Decreased Serum Adiponectin Levels Research Articles

Serum Adiponectin Predicts COVID-19 Severity.

Adiponectin is primarily known for its protective role in metabolic diseases, and it also possesses immunoregulatory properties. Elevated levels of adiponectin have been observed in various inflammatory diseases. However, studies investigating adiponectin levels in the serum of COVID-19 patients have yielded conflicting results. This study aimed to assess serum adiponectin levels in 26 healthy controls, as well as in 64 patients with moderate and 60 patients with severe COVID-19, to determine a potential association between serum adiponectin and the severity of COVID-19. Serum adiponectin levels in severe COVID-19 patients were significantly lower than in those with moderate disease and healthy controls, who exhibited similar serum adiponectin levels. Among patients with moderate disease, positive correlations were observed between serum adiponectin and C-reactive protein levels. Of note, serum adiponectin levels of severe COVID-19 cases were comparable between patients with and without dialysis or vasopressor therapy. Superinfection with bacteria did not exert a notable influence on serum adiponectin levels in patients with severe disease. Patients who were diagnosed with severe COVID-19 and vancomycin-resistant enterococci bacteremia showed a significant reduction in their serum adiponectin levels. An analysis conducted on the entire cohort, including both moderate and severe COVID-19 patients, showed that individuals who did not survive had lower serum adiponectin levels when compared to those who survived. In summary, this study highlights a decrease in serum adiponectin levels in severe COVID-19 cases, indicating the potential utility of adiponectin as an additional biomarker for monitoring disease severity in COVID-19 or critical illnesses in general.

Serum Levels of Adiponectin Are Strongly Associated with Lipoprotein Subclasses in Healthy Volunteers but Not in Patients with Metabolic Syndrome.

Metabolic syndrome (MS) is a widespread disease in developed countries, accompanied, among others, by decreased adiponectin serum levels and perturbed lipoprotein metabolism. The associations between the serum levels of adiponectin and lipoproteins have been extensively studied in the past under healthy conditions, yet it remains unexplored whether the observed associations also exist in patients with MS. Therefore, in the present study, we analyzed the serum levels of lipoprotein subclasses using nuclear magnetic resonance spectroscopy and examined their associations with the serum levels of adiponectin in patients with MS in comparison with healthy volunteers (HVs). In the HVs, the serum levels of adiponectin were significantly negatively correlated with the serum levels of large buoyant-, very-low-density lipoprotein, and intermediate-density lipoprotein, as well as small dense low-density lipoprotein (LDL) and significantly positively correlated with large buoyant high-density lipoprotein (HDL). In patients with MS, however, adiponectin was only significantly correlated with the serum levels of phospholipids in total HDL and large buoyant LDL. As revealed through logistic regression and orthogonal partial least-squares discriminant analyses, high adiponectin serum levels were associated with low levels of small dense LDL and high levels of large buoyant HDL in the HVs as well as high levels of large buoyant LDL and total HDL in patients with MS. We conclude that the presence of MS weakens or abolishes the strong associations between adiponectin and the lipoprotein parameters observed in HVs and disturbs the complex interplay between adiponectin and lipoprotein metabolism.

Co-occurrence of non-alcoholic steatohepatitis exacerbates psoriasis associated with decreased adiponectin expression in a murine model.

Clinical studies have suggested a bidirectional association between non-alcoholic steatohepatitis (NASH) and psoriasis, affecting each other's development and severity. Here, we explored bidirectional causal linkages between NASH and psoriasis using a murine model. NASH was induced in mice by streptozotocin injection at 2 days of age and by high-fat diet feeding (STAM™ model). Psoriasis was induced by topical application of imiquimod (IMQ) on the ear. The severities of liver damage and psoriatic skin changes were determined using histological analysis. Gene expression in the skin tissues was evaluated using quantitative PCR analysis. Serum cytokine levels were determined using enzyme-linked immunosorbent assay. To examine the innate immune responses of normal human epidermal keratinocytes (NHEKs), the cells were treated with interleukin (IL)-17A, tumor necrosis factor (TNF)-α, and AdipoRon, an adiponectin receptor agonist. There were no differences in the degree of liver tissue damage (fat deposition, inflammation, and fibrosis) between NASH mice with and those without psoriasis. Conversely, the co-occurrence of NASH significantly augmented psoriatic skin changes, represented by epidermal hyperplasia, in psoriatic mice. Pro-inflammatory cytokines were expressed in the inflamed skin of psoriatic mice, and the expression of genes, especially Il23a, Il1b, Il36g, and Mip2, was significantly upregulated by the co-occurrence of NASH. The expression of keratinocyte activation marker genes Defb4b and Krt16 was also upregulated by the co-occurrence of NASH. The serum TNF-α and IL-17 levels were increased by the co-occurrence of NASH and psoriasis. The serum adiponectin levels decreased in NASH mice compared with that in non-NASH mice. In NHEK culture, TNF-α and IL-17A synergistically upregulated CXCL1, CXCL8, and IL1B expression. The upregulated pro-inflammatory gene expression was suppressed by AdipoRon treatment, reflecting the anti-inflammatory capacity of adiponectin. The co-occurrence of NASH exacerbated psoriatic skin changes associated with increased serum inflammatory cytokine levels and decreased serum adiponectin levels. Combined with in vitro findings, increased inflammatory cytokine levels and decreased adiponectin levels likely promote innate immune responses in epidermal keratinocytes in psoriatic skin lesions. Overall, therapeutic intervention for co-occurring NASH is essential to achieve a favorable prognosis of psoriasis in clinical practice.

Zinc deficiency and a high-fat diet during growth: Metabolic and adipocyte alterations in rats

Background and aimsTo evaluate the effects of a high-fat diet during post-weaning growth on intermediate metabolism and retroperitoneal adipose tissue, in adult male rats exposed to adequate or deficient zinc intake during prenatal and postnatal life. Methods and resultsFemale Wistar rats were fed low- or control-zinc diets from pregnancy to offspring weaning. Male offspring born from control mothers were fed either control or high-fat, control-zinc diets for 60 days. Male offspring born from zinc deficient mothers were fed either low-zinc or high-fat, low-zinc diets for 60 days. At 74 days of life, oral glucose tolerance test was performed. In 81-day-old offspring, blood pressure, lipid profile, plasmatic lipid peroxidation and serum adiponectin level were determined. In retroperitoneal adipose tissue, we evaluated oxidative stress, morphology and adipocytokines mRNA expression. Low-zinc diet induced adipocytes hypertrophy, increased oxidative stress, and decreased adiponectin mRNA expression in adipose tissue. Low-zinc diet increased systolic blood pressure, triglyceridemia, plasmatic lipid peroxidation and glycemia at 3 h after glucose overload. Animals fed high-fat or high-fat, low-zinc diets showed adipocytes hypertrophy, decreased adiponectin mRNA expression, and increased leptin mRNA expression and oxidative stress in adipose tissue. They also exhibited decreased serum adiponectin levels, increased triglyceridemia, plasmatic lipid peroxidation and area under the oral glucose tolerance curve. High-fat, low-zinc diet induced greater alterations in adipocyte hypertrophy, leptin mRNA expression and glucose tolerance test than high-fat diet. ConclusionZinc deficiency since early stages of intrauterine life could increase susceptibility to metabolic alterations induced by high-fat diets during postnatal life.

Edible red seaweed Campylaephora hypnaeoides J. Agardh alleviates obesity and related metabolic disorders in mice by suppressing oxidative stress and inflammatory response

BackgroundThe obesity epidemic has become a serious public health problem in many countries worldwide. Seaweed has few calories and is rich in active nutritional components necessary for health promotion and disease prevention. The aim of this study was to investigate the effects of the Campylaephora hypnaeoides J. Agardh (C. hypnaeoides), an edible seaweed traditionally eaten in Japan, on high-fat (HF) diet-induced obesity and related metabolic diseases in mice.MethodsMale C57BL/6J mice were randomly divided into the following groups: normal diet group, HF diet group, HF diet supplemented with 2% C. hypnaeoides, and HF diet supplemented with 6% C. hypnaeoides. After 13 weeks of treatment, the weight of the white adipose tissue and liver, and the serum levels of glucose, insulin, adipokines, and lipids were measured. Hepatic levels of adipokines, oxidant markers, and antioxidant markers were also determined. Insulin resistance was assessed by a glucose tolerance test. Polysaccharides of C. hypnaeoides were purified and their molecular weight was determined by high-performance seize exclusion chromatography. The anti-inflammatory effects of purified polysaccharides were evaluated in RAW264.7 cells.ResultsTreatment of HF diet-induced obese mice with C. hypnaeoides for 13 weeks suppressed the increase in body weight and white adipose tissue weight. It also ameliorated insulin resistance, hyperglycemia, hepatic steatosis, and hypercholesterolemia. The ingestion of an HF diet increased serum levels of malondialdehyde (MDA), tumor necrosis factor α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1), while it decreased serum adiponectin levels. In the liver, an HF diet markedly increased the MDA, TNF-α, and interleukin-6 (IL-6) levels, while it decreased glutathione and superoxide dismutase. These metabolic changes induced by HF diet feeding were ameliorated by dietary C. hypnaeoides. Purified polysaccharides and ethanol extract from C. hypnaeoides inhibited the lipopolysaccharide-induced overproduction of nitric oxide and TNF-α in macrophage RAW264.7 cells.ConclusionsThe present results indicated that C. hypnaeoides was able to alleviate HF diet-induced metabolic disorders, including obesity, hyperglycemia, hepatic steatosis, and hypercholesterolemia by attenuating inflammation and improving the antioxidant capacity in mice. Polysaccharides and polyphenols may be involved in these beneficial effects of C. hypnaeoides.

Can improvements in sleep quality positively affect serum adiponectin-levels in patients with obstructive sleep apnea?

BackgroundAssess if changes in sleep quality (Sleep Quality Index, SQI) based on cardiopulmonary coupling-analysis (CPC) impacts serum adiponectin-levels in patients with cardiovascular disease (CVD). MethodsSecondary analysis of electrocardiogram (ECG) data from the Heart Biomarker Evaluation in Apnea Treatment study (HeartBEAT), a multicenter, controlled trial in patients with CVD and moderate-severe sleep apnea, randomly assigned to intervention of Continuous Positive Airway Pressure (CPAP), Nocturnal Supplemental Oxygen (NSO) or Healthy Lifestyle and Sleep Hygiene Education (HLSE; control group). Participants with good-quality ECG-signal (n = 241) were included. ResultsImproving CPC-sleep quality was associated with net average improvements in serum adiponectin-levels 2.69 μg/ml (p = 0.005) irrespective of therapy initiated. After controlling for confounders, a unit increase in SQI was associated with increase in serum adiponectin-levels 0.071 μg/ml (p = 0.012) and decrease in insulin-levels 0.197 μIU/ml (p = 0.0018). Similarly, a percentage point increase in sleep apnea indicator (SAI) was associated with decrease in serum adiponectin-levels of 0.071 μg/ml (p = 0.017) and increase in insulin-levels of 0.218 μIU/ml (p = 0.020). A percentage point increase in CPC-sleep fragmentation (eLFCBB) had a predicted increase in glucose-levels 0.371 mg/dl (p = 0.009) and insulin-levels 0.284 μIU/ml (p = 0.010).In patients receiving CPAP-therapy, a difference in serum adiponictin levels of 3.82 μg/ml (p = 0.025) is observed comparing patients in which SQI-improved to patients that SQI-declined during the study period. The difference is mostly due to a decrease in serum adiponectin levels in patients that decline in SQI (−3.20 μg/ml). ConclusionImprovements in sleep quality were associated with higher serum adiponectin-levels, and improved measures of glycemic metabolism which may have beneficial effects on metabolic syndrome and cardiovascular health. Clinical trial registration name and numberThe Heart Biomarker Evaluation in Apnea Treatment (HeartBEAT) study is registered at https://clinicaltrials.gov/ct2/show/NCT01086800.

Association between serum CTRP9 levels and diabetic retinopathy in patients with type 2 diabetes mellitus

To investigate the relationship between serum C1q tumor necrosis factor-related protein 9 (CTRP9) level and the risk of diabetic retinopathy (DR) in patients with type 2 diabetes mellitus (T2DM). A total of 291 patients with T2DM underwent fundus examination, and their serum levels of CTRP9, insulin and adiponectin were measured using enzyme- linked immunosorbent assay. According to results of fundus examination, the patients were divided into DR group and non-DR (NDR) group, and logistic regression was used to analyze the relationship between serum CTRP9 levels and DR in T2DM patients. Compared with those in NDR group, the patients with DR showed significantly increased serum CTRP9 level (P < 0.001) and decreased serum adiponectin level (P < 0.001). Pearson correlation analysis showed that in patients with T2DM complicated by DR, serum CTRP9 levels had a significant positive correlation with DR stage (P < 0.05) and a negative correlation with serum adiponectin level (P < 0.001). Multivariate logistic regression analysis showed that with the increase of serum CTRP9 level, the risk of DR is significantly increased in patients with T2DM. In patients with T2DM complicated by DR, an increased serum CTRP9 level suggests a compensatory response to DR.

Correlation between Blood Pressure and Obesity Parameter against Cystatin-C and Adiponectin Levels in Serum of Obese Adolescent

Background: Obesity contributes to the increased risk of chronic kidney and systemic inflammation. This condition can occur in obese adolescents. Most researches of cystatin-C (cys-C) and adiponectin have been carried out in adult and children subjects. The purpose of this research is to determine differences in serum cys-C and adiponectin levels between obese and normoweight adolescents and their correlation with blood pressure and obesity parameters.Materials and Methods: Twenty-eight obese adolescents and 22 normoweight adolescents aged 15-18 years old participated in this research. After the measurement of blood pressure and obesity parameters, we examined serum cys-C levels as a biomarker for decreased early stage renal function and adiponectin, an antiinflammatory adipokine. Estimated glomerular filtration rate (eGFR) based on serum cys-C is calculated using the eGFR-Chronic Kidney Disease Epidemiology Collaboration (eGFR-CKD EPI cys-C equation formula). Results: Cys-C levels in obese adolescents were higher than normoweight adolescents. In contrast, serum adiponectin levels in obese adolescents were lower than for normoweight adolescents. Interestingly, eGFR based on serum cys-C showed no difference, although eGFR in obese adolescents was lower than normoweight adolescent. Serum cys-C was positively correlated with systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI) and waist circumference (WC). Serum adiponectin was negatively correlated with SBP, DBP, BMI and WC. SBP is a predictor factor for the increase in serum cys-C and BMI is a predictor factor in the decrease in serum adiponectin levels. Conclusion: There is a decline in early stage kidney function and inflammation in obese adolescents as evidenced by increased serum cyst-C levels and decreased serum adiponectin levels. These two biomarkers correlate with blood pressure, BMI and WC and play a role in the pathomechanism of early stage impairment of kidney function and inflammation in obese adolescents.Keywords: adiponectin, body mass index, cystatin-C, early stage renal diseases, inflammation, systolic blood pressure

Cryptotanshinone alleviates chemotherapy-induced colitis in mice with colon cancer via regulating fecal-bacteria-related lipid metabolism

Patients with colorectal cancer treated with 5-fluorouracil (5-FU) and irinotecan (CPT-11) exhibit a risk for chemotherapy-induced colitis (CIC) that may lead to fatal consequences. Cryptotanshinone (CTS) is a natural compound extracted from the root of Salvia miltiorrhiza Bunge that shows potent antitumor activities. We previously reported CTS relieved 5-FU/ CPT-11 induced colitis in tumor-free mice. In this study, we studied the effect of CTS on 5-FU/ CPT-11 induced colitis in mice with colitis associated colon cancer (CAC). The effects of CTS on CIC were evaluated by disease activity index (DAI) and histological assessment via hematoxylin-and-eosin staining. Serum lipids and lipid-metabolic enzymes were detected by commercial kits. Fecal microbial diversity was detected by 16S ribosomal RNA gene sequencing. To find the role of fecal bacteria in CAC mice with 5-FU/ CPT-11 induced colitis, pseudo-germ-free mice were established by intragastric administration of mixed antibiotics. Except for decreasing tumor number (3 ± 1 vs 6 ± 1, p < 0.05), CTS significantly alleviated DAI (1.9 ± 0.6 vs 2.6 ± 0.5, p < 0.05) and regulated serum lipids in CAC mice with 5-FU/ CPT-11induced colitis. Compared with model group, CTS significantly increased serum triglycerides (TG) (1.13 ± 0.26 mM vs 0.79 ± 0.03 mM, p < 0.05), high density lipoprotein (HDL) (3.88 ± 0.1 mM vs 3.28 ± 0.05 mM, p < 0.001) and oxidized low-density lipoprotein (oxLDL) (288.12 ± 65.92 ng/mL vs 150.72 ± 42.13 ng/mL, p < 0.05) level but decreased serum adiponectin level (1177.47 ± 179.2 pg/mL vs 1523.43 ± 91.8 pg/mL, p < 0.05). Among fecal bacteria significantly correlated with lipid metabolism, CTS significantly decreased the abundance of g__norank_f__Muribaculaceae (21.15 % ± 5.7 % vs 41.84 ± 12.0 %, p < 0.01) but increased that of g_Lactobacillus (11.13 % ± 6.6 % vs 5.7 % ± 4.6 %, p < 0.05), g__Alistipes (3.66 % ± 0.7 % vs 1.47 % ± 1,0%, p < 0.01) and g__Odoribacter (1.31 % ± 0.7 % vs 0.30 % ± 0.2 %, p < 0.01). In addition, the development of CIC and abnormal lipid metabolism were significantly prevented in pseudo-germ-free mice. Therefore, we concluded CTS alleviated 5FU/CPT-11 induced colitis in CAC mice via regulating fecal flora associated lipid metabolism.

Combination of asprosin and adiponectin as a novel marker for diagnosing non-alcoholic fatty liver disease

Background and objectivePatients with non-alcoholic fatty liver disease (NAFLD) have insulin resistance and are at an increased risk of diabetes. Recent evidence suggests that asprosin–a novel hormone secreted by white adipose tissue–may play a role in the pathogenesis of insulin resistance. However, the role of asprosin in NAFLD remains unclear. This study aimed to determine whether serum asprosin level could be used as a biochemical marker for NAFLD diagnosis. MethodsForty-three untreated NAFLD patients and 50 sex- and age-matched healthy controls were included. Circulating serum asprosin and adiponectin (another adipokine) levels were detected by ELISA. Other metabolic parameters related to NAFLD were also determined. ResultsIncreased circulating serum asprosin and decreased serum adiponectin levels were found in NAFLD patients unlike in healthy controls. A positive correlation was observed between asprosin and platelet counts (PLT) (r = 0.3653, p = 0.015), fasting blood glucose (FBG) (r = 0.3592, p = 0.017), triglyceride (TG) levels (r = 0.3383, p = 0.025), serum albumin (ALB) levels (r = 0.3273, p = 0.030), and insulin resistance (HOMA-IR) (r = 0.4799, p = 0.001), whereas a negative correlation existed between adiponectin and TG levels in the NAFLD group. Multivariate linear regression showed that FBG and HOMA-IR were independently related to asprosin levels. Receiver operating characteristic (ROC) curves showed that asprosinAUC and adiponectinAUC were 0.735 (95%CI 0.633–0.836, P < 0.0001) and 0.702 (95%CI 0.597–0.807, p = 0.0007) respectively. Moreover, the combination of both biomarkers showed good sensitivity and specificity with AUC of 0.827, which was better than the single detection of asprosin or adiponectin. ConclusionHigh serum asprosin and low adiponectin level might be associated with the presence of insulin resistance in NAFLD, and the combination of asprosin and adiponectin could be a novel biomarker for diagnosing NAFLD. These data needed to be confirmed and extended in further large-population, well-designed clinical studies.

0720 Study of Serum Adiponectin and Resistin in Patients with Obstructive Sleep Apnea

Abstract Introduction The syndrome of OSA is a very common disorder with several important complications and is still under diagnosed. Obesity is considered to be a chronic disease rather than a life style b. Adipose tissue secretory function is disturbed by chronic intermitted hypoxia occurring in OSA. The aim of this study was to study the level of serum adiponectin and resistin in patients with OSA and we tried to assess their association to different parameters of SDB as well as concomitant co morbidities in each patient Methods This study contained two groups. Patients (group1) included 30 newly diagnosed OSA patients; controls (group 2) included 15 healthy volunteers. All patients were subjected to overnight polysomnography, routine laboratory investigations, Spirometry and fasting serum adiponectin and resistin Results Patients had statically significant lower serum adiponectin level than controls while serum resistin levels were statistically significant higher in patients than controls also serum adiponectin levels were significantly decreased with increase severity of OSA while serum resistin levels were increased significantly with increase severity of OSA, moreover there was a statistical significant decrease in serum adiponectin levels in patients group with increasing number of comorbidities existing in every patient a. There was a statistical significant increase in serum resistin levels in patients group with increasing number of comorbidities existing in every patient Conclusion this highlights the possible relationship of these hormones to the metabolic complications seen in OSA patients Support no conflict of interest

Dysregulation of the Mitochondrial Proteome Occurs in Mice Lacking Adiponectin Receptor 1.

Decreased serum adiponectin levels in type 2 diabetes has been linked to the onset of mitochondrial dysfunction in diabetic complications by impairing AMPK-SIRT1-PGC-1α signaling via impaired adiponectin receptor 1 (AdipoR1) signaling. Here, we aimed to characterize the previously undefined role of disrupted AdipoR1 signaling on the mitochondrial protein composition of cardiac, renal, and hepatic tissues as three organs principally associated with diabetic complications. Comparative proteomics were performed in mitochondria isolated from the heart, kidneys and liver of Adipor1−/− mice. A total of 790, 1,573, and 1,833 proteins were identified in cardiac, renal and hepatic mitochondria, respectively. While 121, 98, and 78 proteins were differentially regulated in cardiac, renal, and hepatic tissue of Adipor1−/− mice, respectively; only 15 proteins were regulated in the same direction across all investigated tissues. Enrichment analysis of differentially expressed proteins revealed disproportionate representation of proteins involved in oxidative phosphorylation conserved across tissue types. Curated pathway analysis identified HNF4, NRF1, LONP, RICTOR, SURF1, insulin receptor, and PGC-1α as candidate upstream regulators. In high fat-fed non-transgenic mice with obesity and insulin resistance, AdipoR1 gene expression was markedly reduced in heart (−70%), kidney (−80%), and liver (−90%) (all P < 0.05) as compared to low fat-fed mice. NRF1 was the only upstream regulator downregulated both in Adipor1−/− mice and in high fat-fed mice, suggesting common mechanisms of regulation. Thus, AdipoR1 signaling regulates mitochondrial protein composition across all investigated tissues in a functionally conserved, yet molecularly distinct, manner. The biological significance and potential implications of impaired AdipoR1 signaling are discussed.

P3480Tissue-specific regulation of the mitochondrial proteome by adiponectin receptor 1

Abstract Lack of the adiponectin target receptor adiponectin receptor 1 (AdipoR1) impairs gene expression of mitochondrial OXPHOS proteins due to impaired AMPK-SIRT1-PGC-1α signaling. Since decreased adiponectin serum levels in diabetes mellitus should thus compromise AdipoR1 signaling, we hypothesized that impaired AdipoR1 signaling may causally contribute to typically observed mitochondrial defects in diabetes complications. Thus, we performed comparative proteomics in cardiac, renal and hepatic tissue of AdipoR1−/− mice using LC-MS/MS. Using principal component analysis, heatmapping and hierarchical clustering, a significant separation of genotypes was observed across tissues. Enrichment analysis of differentially expressed proteins revealed disproportionate representation of proteins involved in oxidative phosphorylation, TCA cycle and fatty acid oxidation in all tissues. While 121 or 98 or 78 proteins were differentially regulated in cardiac or renal or hepatic tissue, respectively, only 15 proteins were regulated in the same direction across all tissues. Pathway analysis identified HNF4, NRF1, LONP, RICTOR, SURF1, insulin receptor and PGC-1α as most likely upstream regulators. Importantly, we found a dramatic downregulation of AdipoR1 expression in heart (−70%), liver (−90%) and kidney (−80%; all p&lt;0.05) of high fat-fed and prediabetic non-transgenic mice compared to low fat-fed mice. In addition and beyond diabetes, AdipoR1 expression was also decreased in endstage failing hearts of non-diabetic human subjects compared to non-failing donor hearts. Thus, we conclude that AdipoR1 signaling regulates mitochondrial protein composition across all tissues in a functionally conserved, yet molecularly distinct, manner. Impaired AdipoR1 signaling may causally contribute to mitochondrial defects in diabetic complications and even human heart failure.

Associations of SNPs of the ADIPOQ Gene with Serum Adiponectin Levels, Unstable Angina, and Coronary Artery Disease

Adiponectin is encoded by the ADIPOQ gene and participates in the pathogenesis of cardiovascular and metabolic diseases. The goal of the study was to assess associations of rs17300539, rs266729, rs182052, rs2241766, and rs17366743 single nucleotide polymorphisms (SNPs) of the ADIPOQ gene with concentrations of serum adiponectin and with coronary atherosclerosis and type 2 diabetes mellitus in 447 patients (316 men and 131 women) subjected to coronary angiography. SNPs of the ADIPOQ gene of the study participants were genotyped using real-time PCR. Multivariate linear regression adjusted for covariates revealed significant association between rs182052 SNP and serum adiponectin concentration (β= –0.11; 95% confidence interval (95%CI): –0.19, –0.03; p = 0.016). Regression analysis revealed an increase in prevalence of unstable angina (OR (odds ratio) = 2.55; 95%CI 1.4–4.82; p = 0.018) and coronary artery disease (OR = 1.55; 95%CI 1.15–2.09; p = 0.021) per copy of the rs182052 A allele. Prevalence of type 2 diabetes mellitus was higher in subjects with the rs182052 A allele (OR = 2.29; 95%CI 1.29-4.21; p = 0.024). Regression analysis of rs266729 showed that prevalence of unstable angina was increased (OR = 3.59; 95%CI 1.17–10.01; p = 0.045) in the subjects with the GG genotype and prevalence of coronary artery disease (CAD) was significantly increased (OR = 1.48; 95%CI 1.09–2.03; p = 0.045) per copy of the G allele. Haplotype analysis revealed that the subjects with the GCATT haplotype have lower adiponectin levels (β= –0.15; p = 0.042) and higher prevalence of unstable angina (OR = 3.597; p = 0.007) compared with reference haplotype carriers. Thus, the results indicate that minor A allele of rs182052 of the ADIPOQ gene is significantly associated with a decrease in serum adiponectin levels, and two SNPs (rs182052 and rs266729) of the ADIPOQ gene are significantly associated with cardiovascular and metabolic diseases.

Association of serum adiponectin level with cystatin C in male patients with obstructive sleep apnea syndrome.

Obstructive sleep apnea syndrome (OSAS) was suggested to exert an effect on renal function. However, the specific mechanism was still unknown. We try to find the association among OSAS, adiponectin, and cystatin C and the effect of adiponectin on renal function in OSAS patients. Seventeen healthy men and seventy-three men which only had OSAS were included in the end. Apnea-hypopnea index (AHI), oxygen desaturation index (ODI), the percentage of total sleep time spent with SpO2 < 90% (T90%), lowest O2 saturation (LaSO2), Epworth Sleepiness Scale (ESS) score, serum adiponectin, and high-sensitive C-reactive protein (hsCRP) were detected in all subjects, and renal function was evaluated with creatinine, cystatin C, and estimated glomerular filtration rate (eGFR). Demographic data, creatinine, and eGFR did not differ among the studied groups. Decreased serum adiponectin levels were associated with severe OSAS. OSAS patients had a higher hsCRP and cystatin C than those without OSAS. Serum adiponectin levels had a negative association with cystatin C. After adjusted for confounders, adiponectin, hsCRP, and ODI had a significant prediction on the cystatin C (β = - 0.218, p = 0.011; β = 0.226, p = 0.037; and β = 0.231, p = 0.029). Decreased serum adiponectin was associated with increased cystatin C in male OSAS patients. These results suggest that serum adiponectin might be a regulatory factor for renal function in OSAS.

Adipocytokines in Non-functional Adrenal Incidentalomas and Relation with Insulin Resistance Parameters.

Adrenal incidentalomas are diagnosed incidentally during radiological screenings and require endocrinological investigations for hormonal activity and malignancy. In certain studies, it has been reported that non-functional incidentalomas can be associated with high adipocytokines levels affecting the insulin resistance just like the adipose tissue with metabolic syndrome. Here, we studied serum adipocytokine levels including leptin, resistin, visfatin, omentin 1 and adiponectin in subjects with non-functional adrenal incidentaloma. Seventy-seven (77) patients (Female 57; Male 20) with non-functional adrenal incidentaloma (NFAI) were enrolled in the study. All patients' past medical history, physical examination including Body Mass Index (BMI) and waist circumference were performed. The patients' demographic, radiologic, hormonal and biochemical parameters were recorded. To compare the parameters, a control group (CG) (n=30) was formed from healthy volunteers. Both groups were matched for age, gender, waist circumference and BMI. Serum adipocytokines including leptin, resistin, visfatin, omentin 1 and adiponectin were measured quantitatively by ELISA. Fasting plasma glucose, insulin, sodium, potassium, cortisol, adrenocorticotropic hormone (ACTH), lipid profiles, and dehidroepiandrostenedion sulphate (DHEAS) were measured. Mean age of the patients was 52.2±10.4 years. BMI and waist circumference of NFAI patients were 26.2±3.28 kg/m2 and 90.2 ±7.5cm, respectively. The mean age of the control group was 48.0±8.16. BMI and waist circumference values for the control group were 25.3±3.5 kg/m2 and 88.3±9.6 cm, respectively. When both groups were compared for age, gender, BMI and waist circumference were non-significant (p>0.05). Serum fasting insulin, total cholesterol, LDL, triglyceride levels of the NFAI group were significantly higher than CG (p<0.05). The insulin resistance index (HOMAIR) values of the NFAI subjects were found to be higher than CG (2.5±1.37, 1.1±0.3 p=0.00). Resistin level of NFAI group was also found to be higher than CG [286.6 ng/L vs. 197 ng/L; (P=0,00)], respectively. Leptin levels of NFAI were significantly higher than CG [441.1 ng/mL vs. 186.5 ng/mL; (P=0.00)] respectively. Adiponectin levels were significantly reduced in the NFAI group than in the CG [10.7 mg/L vs. 30.8 mg/L; (P=0.00)]. Comparision of visfatin and omentin levels was nonsignificant. In this study on subjects with non-functional adrenal incidentaloma, we found not only significantly decreased serum adiponectin levels but also increased leptin, resistin levels as well as dyslipidemia, hypertension and high insulin resistance index. All of which could affect insulin resistance and cardiovascular risk factors. The underlying mechanisms of these findings are unknown, hence further studies are needed.

Association of serum adiponectin with breast cancer: A meta-analysis of 27 case-control studies.

Background:Emerging published studies have indicated that adiponectin is involved in tumorigenesis of breast cancer. However, the results of available studies were inconsistent. The aim of this updated meta-analysis was to assess the association of adiponectin with breast cancer.Materials and methods:PubMed, EMBASE, Wanfang databases, and the China National Knowledge Infrastructure (CNKI) were systematically searched from inception to June 2018. The mean difference (MD) with 95% confidence interval (CI) were estimated and pooled to investigate the effect sizes.Results:Twenty-seven eligible articles that met the study criteria were included in the current meta-analysis. Overall, there was an evident inverse association between serum adiponectin levels and breast cancer (MD = −0.29, 95%CI = (−0.38, −0.21), P < .001). Asian subgroup showed a significant negative association between serum adiponectin concentrations and breast cancer in subgroup analysis by ethnicity (MD = −2.19, 95%CI = (−3.45, −0.94), P < .001). However, no statistical significance was found in Caucasian subgroup (MD = −0.65, 95%CI = (−1.47, 0.17), P = 0.12). Additionally, a further subgroup analysis of Asian stratified by menopausal status showed higher concentrations of adiponectin in healthy control group, whether they were premenopausal (MD = −0.85, 95%CI = (−1.50, −0.19), P = .01) or postmenopausal (MD = −2.17, 95%CI = (−4.17, −0.18), P = .03). No significant difference was observed concerning the association between serum adiponectin and breast cancer metastasis (MD = −1.56, 95%CI = (−4.90, 1.78), P = .36).Conclusion:The current meta-analysis suggests that the serum adiponectin may be inversely associated with breast cancer. Decreased serum adiponectin levels in premenopausal women may also be inversely associated with breast cancer risk other than postmenopausal status. In addition, low serum adiponectin levels in Asian women were more likely to be associated with breast cancer risk than Caucasian women.

Study of serum adiponectin and resistin in patients with obstructive sleep apnea

Background The syndrome of obstructive sleep apnea (OSA) is a very common disorder with several important complications and is still underdiagnosed. Obesity is considered to be a chronic disease rather than a lifestyle disorder. Adipose tissue secretory function is disturbed by chronic intermitted hypoxia occurring in OSA. The aim of this study was to study the level of serum adiponectin and resistin in patients with OSA and we tried to assess their association to different parameters of sleep disordered breathing (SDB) as well as concomitant comorbidities in each patient. Patients and methods This study contained two groups: Patients of group 1 included 30 newly diagnosed OSA patients and controls (group 2) included 15 healthy volunteers. All patients were subjected to overnight polysomnography, routine laboratory investigations, spirometry, and fasting serum adiponectin and resistin. Results Patients had statistically significant lower serum adiponectin level than controls while serum resistin levels were statistically significant higher in patients than controls. Moreover, serum adiponectin levels were significantly decreased with increased severity of OSA while serum resistin levels were increased significantly with increased severity of OSA. Moreover, there was a statistically significant decrease in serum adiponectin levels in the patients’ group with increasing number of comorbidities existing in every patient. There was a statistically significant increase in serum resistin levels in the patients’ group with increasing number of comorbidities existing in every patient. Conclusion This highlights the possible relationship of these hormones with the metabolic complications seen in OSA patients.

Roles of Adiponectin Signaling Related Proteins in Mammary Tumor Development.

Objective:This study aims to investigate the expression levels of adiponectin signaling related proteins in mammary tissue, liver and breast cancer tissue in mice. Adiponectin, an adipocytokine, is secreted from adipose tissue and has been documented to have roles in diabetes, inflammation, and cancer development. In particular, levels of serum adiponectin are inversely associated with obesity and a decrease in serum adiponectin levels have been reported to be associated with breast cancer. There are two adiponectin receptor subtypes, AdipoR1 and AdipoR2, which have been identified in mammalian tissues, including human cancer cell lines and also in human mammary tumors. However, the role of adiponectin receptors in breast cancer development remains to be established.Methods:In this study, MMTV-TGF-α transgenic mice were fed from week 10 up to week 74 of age. Expression levels of adiponectin, AdipoR1 and AdipoR2 proteins were measured in the mammary fat pad (MFP), mammary tumor (MT) and liver tissues from 74 weeks old MMTV-TGF-α transgenic mice with and without MT using Western Blot. Adiponectin levels were measured using ELISA assay.Results:Protein expression levels of Adiponectin and AdipoR1 were significantly lower in MTs compared to control tissues. However, AdipoR2 protein expression levels were similar in MT and MFP tissues from MT-positive and MT-negative mice. The expression levels of adiponectin, AdipoR1 and AdipoR2 proteins in liver tissues were also similar in MT-positive and MT-negative mice. Serum adiponectin levels of the MT-positive and MT-negative mice were similar.Conclusion:These results indicate that adiponectin and its receptors are differentially regulated depending upon the specific tissue analyzed. AdipoR1 and adiponectin may play important roles in MT development.

Adiponectin expression in visceral adiposity is an important determinant of insulin resistance in morbid obesity.

Visceral adiposity is associated with decreased serum adiponectin levels, peripheral resistance to insulin and an increased risk of cardio-metabolic complications. However, the link between adiponectin expression in visceral adipose tissue (VAT), its serum levels and metabolic protection is controversial. The aim of this study was to investigate the relationship between the adiponectin gene expression in VAT and clinical and metabolic parameters in patients with severe obesity. This is a cross-sectional study that included 51 severely obese patients (age 43.24±11.29 years, BMI 45.13±8.67 kg/m2), extensively evaluated clinically and biologically (metabolic tests, serum adiponectin measurements, HOMA-IR) before bariatric surgery. Omental adipose tissue was sampled during the intervention and the relative quantification of adiponectin gene expression was performed by real-time PCR, using beta-actin as reference gene. Adiponectin mRNA in VAT was significantly higher in obese insulin-sensitive patients than in the rest of obese patients (p < 0.05) and negatively correlated with HOMA-IR (r =-0.354, p=0.016) and uric acid (r =-0.304, p=0.045). After adjustment for gender, TG/HDL ratio and uric acid, adiponectin expresion (β= -0.439, p=0.001), waist circumference (β=0.467, p=0.001) and serum adiponectin (β =-0.339, p=0.011) remained significantly associated with HOMA-IR, together explaining more than 50% of its variation. In severely obese patients, adiponectin gene expression in VAT is negatively correlated with serum levels of uric acid and is an independent determinant, together with anthropometric parameters of visceral obesity and serum adiponectin levels, of insulin resistance.