes treated with or without tumor necrosis factor-α (TNF-α: 5 ng/mL). On day 14 of culture, the following adipocyte differentiation marker levels were measured: intracellular lipids, extracellular (i.e., medium) adiponectin, and intracellular differentiation-related genes (PPARγ, CCAAT/enhancer binding protein, adiponectin, differentiation cluster 36, glucose transporter type 4). BOT and TRG increased factors associated with differentiation including lipid, adiponectin, and differentiation-related gene expression levels compared with the controls. The increases in these differentiation markers were inhibited by the PPARγ antagonist GW9662 (20 μM). Furthermore, TNF-α decreased all differentiation marker levels. The decreases in differentiation markers were inhibited by BOT and TRG;however, these inhibitory effects were blocked by GW9662. The results suggest that BOT increases the synthesis and secretion of adiponectin by promoting differentiation similar to TRG. This study is the first to demonstrate that adipocyte differentiation-promoting activity is a mechanism for the beneficial effects of BOT on diabetes and insulin resistance.

Study on Cloning and Polymorphism of Porcine Adiponectin Promoter

[ Objective] The aim of this study was to provide a basis for study on adiponectin as a candidate gene for fat deposition. [ Method] The promoter sequence of adiponectin was obtained by porcine BAC library screening and primer-walking method. The polymorphisms of adiponectin promoter from 290 pigs, including 5 breeds of Lantang pig, Large spotted pig, Large white pig, Landrace and Duroc, were analyzed with PCR-RFLP. [ Result] At SNP site of adiponectin 5＇-flanking region -1 010 bp （G/A）, GG genotype frequency in Chinese indigenous pigs was significantly higher than that in exotic pigs. At SNP site of adiponectin 5＇-flanking region -394 bp （T/C）, the genotype distribution of Chi- nese indigenous pigs was abundant, while no CC genotype was detected in exotic pigs, and T allele frequency was higher in exotic pigs. [ Conclusion] SNP site mutation of - 1 010 bp （G/A） may lead to changes of the gene transcription level, while SNP site of -394 bp （T/C） properly has no relationship with gene transcription level and fat deposition.

Effect of Ovariectomy on Serum Adiponectin Levels and Visceral Fat in Rats

This study was aimed to examine the effect of ovariectomy on visceral fat, serum adi- ponectin levels and lipid profile. Forty-five female Sprague DawIey rats were divided into three groups （n=15 each）： ovariectomized group （OVX）, ovariectomized plus estrogen-treated group （OVX＋E2）, and sham-operated group （SHAM）. Body weight, abdominal adipose tissues, serum adiponectin and lipid profile were measured and compared among the groups after three-month feeding post-surgery. Signifi- cant increases in body weight and visceral fat were found in ovariectomized rats when compared with sham-operated ones and significant increases were also observed in serum adiponectin, triglyceride and very low density lipoprotein cholesterol levels in ovariectomized rats. Body weight, visceral fat and se- rum adiponectin levels were profoundly reduced in OVX＋E2 group as compared with OVX group. It was concluded that ovarian hormone deficiency induced by ovariectomy leads to significant increases in body weight and visceral fat, along with increased serum adiponectin, triglyceride and very low density lipoprotein cholesterol levels in rats. Attenuation in these changes can be achieved by estrogen supple- mentation.

Globular adiponectin induces differentiation and fusion of skeletal muscle cells

The growing interest in skeletal muscle regeneration is associated with the opening of new therapeutic strategies for muscle injury after trauma, as well as several muscular degenerative pathologies, including dystrophies, muscu- lar atrophy, and cachexia. Studies focused on the ability of extracellular factors to promote myogenesis are therefore highly promising. We now report that an adipocyte-derived factor, globular adiponectin （gAd）, is able to induce mus- cle gene expression and cell differentiation, gAd, besides its well-known ability to regulate several metabolic func- tions in muscle, including glucose uptake and consumption and fatty acid catabolism, is able to block cell cycle entry of myoblasts, to induce the expression of specific skeletal muscle markers such as myosin heavy chain or caveolin-3, as well as to provoke cell fusion into multinucleated syncytia and, finally, muscle fibre formation, gAd exerts its pro- differentiative activity through redox-dependent activation of p38, Akt and 5＇-AMP-activated protein kinase path- ways. Interestingly, differentiating myoblasts are autocrine for adiponectin, and the mimicking of pro-inflammatory settings or exposure to oxidative stress strongly increases the production of the hormone from differentiating cells. These data suggest a novel function of adiponectin, directly coordinating the myogenic differentiation program and serving an autocrine function during skeletal myogenesis.

Cloning and Sequence Analysis of Adiponectin Receptor 1 and Receptor 2 cDNA from Guangxi Bama Mini-pig

[ Objective] To clone and analyze the sequence of Adiponectin receptor 1 （ AdipoR1 ） and receptor 2 （AdipoR2） cDNA of Guangxi Bama mini-pig. [Method] The Adiponectin receptors cDNAs were amplified by RT-PCR using skeletal muscle total RNA as template and then ligated into pMD18-T vector after purification. The recombinant pMD18-T vector was transformed into the E. coil DH5α for identification and sequencing. And the results were compared with the cDNA sequence from other species. [Result] The fragments, 1 128 bp and 1 161 bp in size, were amplified by RT-PCR and respectively consistent with the coding sequence of AdipoR1 gene and AdipoR2 gene. The homology analysis showed that the sequences of AdipoR1 gene and AdipoR2 gene were respectively 99.8% and 99.7% homologous to the sequence of domestic pig reported in GenBank with one base and three base missense mutations correspondingly. [ Conclusion] The AdipoR1 gene and AdipoR2. gene were successfully amplified from Guangxi Bama mini-pig, laying the foundation for the further study of the biological function of AdipoR genes and the design of novel drugs with AdipoR as target.

STUDY ON OBESITY RELATED FACTORS: FFA, LEPTIN AND ADIPONECTIN IN SUBJECTS WITH VARYING GLUCOSE TOLERANCE

Objective To study the fasting serum levels of obesity related factors: FFA, leptin and adi-ponectin in subjects with varying glucose tolerance and their relationship with BMI, insulin sensitivity index and isletbeta-cell function. Methods Serum levels of FFA, leptin and adiponectin in 24 normal, 32 simple obese, 34IGT and 36 T2DM subjects were measured by ACS-ACOD assay or RIA. Results The serum levels of leptin andFFA in three groups:simple obese, IGT and DM were much higher than those in normal control (P <0. 001). Incontrast, serum level of adiponectin of simple obese, IGT and DM groups were significant lower than that of normalcontrol, among them DM subjects had the lowest level (P <0. 001). Correlation analysis showed that FFA was pos-itively correlated to BMI, WHR, FBG, fasting insulin level and negatively correlated to SI; adiponectin was negativelycorrelated to BMI, WHR, FBG, PBG, but positively correlated to SI and AIRg; and leptin was positively correlated toBMI, fasting insulin and AIRg when negatively correlated to FBG and SI. None of them was correlated to age.Conclusion Subjects with insulin resistance have high serum FFA and leptin levels but low serum adiponectin level.With the glucose tolerance deterioration, serum FFA level increases much higher while the adiponectin deceases muchlower. Unlike insulin, none of these obesity related factors can be used as the simple indicating or determining factorof SI, though each of them, to different extent, takes part in the development of insulin resistance.

Correlation between Serum Level of Adiponectin and Severity of Coronary Artery Atherosclerosis

Objectives To investigate the correlation between serum level of adiponectin and severity of coronary artery atherosclerosis. Methods Coronary angiographies were performed and serum levels of adiponectin were measured in 88 patients with suspected coronary heart disease （CHD）. Patients were divided into groups according to the coronary angiographies and Gensini＇s scores of coronary artery atherosclerosis. The serum levels of adiponectin were compared in different groups, and multiple regressions were used to analyze the correlation factors of adiponectin. Results （1）Serum adiponectin concentration in CHD group [ 7. 1 mg/L （2.4 - 21.1 mg/L） ] was decreased as compared with that in control group [ 11.6 mg/L （4.4 - 28.2 mg/L ）, P 〈 0. 01 ] ; （2）The serum levels of adiponectin fell while the Gensini＇ s scores of coronary artery atherosclerosis increased （P 〈 0. 05, P 〈 0. 01 ） ; （3）Serum level of adiponectin was positively correlated with the high-density lipoprotein cholesterol, while negatively correlated with the Gensini＇ s score of coronary artery atherosclerosis and triglyceride （P 〈 0. 01 ）. Conclusions Serum adiponectin concentration was decreased in patients with CHD. Low serum levels of adiponectin reflected the severity of coronary artery atherosclerosis. Adiponectin was a protective factor of cardiovascular system.

The Study on the Correlation Between Plasma Adiponectin Level and Coronary Heart Disease

Objectives To investigate the relationship between plasma adiponectin level and coronary heart disease （CHD）, and some established cardiovascular risk factors and to probe its probable pathogenesis which adiponectin results in CHD. Methods The levels of plasma adiponectin, fasting plasma insulin （FINS）, C-reactive protein （CRP） and P-selectin were measured by ELISA, plasma ET-1 was measured by radioimmunoassay （RIA） in 75 male patients with CHD and 30 healthy male people. Body mass index （BMI）, waist / hip ratio （WHR） and insulin resistance index （Homa-IR） were calculated respectively. Results （1）The plasma adiponectin levels in CHD group were lower compared with control group[（5.18±2.57）mg / L vs（8.94±2.59）mg / L, P〈 0.001 ], there was no significant difference of plasma adiponectin levels in CHD sub-groups （P 〉 0.05）.（2） Based on multinominal stepwise logistic regression analysis, adiponectin was one of significant and independent risk factors for CHD. （3） Multivariate liner stepwise regression analysis showed that adiponectin had significant correlation with BMI and TG, BMI and TG were independent factors influencing on plasma adiponectin levels. （4） Pearson correlation analysis indicated plasma adiponectin levels were inversely related to FINS levels , Homa-IR, CRP, P-selectin and ET-1. Conclusions （ 1 ）Plasma adiponectin levels are lower in CHD patients compared the control subjects, there are no significant difference of plasma adiponectin levels in patients with SAP, UAP and AMI. （2） Plasma adiponectin levels are relative with CHD. Hypoadiponectinemia is an independent risk factor for CHD. （3）Established cardiovascular risk factors such as BMI and TG have an obvious influence on adiponectin. （4）The probable pathogenesis by which adiponectin involves in CHD is suggested that adiponectin relates to insulin resistance, inflammatory reaction and dysfunction of vessel endothelium.

What is the role of adiponectin in obesity related non-alcoholic fatty liver disease?

Non-alcoholic fatty liver disease (NAFLD) is recognized as the most common type of chronic liver disease in Western countries.Insulin resistance is a key factor in the pathogenesis of NAFLD,the latter being considered as the hepatic component of insulin resistance or obesity.Adiponectin is the most abundant adipose-specific adipokine.There is evidence that adiponectin decreases hepatic and systematic insulin resistance,and attenuates liver inflammation and fibrosis.Adiponectin generally predicts steatosis grade and the severity of NAFLD;however,to what extent this is a direct effect or related to the presence of more severe insulin resistance or obesity remains to be addressed.Although there is no proven pharmacotherapy for the treatment of NAFLD,recent therapeutic strategies have focused on the indirect upregulation of adiponectin through the administration of various therapeutic agents and/or lifestyle modifications.In this adiponectin-focused review,the pathogenetic role and the potential therapeutic benefits of adiponectin in NAFLD are analyzed systematically.

Fat cell-secreted adiponectin mediates physical exercise-induced hippocampal neurogenesis: an alternative anti-depressive treatment?

Psychological depression is drawing accumulating attention nowadays, due to the skyrocketing incidence worldwide and the enormous burdens it incurs. Physical exercise has been long recog- nized for its therapeutic effects on depressive disorders, although knowledge of the underlying mechanisms remains limited. Suppressed hippocampal neurogenesis in adult brains has been regarded, at least partly, contributive to depression, whereas physical exercise that restores neuro- genesis accordingly exerts the anti-depressive action. Several recent publications have suggested the potential role of adiponectin, a protein hormone secreted by peripheral mature adipocytes, in mediating physical exercise-triggered enhancement of hippocampal neurogenesis and alleviation of depression. Here, we briefly review these novel findings and discuss the possibility of counter- acting depression by modulating adiponectin signaling in the hippocampus with interventions including physical exercise and administration of pharmacological agents.

Serum Adiponectin and Resistin Levels in Patients with Polycystic Ovarian Syndrome and Their Clinical Implications

In this study, serum adiponectin and resistin levels were determined in 46 patients with polycystic ovarian syndrome (PCOS), and their correlation with serum sexual hormones and insulin resistance (IR) were examined.The subjects included 26 obese patients with body mass index (BMI)】25 and 20 non-obese patients with BMI≤25, with 25 obese and 25 non-obese healthy volunteers without PCOS serving as controls.Serum adiponectin and resistin levels in all subjects were measured, and endocrinal and metabolic indices were also analysed.Our results showed that the serum adiponectin levels in both obese and non-obese PCOS groups were significantly lower than their controls, while the serum resistin levels in obese and non-obese PCOS group were significantly higher than in their controls (P【0.001).The serum adiponectin level was significantly lower and serum resistin level significantly higher in the non-obese PCOS group as compared with the obese control group (P【0.05).Serum adiponectin level was negatively correlated with FIN, HOMA-IR, LH and LH/FSH (P【0.05), but serum resistin level was positively correlated with FIN, HOMA-IR, LH and LH/FSH (P【0.05).We are led to conclude that PCOS patients have obvious IR, low serum adiponectin and high serum resistin, and adiponectin and resistin might play important roles in the pathogenesis of IR in PCOS patients.

Significance of serum leptin and adiponectin levels in Egyptian patients with chronic hepatitis C virus associated hepatic steatosis and fibrosis

AIM:To study serum levels of leptin and adiponectin in patients with chronic hepatitis C virus infection genotype-4(HCV-4) related steatosis and fibrosis.METHODS:We prospectively studied 45 untreated men with chronic HCV-4,with proven steatosis(group Ⅰ,30 patients),and fibrosis(group Ⅱ,15 patients),on liver biopsy.In addition,15 healthy men(group Ⅲ),matched for age,and body mass index were included.However,we excluded another five patients with steatohepatitis,and six patients with cirrhosis.We measured total serum leptin and adiponectin levels,as potential predictors for liver steatosis and fibrosis.Also,a correlation between these adipokines and various clinical and laboratory data were evaluated.All subjects were selected from Tropical and Internal medicine departments,Menoufiya University Hospital,Menoufiya,Egypt,during the period from February 2010 to August 2011.RESULTS:In group Ⅰ,severity of hepatic steatosis was mild,moderate,and severe,in 19 patients(63.5%),8 patients(26.5%),and 3 patients(10%),respectively.In contrast,in group Ⅱ,hepatic fibrosis was found to be in stage 1,2,and 3,in 6 patients(40%),in 6 patients(40%),and in 3 patients(20%),respectively.On comparing group Ⅰ with group Ⅱ,there was a significant decrease in serum adiponectin levels(131.4 ± 7.91 pg/mL vs 436 ± 9.75 pg/mL,P < 0.001),while there was no significant difference between both groups regarding serum leptin levels(34.69 ± 7.69 ng/mL vs 35.17 ± 1.06 ng/mL,P > 0.05).However,in the same group,when compared with group Ⅲ,there was a significant increase in serum leptin levels(34.69 ± 7.69 ng/mL vs 10.69 ± 0.84 ng/mL,P < 0.001),while there was a significant decrease in serum adiponectin levels(131.4 ± 7.91 pg/mL vs 342.4 ± 44.48 pg/mL,P < 0.001).In contrast,in group Ⅱ,when compared with group Ⅲ,there was a significant increase in serum leptin and adiponectin levels(35.17 ± 1.06 ng/mL vs 10.69 ± 0.84 ng/mL,P < 0.001,and 436 ± 9.75 pg /mL vs 342.4 ± 44.48 pg/mL,P < 0.05,respectively),while there was no significant difference between both groups regarding serum creatinine(0.83 ± 0.34 vs 0.89 ± 0.24,P > 0.05).On the other hand,serum leptin was not correlated with serum adiponectin in group Ⅰ and in group Ⅱ(r = 0.09,P > 0.05,and r =-0.1,P > 0.05,respectively).However,serum adiponectin was significantly negatively correlated with serum aspartate transaminase in group Ⅰ,but no correlation detected in group Ⅱ(r =-0.39,P > 0.05,and r =-0.03,P > 0.05).CONCLUSION:In male patients with chronic HCV-4,serum adiponectin levels are elevated in hepatic fibrosis,but decreased in steatosis.Therefore,in contrast to leptin,adiponectin may be used as a non-invasive marker.

Gene Expression of Adiponectin and Adiponectin Receptor 1 in Type 2 Diabetic Rats and the Relationship with the Parameters of Glucose and Lipid Metabolism

In order to confirm whether the mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were correlated with the serum parameters of glucose and lipid metabolism and to clarify the regulation of adiponectin receptor gene expression in diabetic states, serum adiponectin, mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were examined in type 2 diabetic rats. The model of type 2 diabetes was prepared by feeding high fat diet and injecting low dosage of streptozotocin (STZ). The diabetic rats were screened out by oral glucose tolerance test. One group of type 2 diabetic rats received rosiglitazone. The serum adiponectin concentration was detected by using ELISA and mRNA levels were examined by RT-PCR. The serum adiponectin levels and mRNA levels of adiponectin in adipose tissue of type 2 diabetic rats were significantly decreased as compared with the normal control rats (P<0.05, P<0.01 respectively). No siglificant changes were observed in the expression of adiponectin receptor 1 in the skeletal muscle of type 2 diabetic rats. The mRNA levels of adiponectin in adipose tissue were reversely correlated with serum insulin (r=-0.66, P<0.05), triglyceride (r=-0.58, P<0.05), cholesterol (r=-0.49, P<0.05), interleukin-6 (r=-0.49, P<0.05) and tumor necrosis factor (r=-0.43, P<0.05). The expression of adiponectin receptors was not altered in the skeletal muscle of Type 2 diabetic rats. The decreased serum adiponectin was caused by the decreased expression of adiponectin mRNA in adipose tissue rather than the adiponectin receptors in the skeletal muscle, which could be improved by rosiglitazone.

Identification of a Regulatory Single Nucleotide Polymorphism in the Adiponectin (APM1) Gene Associated with Type 2 Diabetes in Han Nationality

Objective To identify the genetic defects of the the adiponectin （APM1） gene that contribute to the development of type 2 diabetes （T2DM） and determine the functional single nucleotide polymorphisms （SNPs） in the APMI gene associated with T2DM in Han nationality. Methods The APMI gene 5＇-UTR was screened by direct sequencing to identify common polymorphisms. Identified SNPs were genotyped in 585 nondiabetic controls, 278 subjects with impaired glucose intolerance （IGT） and 212 patients with T2DM. The functions of SNPs in the regulatory region were assessed by reporter gene assay. Possible association between SNPs and plasma APMI levels or metabolic parameters was statistically asses,sed. Results Three SNPs were identified in the APMI gene 5＇-UTR. A case-control study revealed that SNP -11377 G/C had significant differences in allele frequencies between T2DM patients and nondiabetic controls （G 0.314/C 0.686 vs. G 0.265/C 0.735, P=0.03）. Haplotype analysis of three SNPs in the APM1 gene showed that no significant association of haplotypes with T2DM. IGT was detected in the present study. Reporter gene assay showed that SNP did not influence the transcription efficiency in the 3T3-LI cell line. Conclusion SNP - 11377 G/C in the proximal promoter region of the APM 1 gene contributes to the development of T2DM in Han nationality but may not be a functional SNP in the APM1 gene.

Protective role of adiponectin in a rat model of intestinal ischemia reperfusion injury

AIM: To determine the potential protective role of adiponectin in intestinal ischemia reperfusion(I/R) injury.METHODS: A rat model of intestinal I/R injury was established. The serum level of adiponectin in rats with intestinal I/R injury was determined by enzymelinked immunosorbent assay(ELISA). The serum levels of interleukin(IL)-1β, IL-6, and tumor necrosis factor(TNF)-α were also measured by ELISA. Apoptosis of intestinal cells was detected using the terminal deoxynucleotidyl transferase d UTP nick end labeling assay. The production of malondialdehyde(MDA) and superoxide dismutase(SOD) and villous injury scores were also measured.RESULTS: Adiponectin was downregulated in the serum of rats with intestinal I/R injury compared with sham rats. No significant changes in the expression of adiponectin receptor 1 and adiponectin receptor 2 were found between sham and I/R rats. Pre-treatment with recombinant adiponectin attenuated intestinal I/R injury. The production of pro-inflammatory cytokines,including IL-6, IL-1β, and TNF-α, in rats with intestinal I/R injury was reduced by adiponectin pre-treatment. The production of MDA was inhibited, and the release of SOD was restored by adiponectin pre-treatment in rats with intestinal I/R injury. Adiponectin pre-treatment also inhibited cell apoptosis in these rats. Treatment with the AMP-activated protein kinase(AMPK) signaling pathway inhibitor, compound C, or the heme oxygenase 1(HO-1) inhibitor, Snpp, attenuated the protective effects of adiponectin against intestinal I/R injury. CONCLUSION: Adiponectin exhibits protective effects against intestinal I/R injury, which may involve the AMPK/HO-1 pathway.

Association between Adiponectin and Metabolic Syndrome in Older Adults from Major Cities of China

Objective To investigate the association between adiponectin and metabolic syndrome （MetS） and related diseases in older adults from major cities of China. Methods A total of 2 049 adults at the age of 60-96 years from18 major cities of China were enrolled in the study. Plasma adiponectin and insulin concentrations were measured. Insulin resistance was assessed by homeostasis model assessment of insulin resistance （HOMA-IR）. The definitions proposed by International Diabetes Federation （IDF） and American Heart Association/National Heart, Lung, and Blood/nstitute （AHA/NLHBI） were used to identify MetS. Results The adiponectin concentration increased with the advance of age and was higher in women than in men. The sex specific adiponectin concentration was inversely correlated with body mass index （BMI）, waist circumference, diastolic blood pressure, triglycerides, glucose and fasting blood insulin, and positively correlated with HDL-C （P〈0.001）. The adiponectin concentration decreased with increasing MetS components. Compared with the 4th sex-specific adiponectin quartile, the odds ratio （OR） for prevalent MetS-IDF and MetS-AHA/NLHBI in subjects of the 1st quartile group was 3.25 （95% CI： 2.24, 4.71） and 3.21 （95% CI： 2.26, 4.55）, respectively. The association was independent of age, sex, life-style factors, medication, family history of chronic diseases, BMI, and HOMA-IR, The OR for MetS was much higher than those of MetS components and its related diseases. Conclusion Adiponectin is strongly associated with MetS independent of insulin resistance and obesity in older adults from major cities in China. The adiponectin concentration is a useful predictor for the risk of MetS.