Lower Serum Adiponectin Levels Research Articles

Cytokine and adipokine are biofactors can act in blood and colostrum of obese mothers.

Breast milk contains bioactive components that contribute to newborn development. However, colostrum may undergo biochemical and immunological changes as a function of maternal overweight and obesity. To investigate this hypothesis, this study determined the levels of hormones and immunological markers in the serum and colostrum of overweight and obese mothers. Colostrum and serum samples were collected from 15 normoweight, 15 overweight, and 15 obese women for determination of leptin, adiponectin, cytokines (TNF-α, IL-6, IL-10), and C-reactive protein (CRP). Obese mothers exhibited higher levels of serum TNF-α, IL-6, and CRP, serum and colostrum leptin and colostrum adiponectin and lower levels of serum adiponectin. Leptin levels in maternal serum and colostrum were positively correlated, as was pre-pregnancy BMI and serum TNF-α, IL-6, CRP, and leptin. Adiponectin levels in colostrum and serum were negatively correlated. The results suggest that obesity changes hormonal and immunological components of maternal serum and colostrum. The modifications can have short-term and long-term effects on newborn development. © 2016 BioFactors, 43(2):243-250, 2017.

Low serum adiponectin levels in childhood and adolescence predict increased intima-media thickness in adulthood. The Cardiovascular Risk in Young Finns Study

Introduction: Low adiponectin levels may predict the development of atherosclerosis. We examined the association of childhood adiponectin with preclinical carotid atherosclerosis that is defined as plaque and/or high (≥95th percentile) intima-media thickness (IMT) at the carotid bifurcation in adulthood.Methods: The Cardiovascular Risk in Young Finns Study is a cohort study on cardiovascular risk factors. We used risk factor data from the baseline study (1980) and ultrasound findings from the follow-ups (2001 and 2007). The study population included 1708 participants, aged 3–18 years at baseline.Results: In multivariate analysis, childhood adiponectin was inversely associated with preclinical carotid atherosclerosis: odds ratio 0.68, 95% confidence interval (CI) 0.53–0.86, p = .001, for 1-SD increase in childhood adiponectin after adjusting for childhood non-high-density lipoprotein cholesterol, body mass index, and blood pressure. When examining the incremental predictive ability, we observed that compared to an approach utilizing only conventional risk factors, the model additionally including adiponectin levels improved c-statistics area under curve from 0.733 (95% Cl 0.694–0.771) to 0.748 (95% Cl 0.710–0.786), p = .02.Conclusions: Childhood adiponectin levels improve the prediction of carotid atherosclerosis in adulthood over conventional risk factors. This supports the idea that low adiponectin levels may have a role in the development of preclinical atherosclerosis.Key messagesChildhood adiponectin levels improve the prediction of increased carotid intima-media thickness in adulthood over conventional cardiovascular risk factors.These results suggest that adiponectin levels measured in childhood may have a role in the atherosclerotic process.

Associations between single-nucleotide polymorphisms of ADIPOQ, serum adiponectin and increased type 2 diabetes mellitus risk in Bahraini individuals.

This study aimed to estimate the frequency of the SNPs (+45T>G and +276G>T) genotypes and investigate the association between the two SNPs and adiponectin concentration, metabolic parameters and risk of T2DM in the Bahraini population. We genotyped the two ADIPOQ SNPs in 140 unrelated T2DM patients and 66 nondiabetic controls using the polymerase chain reaction-restriction fragment length polymorphism assay. Lipid profile was measured by enzymatic methods. Total serum adiponectin levels were measured by immunoassay. T2DM patients had reduced adiponectin levels compared with controls. +45T>G was more prevalent in patients than controls. The rare G allele of +45T>G occurred more frequently than the common T allele in T2DM patients compared with controls, and was associated with lower serum adiponectin levels. There was no significant difference in allele and genotype frequencies of +276G>T between type T2DM patients and controls. There was no association between both SNPs and metabolic parameters.

Association of asthma diagnosis with leptin and adiponectin: a systematic review and meta-analysis

There is some evidence which shows that higher levels of serum leptin and lower levels of serum adiponectin are associated with the diagnosis of asthma. This meta-analysis evaluated the association...

Natural History of Congenital Generalized Lipodystrophy: A Nationwide Study From Turkey.

Congenital generalized lipodystrophy (CGL) is a rare autosomal recessive disorder characterized by near-total lack of body fat. We aimed to study natural history and disease burden of various subtypes of CGL. We attempted to ascertain nearly all patients with CGL in Turkey. This was a nationwide study. Participants included 33 patients (22 families) with CGL and 30 healthy controls. We wanted to ascertain genotypes by sequencing of the known genes. Whole-body magnetic resonance imaging was used to investigate the extent of fat loss. Metabolic abnormalities and end-organ complications were measured on prospective follow-up. Analysis of the AGPAT2 gene revealed four previously reported and four novel mutations (CGL1; c.144C>A, c.667_705delinsCTGCG, c.268delC, and c.316+1G>T). Analysis of the BSCL2 gene revealed four different homozygous and one compound heterozygous possible disease-causing mutations (CGL2), including four novel mutations (c.280C>T, c.631delG, c.62A>T, and c.465-468delGACT). Two homozygous PTRF mutations (c.481-482insGTGA and c.259C>T) were identified (CGL4). Patients with CGL1 had preservation of adipose tissue in the palms, soles, scalp, and orbital region, and had relatively lower serum adiponectin levels as compared to CGL2 patients. CGL4 patients had myopathy and other distinct clinical features. All patients developed various metabolic abnormalities associated with insulin resistance. Hepatic involvement was more severe in CGL2. End-organ complications were observed at young ages. Two patients died at age 62 years from cardiovascular events. CGL patients from Turkey had both previously reported and novel mutations of the AGPAT2, BSCL2, and PTRF genes. Our study highlights the early onset of severe metabolic abnormalities and increased risk of end-organ complications in patients with CGL.

Correlation between serum adiponectin level and cognitive function in patients with Alzheimer's disease

To investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function. This case-control study was conducted in 90 patients with a highly probable diagnosis ofAD, who were divided into mild, moderate and severe group saccording to the MMSE score. Ninety healthy subjects matched for age and gender with the AD patients were selected as the control group. The serum levels ofadiponectin in the participants were detected using enzyme-linked immunosorbent assay. Serum adiponectin level was significantly lower in the AD group than in the control group (P<0.05). Of the 3 subgroups of the AD patients, the moderate and severe AD groups showed significantly lower serum adiponectin level sthan the control group (P<0.05), but the difference in adiponectin levels was not significant between the mild AD group and the control group (P>0.05); serum adiponectin levels also differed significantly among the 3 subgroups of AD patients (P<0.05). Serum adiponectin level was positively correlated with the MMSE score in the AD patients (r=0.683, P<0.001). Serum adiponectin levels are reduced in AD patients and associated with the degree of cognitive impairment.

Serum adiponectin, insulin resistance, and uveal melanoma: clinicopathological correlations.

To investigate the status of insulin resistance, metabolic syndrome, dyslipidemia, and serum adiponectin levels in patients with uveal melanoma and choroidal nevus were investigated. Our study included 86 patients with uveal melanoma, 38 patients with choroidal nevus, and 86 controls. Uveal melanomas were classified as small, medium, and large on the basis of Collaborative Ocular Melanoma Study (COMS) criteria. Patients with uveal melanoma had significantly higher homeostatic model assessment scores compared with patients with choroidal nevus (P<0.001). Patients with uveal melanoma and choroidal nevus had significantly lower levels of serum adiponectin compared with controls (P<0.001). Patients with uveal melanoma who developed systemic metastases had significantly lower levels of serum adiponectin levels compared with patients with nonmetastases during follow-up (P=0.018). When the largest tumors (COMS III) were compared, ciliary body melanomas were associated with significantly lower levels of serum adiponectin than choroidal melanomas. In patients who were treated with enucleation, epitheloid predominant and mixed cell-type tumors were associated with lower levels of serum adiponectin compared with tumors with spindle cell type, but this did not reach statistical significance. By providing an antiapoptotic and proangiogenic environment, low serum adiponectin levels and insulin resistance may play a role in promoting the growth of uveal melanocytic tumors and may contribute toward a more aggressive clinical course, adversely affecting the prognosis.

The clinical and biochemical characteristics associated with insulin resistance in non-obese young women

Aim: The aim of this study was to investigate the biomarkers of insulin resistance in non-obese women.Design: This was a retrospective study.Patients: A total 229 non-obese women (Body mass index: BMI < 25) were evaluated.Main outcome measure(s): Serum levels of various androgens, cardiovascular risk and metabolic components.Results: There were no significant differences in the prevalence of polycystic ovary syndrome (PCOS), hyperprolactinemia, or premature ovarian failure (POF) between the non-obese women with and without insulin resistance. Non-obese women with insulin had significantly higher serum thyroid stimulation hormone (TSH) levels and resistin and lower serum adiponectin levels than non-obese women without insulin resistance; however, the inflammatory biomarkers and serum androgen levels did not differ between the two groups. Furthermore, using step-wise multivariate regression analysis applied by the risk factors listed above, TSH was the only predictive factor for insulin resistance in non-obese reproductive-aged women.Conclusions: Thyroid function should play an important role in developing insulin resistance for non-obese women. Serum androgens and inflammation might not contribute to insulin resistance in these women.

Association between serum adiponectin levels and muscular fitness in Portuguese adolescents: LabMed Physical Activity Study

Background and aimParadoxically, recent investigations have showed that adiponectin levels are inversely associated with muscle strength. However, to date, there is a lack of knowledge on the relationship between muscular fitness (MF) and adiponectin levels in adolescents. We aimed to examine the independent associations between MF and adiponectin levels in adolescents, controlling for several potential confounders. Methods and resultsThis is a cross-sectional analysis with 529 Portuguese adolescents aged 12–18 years. A MF score was computed as the mean of the handgrip strength and standing long jump standardized values by age and gender. We measured fasting glucose, insulin, HDL-cholesterol, C-reactive protein and adiponectin. Linear regression analysis showed a significant inverse association between adiponectin (Z-score by age and sex) and MF score, after adjustments for age, sex, pubertal stage, socioeconomic status, adherence to the Mediterranean diet, body mass index, HOMA-IR, HDL-cholesterol, C-reactive protein and cardiorespiratory fitness (unstandardized β = −0.176; p < 0.005). Analysis of covariance showed a significant difference between the Low MF/Non-overweight group and the High MF/Non-overweight Group (p < 0.05) and between the Low MF/Non-overweight and High MF/Overweight Group (p < 0.05) (F (5, 523) = 2.262, p = 0.047). ConclusionAdiponectin circulating levels are inversely and independently associated with MF. In non-overweight adolescents, those with high levels of MF presented lower levels of adiponectin compared to those with Low MF. Likewise, overweight adolescents with High MF presented lower levels of serum adiponectin than non-overweight adolescents with Low MF.

In Utero Nutritional Manipulation Provokes Dysregulated Adipocytokines Production in F1 Offspring in Rats.

Background. Intrauterine environment plays a pivotal role in the origin of fatal diseases such as diabetes. Diabetes and obesity are associated with low-grade inflammatory state and dysregulated adipokines production. This study aims to investigate the effect of maternal obesity and malnutrition on adipokines production (adiponectin, leptin, and TNF-α) in F1 offspring in rats. Materials and Methods. Wistar rats were allocated in groups: F1 offspring of control mothers under control diet (CF1-CD) and under high-fat diet (CF1-HCD), F1 offspring of obese mothers under CD (OF1-CD) and under HCD (OF1-HCD), and F1 offspring of malnourished mothers under CD (MF1-CD) and under HCD (MF1-HCD). Every 5 weeks postnatally, blood samples were obtained for biochemical analysis. Results. At the end of the 30-week follow-up, OF1-HCD and MF1-HCD exhibited hyperinsulinemia, moderate dyslipidemia, insulin resistance, and impaired glucose homeostasis compared to CF1-CD and CF1-HCD. OF1-HCD and MF1-HCD demonstrated low serum levels of adiponectin and high levels of leptin compared to CF1-CD and CF1-HCD. OF1-CD, OF1-HCD, and MF1-HCD had elevated serum levels of TNF-α compared to CF1-CD and CF1-HCD (p < 0.05). Conclusion. Maternal nutritional manipulation predisposes the offspring to development of insulin resistance in their adult life, probably via instigating dysregulated adipokines production.

Peroxisome proliferator activated receptor gamma 2 modulates late pregnancy homeostatic metabolic adaptations.

Pregnancy requires the adaptation of maternal energy metabolism including expansion and functional modifications of adipose tissue. Insulin resistance (IR), predominantly during late gestation, is a physiological metabolic adaptation that serves to support the metabolic demands of fetal growth. The molecular mechanisms underlying these adaptations are not fully understood and may contribute to gestational diabetes mellitus. Peroxisome proliferator-activated receptor gamma (PPARγ) controls adipogenesis, glucose and lipid metabolism and insulin sensitivity. The PPARγ2 isoform is mainly expressed in adipocytes and is thus likely to contribute to adipose tissue adaptation during late pregnancy. In the present study, we investigated the contribution of PPARγ2 to the metabolic adaptations occurring during the late phase of pregnancy in the context of IR. Using a model of late pregnancy in PPARγ2 knockout (KO) mice, we found that deletion of PPARγ2 exacerbated IR in association with lower serum adiponectin levels, increased body weight and enhanced lipid accumulation in liver. Lack of PPARγ2 provoked changes in the distribution of fat mass and preferentially prevented the expansion of the perigonadal depot while at the same time exacerbating inflammation. PPARγ2KO pregnant mice presented adipose tissue depot-dependent decreased expression of genes involved in lipid metabolism. Collectively, these data indicate that PPARγ2 is essential to promote healthy adipose tissue expansion and immune and metabolic functionality during pregnancy, contributing to the physiological adaptations that lead gestation to term.

Adiponectin, leptin and insulin levels at birth and in early postnatal life in neonates with hypoxic ischemic encephalopathy.

BackgroundHypoxic ischemic encephalopathy (HIE) occurs in one to three per 1000 live full-term births. Fifteen to twenty percent will die in the postnatal period, and an additional 25 % will develop severe and permanent neuropsychological sequalae. The control of growth and nutritional status in the fetus and neonate is a complex mechanism, in which also hormones produced by adipose tissue, such as adiponectin and leptin are involved. The aim of this study was to measure the levels of adiponectin, leptin and insulin in neonates with HIE at birth and in early postnatal life and comparing them with normal healthy AGA and SGA neonatesMethodsThis study carried out on 80 full-term neonates born in Minia university hospital during the period from May 2013 to December 2014. They were divided into group I included 25 neonates with HIE and group II included 55 normal healthy neonates (30 appropriate for gestational age (AGA) and 25 small for gestational age (SGA)). Weight, length, head circumference, body mass index (BMI), glucose, adiponectin, leptin and insulin levels were measured for all neonates. Adiponectin, leptin and insulin levels were compared between neonates with HIE and normal healthy neonates as well as between AGA and SGA neonates at birth, 2nd and 6th days of life.ResultsAdiponectin and leptin levels were significantly higher at birth then began to decrease during the first postnatal week in all neonates while insulin level increased during the same period. Serum adiponectin levels were significantly lower while serum leptin and insulin levels were significantly higher in neonates with HIE than healthy neonates. In all neonates, the serum adiponectin level was positively correlated at birth with weight, length, BMI and leptin levels but not with insulin level. In neonates with HIE, serum adiponectin level was not correlated with weight, BMI, leptin level or insulin level. In all neonates, the serum leptin level was positively correlated at birth with body weight, height and BMI. In neonates with HIE serum leptin levels were not correlated with weight, BMI or insulin level after birth. There were no correlations between either leptin or adiponectin serum levels or any of the studied parameters in neonates with HIEConclusionsNeonates who are suffering from HIE had lower serum levels of adiponectin and higher serum levels of leptin and insulin than normal healthy neonates at birth and during the early postnatal period. The decline of leptin and increased the insulin levels after birth in all neonates may be important for the stimulation of feeding behavior and the acquisition of energy homeostasis during the early postnatal life. Positive significant correlations between adiponectin, leptin, body weight and body mass indices were present in normal healthy neonates but not in neonates with HIE reflecting the effect of hypoxia on the regulatory mechanisms controlling the adipose tissue functions.

Type 2 diabetes mellitus is associated with lower serum adiponectin level in Bangladeshi population

The aim of the observational case control study was to find out the association of type 2 diabetes mellitus (T2DM) with serum adiponectin level in Bangladeshi population. This was conducted in the Biomedical Research Group, Research Division, Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic Disorders (BIRDEM), Dhaka, Bangladesh. Sixty six T2DM subjects and seventy four healthy control subjects were included. Diabetes was diagnosed and classified as per World Health Organization criteria. Serum adiponectin was measured by Enzyme Linked Immunosorbent Assay (ELISA) method. Serum glucose was measured by glucose-oxidase method; serum insulin was measured by chemiluminescence- based ELISA technique. The insulin secretory capacity (HOMA%B), insulin sensitivity (HOMA%S) &amp; insulin resistance (HOMA-IR) were assayed by homeostasis model assessment method. Statistical analysis was performed using SPSS Windows version 11.5. The median (range) fasting serum insulin of control and T2DM subjects were 14.7 (1.9-45.9) and 18.1 (4.1-42.8), respectively. The median (range) serum adiponectin (?g/ml) of the control and T2DM subjects were 8.7 (0.8-16.0) and 6.2 (1.1-22.4). The serum adiponectin of T2DM was significantly lower than the control subjects (p &lt; 0.001). The median (range) HOMA%B values of control and T2DM subjects were 160.1 (33.4-493.4) and 100.5 (17.7-349.3), respectively. The median HOMA%B of T2DM subjects was significantly lower than the control subjects (p &lt; 0.001). The median (range) HOMA%S values of control and T2DM subjects were 44.2 (9.8-339.4) and 32.8 (14.3-154.7), respectively. The median HOMA%S of T2DM group was significantly lower than the control subjects (p &lt; 0.05). The median (range) HOMA-IR of control and T2DM subjects were 3.5 (0.5-11.4) and 5.8 (1.0-28.3), respectively. The median HOMA-IR of T2DM subjects was significantly higher than the control subjects (p &lt; 0.001). The results of the study suggest that T2DM subjects have both insulin secretory defects, insulin resistance and associated with lower serum adiponectin level in Bangladeshi population.Mediscope Vol. 2, No. 2: July 2015, Pages 16-21

Association of polymorphism in adiponectin (+45 T/G) and leptin (-2548 G/A) genes with type 2 diabetes mellitus in male Egyptians.

IntroductionAdiponectin is an adipose tissue-specific protein with insulin-sensitizing properties. Many investigators have explored the association between adiponectin single nucleotide polymorphisms (SNPs) and type 2 diabetes mellitus (T2DM) in different ethnic populations from different regions. Leptin is a protein hormone constituting an important signal in the regulation of adipose tissue mass and body weight. The aim of this study was to explore potential associations between SNP +45 T>G of the adiponectin gene and SNP 2548G/A of leptin with T2DM and the effect of SNPs on serum adiponectin and leptin levels.Material and methodsFrom the Egyptian population, we enrolled 110 T2DM patients and 90 non-diabetic controls. Serum lipid profile, blood glucose, serum adiponectin, and leptin were measured. Genotyping for two common SNPs of the adiponectin and leptin genes was performed by polymerase chain reaction–restriction fragment length polymorphism.ResultsThe G allele and TG/GG genotype of SNP 45 occurred more frequently than the T allele and TT genotype in T2DM patients compares to the controls. Subjects with the GG + TG genotype of SNP 45 were at increased risk for T2DM (OR = 6.476; 95% CI: 3.401–12.33) and associated with a low serum adiponectin level compared with the TT genotype. The serum leptin concentration of GA + AA genotype carriers was not significantly different from that of the GG genotype in the diabetic group.ConclusionsThe G allele carriers who have reduced plasma concentrations of adiponectin may have an association with T2DM, while leptin SNP 2548 G/A is not associated with the risk of development of T2DM in the Egyptian population.

Type 2 Diabetes Mellitus is Associated with Lower Serum Adiponectin Level in Bangladeshi Population

Background: The physiological role of adiponectin is not yet fully clear, but it is now generally accepted that it has a protective role against the development of lifestyle disorders, related to insulin resistance and atherosclerosis. Insulin resistance is one of the basic defects of type 2 diabetes (T2DM) and adiponectin is inversely associated with T2DM. As serum adiponectin level has not yet been investigated in Bangladeshi T2DM subjects,so that the present study has been under taken to find out the association of T2DM with serum adiponectin level in Bangladeshi population.Methodology: In this observational case control study, sixty six (66) T2DM subjects, seventy four (74) healthy control subjects were included. Diabetes was diagnosed and classified as per WHO criteria. Serum Adiponectin was measured by Enzyme Linked Immunosorbent Assay (ELISA) method. Serum glucose was measured by glucose-oxidase method; serum insulin was measured by chemiluminescence-based ELISA technique. The insulin secretory capacity (HOMA%B), insulin sensitivity (HOMA%S) &amp; insulin resistance (HOMA IR) were assayed by homeostasis model assessment method.Results: The study subjects were BMI matched. BMI of the Control subjects and T2DM subjects (Mean±SD) were 25.02±3.55 and 25.85±3.62. Age (year) of the Control subjects and T2DM subjects (Mean±SD) were 42.46±9.24 and 48.49±8.09. Median (range) fasting serum insulin in the control and T2DM was 14.68 (1.86-45.92) and 18.09 (4.10-42.78) respectively which was not statistically significant (p=0.214). Median (range) HOMA%B values in the control and T2DM subjects was 160.10(33.40-493.40) and 100.45(17.70-349.30). Median HOMA%B in the T2DM group was significantly lower compared to the control (p=0.0001). Median (range) HOMA%S values in the control and T2DM subjects was 44.20(9.80- 339.40) and 32.80(14.30-154.70) respectively. Median HOMA%S in the T2DM group was significantly lower compared to the control (p=0.036). Median (range) serum adiponectin (?g/ml) of the control and T2DM subjects was 8.70 (0.76-15.96) and 6.19 (1.13-22.37). Serum adiponectin was significantly lower in T2DM compared to the control (p=0.0001).Conclusions: From this study it may be concluded that, T2DM subjects have both insulin secretory defects and insulin resistance and associated with lower serum adiponectin level in Bangladeshi population.Anwer Khan Modern Medical College Journal Vol. 6, No. 1: January 2015, Pages 10-13

Association of adiponectin gene polymorphism with nonalcoholic fatty liver disease in Taiwanese patients with type 2 diabetes.

ObjectivePatients with type 2 diabetes and nonalcoholic fatty liver disease (NAFLD) have a higher prevalence of cardiovascular diseases. In this study we investigated the frequency of single nucleotide polymorphisms (SNPs) of several candidate genes associated with NAFLD in Taiwanese patients with type 2 diabetes mellitus (DM) and NAFLD and in those with DM but without fatty liver disease.MethodsWe enrolled 350 patients with type 2 DM and NAFLD and 209 patients with DM but without NAFLD. Body mass index (BMI), % body fat (% BF), glycated hemoglobin (HbA1c), high molecular weight (HMW) isoform of adiponectin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglyceride (TG) levels were measured. Thirteen SNPs in 5 genes (adiponectin, leptin, peroxisome proliferator-activated receptor alpha, adiponutrin/patatin-like phospholipase domain-containing protein 3 and peroxisome proliferator-activated receptor γ co-activator 1α ) were measured.ResultsOnly adiponectin rs266729 polymorphism was associated with susceptibility to NAFLD (p = 0.001). Subgroup analysis revealed that the proportion of subjects with homozygous genotype GG was higher in patients with NAFLD (31%) than in controls (11%) and that the proportions of heterozygous CG and homozygous CC were higher in controls (37% and 52%, respectively) than in patients with NAFLD (33% and 36%, respectively). Patients with NAFLD carrying the GG genotype of rs266729 showed significantly lower serum HMW adiponectin levels than patients carrying the GC or CC genotype (3.75±0.37 vs. 3.99±0.66 vs. 4.79±0.58 μg/ml, p< 0.001). Body fat and serum HMW adiponectin levels were the strongest predictors of developing NAFLD (p < 0.001 and 0.004, respectively).ConclusionsIn patients with type 2 diabetes gene polymorphism of adiponectin rs266729 is associated with risk of NAFLD. G allele of rs266729 is associated with hypoadiponectinemia. Low serum adiponectin level may precipitate liver steatosis in patients with type 2 diabetes.

Aortic valve sclerosis is associated with lower serum adiponectin levels.

The sclerotic lesions of the aortic valve share common features with atherosclerosis. An anti-inflammatory protein, adiponectin, seems to have a protective effect on the cardiovascular system. The goal of our study is to determine adiponectin levels in patients with aortic sclerosis and to compare these values with the control group with similar age and cardiovascular risk profile. Sixty-eight patients with aortic sclerosis and 40 controls were included. Serum adiponectin levels were measured by solid-phase enzyme-linked immunosorbent assay. There were no significant differences regarding age, sex and other cardiovascular risk factors between groups. Also, mean body mass index values were similar. The rate of mitral annular calcification and left ventricular hypertrophy were significantly higher in patients with aortic sclerosis. Among laboratory variables, high-sensitive C-reactive protein (hsCRP) levels were significantly higher in patients with aortic sclerosis than in those without (4.0 ± 2.9 vs. 2.9 ± 2.3 mg/dl, P = 0.04). Adiponectin levels were found to be significantly lower in aortic sclerosis group than in controls (9.7 ± 4.4 vs. 11.7 ± 4.9 μg/ml, P = 0.034). In the whole group, adiponectin levels were significantly correlated with BMI (r = -0.22, P = 0.02), white blood cell count (r = -0.2, P = 0.03), hsCRP (r = -0.25, P = 0.008), total cholesterol (r = -0.18, P = 0.05), high-density lipoprotein (HDL) cholesterol (r = 0.31, P = 0.001) and triglyceride (r = -0.36, P < 0.001). In patients with aortic sclerosis, serum adiponectin levels were significantly lower compared with those with normal aortic valves. Our findings suggested that adiponectin might play a role in the progression of degenerative aortic valve disease.

Abstract P4-11-16: Low serum adiponectin level is an independent risk factor of DCIS in postmenopausal women at increased risk of breast cancer

Abstract Background:The assessment of breast cancer (BC) risk is a key step for an effective preventive treatment. Besides the established risk assessment models, validation of independent predictive factors such as circulating biomarkers would improve patient selection and treatment efficacy. Obesity and metabolic imbalance play an important role in BC risk in menopausal women. The role of adipocytes in energy homeostasis is currently under investigation for their emerging relationship with BC. Adipokines (such as leptin and adiponectin) are linked to insulin sensitivity and have been related to BC risk and prognosis. Adiponectin, a peptide hormone secreted by the adipose tissue, has been inversely related to BC risk both in observational studies and in a phase II chemoprevention trial in premenopausal women at increased risk. Aim:We measured baseline serum adiponectin and leptin levels as well as HOMA index, in 534 postmenopausal women enrolled in 16 Italian centers and randomized in one of the two international phase III trials for BC prevention -the IBIS-II(Prevention) and IBIS-II(DCIS) trials- to assess whether these biomarkers were different in the healthy women at increased risk for BC cohort compared to the DCIS cohort. Methods:Healthy postmenopausal women (aged 40-70) at increased risk for BC (on an age-dependent risk model; n=186) or DCIS patients who underwent radical surgery in the previous 6 months (n=348) were eligible according to the two separate protocol entry criteria. At baseline, fasting blood was collected, processed and stored at -80°C till biomarkers measurement. Insulin and glucose levels were measured with the Architect system (Abbott Laboratories, Abbott Park, IL 60064 USA). Serum adiponectin and leptin levels were determined with Immunoassays by R&amp;D (Minneapolis, USA). Results:Participant characteristics and biomarker levels (median, IQ range) by disease status are reported below. Table 1Healthy (n=186)DCIS (n=348)Age at entry59 (55, 63)60 (56, 65)BMI (kg/m2)25.2 (22.9, 28.4)25.0 (22.4, 28.1)Adiponectin (ng/mL)13063 (10279, 18157)11498 (7722, 16909)Leptin (pg/mL)16181 (9594, 26391)17284 (9675, 26173)L/A ratio1.33 (0.60, 2.09)1.46 (0.69, 3.19)Glucose (mg/dL)89 (81, 97)93 (86, 103)Insulin (μU/mL)6.6 (5.0, 9.6)7.5 (5.4, 10.6)HOMA index1.39 (1.04, 2.02)1.79 (1.18, 2.61)L/A, Leptin/Adiponectin ratio Adiponectin was significantly negatively correlated with leptin, L/A ratio, HOMA index and BMI, while leptin was positively correlated with L-A ratio, BMI, HOMA. Logistic regression has been used and Odds Ratios (ORs) have been calculated to assess the association of DCIS with biomarkers.DCIS patients were significantly more frequent in the lowest quartile of adiponectin compared to the highest quartile (60% vs 75%; OR=2.49; 95% CI, 1.39-4.44, p= 0.0003) adjusting for center, BMI, HOMA index and age. Conclusions:Low serum adiponectin levels in postmenopausal women are more frequent in DCIS patients compared to healthy at risk subjects independently of BMI, HOMA index and age and results are similar to premenopausal women. Future investigations in both trials will assess whether adiponectin is also associated with BC events. Acknowledgments: J.Forbes and T.Howell, Co-Chairmen,IBIS-II Steering Committee. Citation Format: Aliana Guerrieri-Gonzaga, Debora Macis, Sara Gandini, Valentina Aristarco, Harriet Johansson, Giorgia Bollani, Teresa Roth, Maria-Teresa Sandri, Jill Knox, Jack Cuzick, Bernardo Bonanni. Low serum adiponectin level is an independent risk factor of DCIS in postmenopausal women at increased risk of breast cancer [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P4-11-16.

Systemic arteriosclerosis and eating behavior in Japanese type 2 diabetic patients with visceral fat accumulation.

BackgroundVisceral fat accumulation is a major etiological factor in the progression of type 2 diabetes mellitus and atherosclerosis. We described previously visceral fat accumulation and multiple cardiovascular risk factors in a considerable number of Japanese non-obese subjects (BMI <25 kg/m2). Here, we investigated differences in systemic arteriosclerosis, serum adiponectin concentration, and eating behavior in type 2 diabetic patients with and without visceral fat accumulation.MethodsThe study subjects were 75 Japanese type 2 diabetes mellitus (age: 64.8 ± 11.5 years, mean ± SD). Visceral fat accumulation represented an estimated visceral fat area of 100 cm2 using the bioelectrical impedance analysis method. Subjects were divided into two groups; with (n = 53) and without (n = 22) visceral fat accumulation. Systemic arteriosclerosis was scored for four arteries by ultrasonography. Eating behavior was assessed based on The Guideline for Obesity questionnaire issued by the Japan Society for the Study of Obesity.ResultsThe visceral fat accumulation (+) group showed significantly higher systemic vascular scores and significantly lower serum adiponectin levels than the visceral fat accumulation (−) group. With respect to the eating behavior questionnaire items, (+) patients showed higher values for the total score and many of the major sub-scores than (−) patients.ConclusionsType 2 diabetic patients with visceral fat accumulation showed 1) progression of systemic arteriosclerosis, 2) low serum adiponectin levels, and 3) differences in eating behavior, compared to those without visceral fat accumulation. Taken together, the findings highlight the importance of evaluating visceral fat area in type 2 diabetic patients. Furthermore, those with visceral fat accumulation might need to undergo more intensive screening for systemic arteriosclerosis and consider modifying their eating behaviors.

Expression of Adiponectin Receptors on Peripheral Blood Leukocytes of Hypertensive Children Is Associated with the Severity of Hypertension.

The aim of the study was to find out whether peripheral blood leukocyte adiponectin receptors 1 and 2 (AdipoR1, AdipoR2) protein expression patterns (flow cytometry) differ between the primary hypertension children (n = 57) and healthy controls (n = 19) and if their expression levels are related to selected clinical parameters. The group of 26 patients [AdipoR(−)] showed lower and the group of 31 patients [AdipoR(+)] showed higher AdipoRs protein expression than the control and each other (P < 0.01 for neutrophils, P < 0.05 for monocytes). The AdipoR(+) leukocytes expressed higher AdipoR1 mRNA levels (RT-PCR) than AdipoR(−) ones and controls (P = 0.022 and P = 0.007, resp.). Despite greater BMI, the AdipoR(−) patients had unchanged serum adiponectin levels. In contrast, AdipoR(+) patients had lower serum adiponectin concentrations than the AdipoR(−) ones and controls (P < 0.001). The AdipoR(+) patients had higher blood pressure (P = 0.042) and greater carotid intima-media thickness (P = 0.017) than the AdipoR(−) ones. The stage of hypertension was associated with increased neutrophil but not monocyte AdipoR1 density (AdipoR1 MFI) (P < 0.05). Severe ambulatory hypertension was presented more often in AdipoR(+) patients than in AdipoR(−) ones (51.6% versus 26.9%, resp.; P < 0.01). In conclusion, neutrophil AdipoRs upregulation was associated with early stages of vascular injury, hypertension severity, and low serum levels of adiponectin.