Higher Adiponectin Concentrations Research Articles

Biomarker signatures associated with ageing free of major chronic diseases: results from a population-based sample of the EPIC-Potsdam cohort.

A number of biomarkers denoting various pathophysiological pathways have been implicated in the aetiology and risk of age-related diseases. Hence, the combined impact of multiple biomarkers in relation to ageing free of major chronic diseases, such as cancer, cardiovascular disease and type 2 diabetes, has not been sufficiently explored. We measured concentrations of 13 biomarkers in a random subcohort of 2,500 participants in the European Prospective Investigation into Cancer and Nutrition Potsdam study. Chronic disease-free ageing was defined as reaching the age of 70years within study follow-up without major chronic diseases, including cardiovascular disease, type 2 diabetes or cancer. Using a novel machine-learning technique, we aimed to identify biomarker clusters and explore their association with chronic disease-free ageing in multivariable-adjusted logistic regression analysis taking socio-demographic, lifestyle and anthropometric factors into account. Of the participants who reached the age of 70years, 321 met our criteria for chronic-disease free ageing. Machine learning analysis identified three distinct biomarker clusters, among which a signature characterised by high concentrations of high-density lipoprotein cholesterol, adiponectin and insulin-like growth factor-binding protein 2 and low concentrations of triglycerides was associated with highest odds for ageing free of major chronic diseases. After multivariable adjustment, the association was attenuated by socio-demographic, lifestyle and adiposity indicators, pointing to the relative importance of these factors as determinants of healthy ageing. These data underline the importance of exploring combinations of biomarkers rather than single molecules in understanding complex biological pathways underpinning healthy ageing.

Plant-based dietary indices and biomarkers of chronic low-grade inflammation: a cross-sectional analysis of adults in Ireland

PurposeThere is increasing interest in the health benefits of plant-based diets (PBDs). Evidence reports favourable associations with inflammatory profiles and reduced cardiovascular disease risk. However, limited studies have examined relationships between PBD indices (PDIs) and inflammatory biomarkers. We explored overall PDI, healthful PDI (hPDI) and unhealthful PDI (uPDI) associations with inflammatory biomarker profiles.MethodsThis cross-sectional analysis included 1986 middle- to older-aged adults from the Mitchelstown Cohort. PDI scores were calculated using validated food frequency questionnaires. PDI score associations with inflammatory biomarkers were assessed via linear regression analysis, with adjustment for potential confounders.ResultsComparison of quintiles (Q5 vs Q1) revealed lower concentrations of C-reactive protein (CRP), interleukin 6 (IL-6), white blood cells (WBCs), neutrophils and monocytes, and the leptin-to-adiponectin ratio (PDI and hPDI P < 0.05); lower leptin (PDI, P < 0.05), and complement component 3 (C3), tumour necrosis factor alpha (TNF-α), plasminogen activator inhibitor 1, lymphocytes and eosinophils (hPDI, P < 0.05); and higher concentrations of adiponectin (PDI and hPDI, P < 0.05). Conversely, higher concentrations of C3, CRP, IL-6, TNF-α, resistin, WBCs, neutrophils, lymphocytes, monocytes and eosinophils, and the neutrophil-to-lymphocyte ratio, and lower adiponectin concentrations were observed comparing uPDI quintiles (P < 0.05). In fully adjusted regression models, higher hPDI scores were associated with lower concentrations of C3, TNF-α, WBCs, neutrophils and monocytes (all P < 0.01). Higher uPDI scores were associated with higher C3 and TNF-α concentrations (all P < 0.01).ConclusionThis study provides evidence that a more healthful PBD is associated with a more favourable inflammatory profile and that a more unhealthful PBD is associated with the reverse.

Metformin versus insulin for gestational diabetes: Adiposity variables and adipocytokines in offspring at age of 9 years

AimsTo compare body composition, visceral adiposity, adipocytokines, and low-grade inflammation markers in prepubertal offspring of mothers who were treated with metformin or insulin for gestational diabetes mellitus (GDM). Methods172 offspring of 311 mothers randomized to receive metformin (n = 82) or insulin (n = 90) for GDMwere studied at 9 years of age (follow-up rate 55%). Measurements included anthropometrics, adipocytokines, markers of the low-grade inflammation, abdominal magnetic resonance imaging (MRI), magnetic liver spectrometry (MRS), and whole body dual-energy X-ray absorptiometry (DXA). ResultsSerum markers of low-grade inflammation, visceral adipose tissue volume, total fat percentage, and liver fat percentage were similar between the study groups. Serum adiponectin concentration was higher in children in the metformin group compared to insulin group (median 10.37 vs 9.50 µg/ml, p = 0.016). This difference between groups was observed in boys only (median 12.13 vs 7.50 µg/ml, p < 0.001). Leptin/adiponectin-ratio was lower in boys in the metformin group than in the insulin group (median 0.30 vs 0.75; p = 0.016). ConclusionsMaternal metformin treatment for GDM had no effects on adiposity, body composition, liver fat, or inflammation markers in prepubertal offspring compared to maternal insulin treatment but was associated with higher adiponectin concentration and lower leptin/adiponectin-ratio in boys.

Serum adiponectin concentrations as a risk factor for cardiovascular complications in type 1 diabetes

AimBy analyzing data from DCCT/EDIC study, we investigated the associations of serum adiponectin concentrations with macrovascular complications and cardiovascular events in T1D. Materials and MethodsAdiponectin concentrations were measured in EDIC year 8. The participants (n = 1040) were divided into four groups by quartiles of adiponectin concentrations. The association of macrovascular complications and cardiovascular events were analyzed by using multivariable regression and Cox proportional hazards models. ResultsHigh adiponectin concentrations were associated with decreased risk of peripheral artery disease represented by ankle brachial index (ORs (95% CI): 0.22 (0.07–0.72), 0.48 (0.18–1.25), and 0.38 (0.14–0.99) in fourth, third, and second quartiles compared with first quartile), with reduced carotid intima-media thickness, and with increased LVEDV index. Moreover, high adiponectin concentrations were also associated with increased risk of any cardiovascular events (HRs (95% CI): 2.59 (1.10–6.06), 2.03 (0.90–4.59), and 1.22 (0.52–2.85)) and major atherosclerotic cardiovascular events (HRs (95% CI): 11.37 (2.04–63.43), 5.68 (1.04–31.07), and 3.76 (0.65–21.77) in fourth, third, and second quartiles compared with first quartile), however, after adjustments with LVEDV index, these associations were diminished. ConclusionsAdiponectin may protect carotid atherosclerosis and peripheral artery disease in T1D. It may be associated with increased cardiovascular events, depending on cardiac structural changes.

Malic Enzyme 1 (ME1) Promotes Adiposity and Hepatic Steatosis and Induces Circulating Insulin and Leptin in Obese Female Mice.

Malic Enzyme 1 (ME1) supports lipogenesis, cholesterol synthesis, and cellular redox potential by catalyzing the decarboxylation of L-malate to pyruvate, and the concomitant reduction of NADP to NADPH. We examined the contribution of ME1 to the development of obesity by provision of an obesogenic diet to C57BL/6 wild type (WT) and MOD-1 (lack ME1 protein) female mice. Adiposity, serum hormone levels, and adipose, mammary gland, liver, and small intestine gene expression patterns were compared between experimental groups after 10 weeks on a diet. Relative to WT female mice, MOD-1 female mice exhibited lower body weights and less adiposity; decreased concentrations of insulin, leptin, and estrogen; higher concentrations of adiponectin and progesterone; smaller-sized mammary gland adipocytes; and reduced hepatosteatosis. MOD-1 mice had diminished expression of Lep gene in abdominal fat; Lep, Pparg, Klf9, and Acaca genes in mammary glands; Pparg and Cdkn1a genes in liver; and Tlr9 and Ffar3 genes in the small intestine. By contrast, liver expression of Cdkn2a and Lepr genes was augmented in MOD-1, relative to WT mice. Results document an integrative role for ME1 in development of female obesity, suggest novel linkages with specific pathways/genes, and further support the therapeutic targeting of ME1 for obesity, diabetes, and fatty liver disease.

Dietary inadequacies overestimate the blood deficiencies of magnesium, zinc, and vitamins A, C, E, and D among residents of Sao Paulo

We aimed to estimate the prevalence of the inadequate intake and status of magnesium, zinc, and vitamins A, C, E, and D and identify factors associated with micronutrient deficiency in serum/plasma among residents of São Paulo, Brazil. Data from 824 individuals aged ≥14 years were obtained from the 2015 ISA-Nutrition, a population-based, cross-sectional survey. Dietary and supplement intakes were assessed using two 24-h dietary recalls, and the micronutrient inadequacies were estimated using the National Cancer Institute method. Micronutrient status was measured in serum or plasma, and deficiency was established according to the lower limit of the reference values. Receiver operating characteristic curve analysis was used to identify the effect of intake on the micronutrient status in serum/plasma. Logistic regression analysis was applied to assess the association between micronutrient status and individual characteristics. More than 80% of the population had an inadequate dietary intake of magnesium, vitamin E, and vitamin D. Males had a high prevalence of inadequate dietary intake of vitamin A and zinc. A high-to-moderate prevalence of inadequate vitamin C intake was observed. Vitamin D was the only nutrient with a deficient status comparable to its dietary inadequacy. The other nutrients demonstrated a lower deficiency prevalence compared to dietary inadequacy, and vitamin A demonstrated the lowest prevalence of deficiency in plasma. Generally, dietary intake showed a non-notable association with micronutrient deficiency in serum/plasma. Individuals with fasting glucose concentrations ≥100mg/dL and those using diuretic drugs had a higher risk of serum magnesium deficiency. Those using lipid-lowering drugs and those with high plasma adiponectin concentrations had a higher risk of serum zinc deficiency. Individuals who smoked and those with hypertension showed a higher risk of plasma vitamin C deficiency. Individuals with average leptin concentrations had a higher risk of plasma vitamin E deficiency. Finally, those with sufficient leisure-time physical activity had a lower risk of serum vitamin D deficiency. Residents of the urban areas of São Paulo demonstrated substantially inadequate intakes of most of the assessed micronutrients; however, micronutrient deficiency in serum/plasma was not associated with dietary inadequacy, and it usually demonstrated a lower prevalence than dietary indicators. Thus, using micronutrient intake to determine the serum/plasma profile should be done with caution. The status of the micronutrients varied according to individual characteristics, indicating the interplay of complex mechanisms underlying micronutrient balance.

Adiponectin System (Rescue Hormone): The Missing Link between Metabolic and Cardiovascular Diseases.

The adipose tissue, regardless of its role in generating and storing energy, acts as a key player as an endocrine tissue, producing a wide scale of cytokines/hormones called adipokines. Adipokines such as leptin, resistin, visfatin and osteopontin own pro-inflammatory effects on the cardiovascular system in some cases. In contrast, some adipokines have cardioprotective and anti-inflammatory impacts including adiponectin, omentin, and apelin. One of the key adipokines is adiponectin, the abundant peptide regulating hormone that is released mainly by adipocytes and cardiomyocytes as well as by endothelial and skeletal cells. It acts through two main receptors: AdipoR1 and AdipoR2, forming the “Adiponectin system” which effectively exerts its cellular mechanisms and responses in target cells. It regulates various metabolic processes, while adiponectin is the adipocyte hormone known for its cardioprotective impact in clinical and experimental research. It is also a well-effector metabolic adipokine, since weight loss or diet restriction show a link with rises in adiponectin concentrations, which is accompanied with increasing insulin sensitivity, glucose, and lipids-regulation via adiponectin’s antioxidant, anti-inflammatory, anti-fibrotic actions. The high adiponectin level made it an attractive player in developing therapeutical treatments for metabolic syndromes and cardiovascular disease. The elevated plasma levels of adiponectin are mostly attributed to its benefits on cardio-metabolism. In some cases, adiponectin has been paradoxically accompanied with elevated risk of cardiovascular disease, so higher adiponectin concentration is a marker of poor prediction. Thus, the adiponectin system is attractive to researchers as a biomarker of heart disease advancement and a predictor of prognosis during the term of some cardiovascular diseases and its mechanical functions in Hypertension and diabetic patients. This review highlights the physiological roles of adiponectin as an anti-inflammatory and cardioprotective hormone as well as how it plays as a biomarker and potential therapeutic tool in the cardiovascular system in adult, children, and adolescents. The adiponectin system may be seen as a rescue hormone aiding in remodeling of the cardiovascular system on both cellular and molecular levels. The paradox role of adiponectin relevant to cardiovascular mortality should be taken into consideration.

0189 High Levels of Sleep Disturbance across Early Childhood Increases Cardiometabolic Disease Risk Index in Early Adolescence: Longitudinal Sleep Analysis Using the HOME Study

Abstract Introduction Sleep is a predictor of cardiometabolic disease (CMD) risk, and new evidence links early childhood sleep to later CMD risk. This study examines the impact of early childhood sleep duration, bedtime timing, and sleep disturbance on a CMD risk score in early adolescence. Methods Within the Health Outcomes and Measures of Environment (HOME) Study, a prospective pregnancy and birth cohort study, we assessed sleep patterns among 346 children using the Children’s Sleep Habits Questionnaire from ages 2 to 8 years. We calculated cardiometabolic risk scores ate age 12 for 183 of these children from visceral adiposity area, blood pressure, fasting serum triglyceride, high density lipoprotein, leptin, and adiponectin concentrations. We used a group-based semi-parametric mixture model to identify distinct trajectories in sleep duration, bedtime timing, and sleep disturbance for the entire sample. We then examined the associations between sleep trajectories and CMD risk score using general linear models for children with a CMD risk score, using both an unadjusted model (no covariates) and an adjusted model (adjusting for child pubertal stage, child sex, duration of breastfeeding, household income, and maternal education). Results Three sleep trajectories emerged for bedtime timing (late timing, medium timing, and early timing) and for sleep disturbance (high, medium, and low), and two for sleep duration (high and low). In the unadjusted model, we found significant differences in CMD risk scores by trajectories of sleep disturbance. Children in the ‘high’ trajectory had higher CMD risk scores (Least Square Mean=1.51; 95% CI: 0.39, 2.64) than those in the ‘low’ trajectory (Least Square Mean =-0.51; 95% CI: -1.16, 0.15; p=.002) and ‘medium’ trajectory (Least Square Mean=-0.15; 95% CI: -1.14, 0.85; p=.03). These findings only approached significance after adjusting for covariates. No significant differences in CMD risk were observed for bedtime timing or total sleep time trajectories in the unadjusted or adjusted models. Conclusion In this cohort, parent-reported sleep disturbance in early childhood was associated with more adverse cardiometabolic profiles in early adolescence. Our findings suggest that trials to reduce CMD risk via sleep interventions – which have been conducted in adolescents and adults – may be implemented too late. Support (If Any) National Institute of Environmental Health Sciences grants PO1 ES11261, R01 ES014575, R01 ES020349, R01 ES027224, R01 ES025214.

Elevations in adipocytokines and mortality in rheumatoid arthritis.

This study assessed whether circulating levels of adiponectin and leptin are associated with higher mortality in patients with RA. Participants were adults from the Veterans Affairs RA Registry. Adipokines and inflammatory cytokines were measured as part of a multi-analyte panel on banked serum at enrolment. Dates and causes of death were derived from the Corporate Data Warehouse and the National Death Index. Covariates were derived from medical record, biorepository and registry databases. Multivariable Cox proportional hazard models evaluated associations between biomarkers and all-cause and cause-specific mortality. A total of 2583 participants were included. Higher adiponectin levels were associated with older age, male sex, white race, lower BMI, autoantibody seropositivity, radiographic damage, longer disease duration, prednisone use and osteoporosis. Higher adiponectin concentrations were also associated with higher levels of inflammatory cytokines but not higher disease activity at enrolment. Leptin was primarily associated with greater BMI and comorbidity. The highest quartile of adiponectin (vs lowest quartile) was associated with higher all-cause mortality [hazard ratio (HR): 1.46 (95% CI: 1.11, 1.93), P = 0.009] and higher cardiovascular mortality [HR: 1.85 (95% CI: 1.24, 2.75), P = 0.003], after accounting for covariates. Higher leptin levels were also associated with greater all-cause and cancer mortality. Elevations in adipokines are associated with age, BMI, comorbidity and severe disease features in RA and independently predict early death. Associations between adiponectin and inflammatory cytokines support the hypothesis that chronic subclinical inflammation promotes metabolic changes that drive elevations in adipokines and yield adverse health outcomes.

Association of circulating leptin, adiponectin, and resistin concentrations with long-term breast cancer prognosis in a German patient cohort

Adipokines including leptin, adiponectin and resistin have been linked to risk of obesity-related cancers potentially through low-grade chronic inflammation pathways. We aimed to assess the role of post-diagnosis circulating adipokines on long-term prognosis in a prospective breast cancer cohort. Adipokines were measured in blood collected at baseline shortly after diagnosis (2002–2005) and at follow-up (2009) from 3112 breast cancer patients enrolled in the population-based MARIE study. Half of the patients had measurements at both time-points. All-cause mortality, breast cancer specific mortality and recurrences were ascertained up to June 2015 (11 years median follow-up). Associations with time-varying adipokine concentrations overall and stratified by estrogen and progesterone receptor (ERPR) were evaluated using adjusted proportional hazard regression. At baseline (n = 2700) and follow-up (n = 2027), median concentrations for leptin, adiponectin and resistin were 4.6 and 2.7 ng/ml, 24.4 and 30.0 mg/l, 15.4 and 26.2 ng/ml, respectively. After adjustment, there was no evidence for associations between adipokines and any outcome overall. In ERPR negative tumors, highest vs. lowest quintile of adiponectin was significantly associated with increased breast cancer specific mortality (HR 2.51, 95%CI 1.07–5.92). Overall, post-diagnosis adipokines were not associated with long-term outcomes after breast cancer. In patients with ERPR negative tumors, higher concentrations of adiponectin may be associated with increased breast cancer specific mortality and warrant further investigation.

Evaluation of the frequency of ADIPOQ c.45 T>G and ADIPOQ c.276 G>T polymorphisms in adiponectin coding gene in girls with anorexia nervosa.

Anorexia nervosa (AN) is a serious chronic psychosomatic disorder, the essence of which are attempts by the sufferer to obtain a slim silhouette by deliberate weight loss (restrictive diet, strenuous physical exercise, provoking vomiting). The aetiology of this disorder is multifactorial. Genetic factors that influence the predisposition to AN have been sought. A broad meta-analysis points to a strong genetic correlation between AN and insulin resistance. Adiponectin (ADIPO) increases insulin sensitivity. In our pilot study we demonstrated that the TT genotype in locus ADIPOQ c.276 G>T of the ADIPO gene and a higher concentration of ADIPO in blood serum occurred significantly more frequently in 68 girls suffering from AN than in 38 healthy girls. The objective of this study was to evaluate the frequency of the occurrence of ADIPOQ c.45 T>G and ADIPOQ c.276 G>T in the ADIPO gene in a larger cohort of girls with AN and healthy girls, as well as an analysis of correlations between variants of the aforementioned polymorphisms and the levels of ADIPO in blood serum. The study covered 472 girls (age: 11-19 years): 308 with the restrictive form of AN (AN) and 164 healthy girls (C). The level of ADIPO in blood serum was determined by means of the ELISA method on a Bio-Vendor, LLC (Asheville, North Carolina, USA). The DNA isolation was carried out by means of Genomic Mini AX BLOOD (SPIN). The PCR reaction was carried out in a ThermoCycle T100 thermocycler. 80-150 ng of the studied DNA and relevant F and R starters were added to the reaction mixture. The reaction products were subjected to digestion by restriction enzymes and separated on agarose gels (RFLP). The distribution of genotypes in the polymorphic site ADP c.45 of the ADIPO gene and ADP c.276 was similar in both groups. In both groups the T allele was most frequent in locus ADIPOQ c.45 and the G allele in locus ADIPOQ c.276. In all the study subjects collectively (AN and C) a statistically significant negative correlation between the levels of ADIPO in blood serum on one hand and body weight (r = -0.46; p < 0.0001) and BMI (r = -0.67; p < 0.0001) on the other was demonstrated. Exclusively in the AN group a significant correlation between the level of ADIPO in blood and the distribution of TG, TT, and GG alleles in loci ADIPOQ c.45 and ADIPOQ c.276 was demonstrated (p = 0.0052 and p < 0.0001, respectively). The genotype in loci ADIPOQ c.45 and ADIPOQ c.276 of the ADIPO gene seems to have no effect on the predisposition to AN. Girls suffering from AN with the TT genotype in loci ADIPOQ c.45 and ADIPOQ c. 276 may demonstrate higher insulin sensitivity because they have significantly higher levels of ADIPO than girls suffering from AN with other genotypes. This may be suggestive of their better adaptation to the state of malnutrition, and it has a potential effect on treatment results.

Mendelian randomization study of the relation between adiponectin and heart function, unravelling the paradox

High adiponectin concentrations are generally regarded as beneficial with regard to cardiometabolic health, but have been paradoxically associated with increased cardiovascular disease risk, specifically heart failure, in individuals at high cardiovascular risk. We aimed to investigate the association between adiponectin and heart function parameters, and inversely, we estimated the effect of genetically-determined heart function and NT-proBNP as the main marker of heart failure on adiponectin using Mendelian randomisation.Observational analyses between adiponectin and measures of heart function, i.e. E/A ratio, left, and right ventricular ejection fraction, were performed in participants of the Netherlands Epidemiology of Obesity (NEO) study, assessed by MRI of the heart (n = 1,138). Two-sample Mendelian randomisation analyses were conducted to estimate the effect of NT-proBNP and heart function on adiponectin concentrations using publicly-available summary statistics (ADIPOGen; the PLATO trial).The mean (standard deviation) age was 56 (6) years and mean body mass index was 26 (4) kg/m2. Per five μg/mL higher adiponectin, the E/A ratio was −0.05 (95 % CI: −0.10, −0.01) lower, left ventricle ejection fraction was −0.5 % (95 % CI: −1.1, 0.1) lower, and right ventricle ejection fraction was 0.5 % (95 % CI: −0.1, 1.2) higher. Genetically-determined NT-proBNP was causally related to adiponectin concentrations in ADIPOGen: per doubling of genetically-determined NT-proBNP, adiponectin concentrations were 11.4 % (95 % CI: 1.7, 21.6) higher.With causal MR methods we showed that NT-proBNP affects adiponectin concentrations, while adiponectin is not associated with heart function parameters. Therefore, reverse causation may explain the adiponectin paradox observed in previous studies.

Altered Adiponectin Response in Older Women Following Dextrose and High-Fat Dietary Challenges.

Despite its beneficialproperties,higheradiponectinconcentrations are paradoxically associated with mortality in advanced age. Several mechanisms are being discussed. However, little is known about postprandial regulation of adiponectin in older adults. We assessed age-specific differences of the adiponectin response to different test meals considering potential determinants. Older(n=20)andyounger(n=22)womenare randomizedtoadextrose(DEX)orhigh-fat(HF)dietarychallenge. Postprandial adiponectin and fibroblast growth factor 21 (FGF21) concentrations are measured before and 60, 120, 240 min after ingestion. We assessed postprandial changes and group differences using linear mixed models controlled for possible determinants. In younger women, postprandial adiponectin remains stable after both test meals. In contrast, adiponectin increases following DEX and decreases after HF in older women, irrespective of control variables. Postprandial adiponectin is positively associated with malondialdehyde and inversely associated with interleukin-6 following DEX and also negatively associated with metabolic parameters after both test meals. In older women, elevated postprandial FGF21 concentrations are associated with a higher adiponectin response (β = 30.7, 95% CI 10.6-50.8, p= 0.007). Adiponectin response is associated with type of dietary challenge, age, and FGF21 response. Age-group differences are partly attributable to metabolic parameters and oxidative stress.

Correlation between age, testosterone and adiponectin concentrations, and sperm abnormalities in Simmental bulls.

Background and Aim:Capacity for sperm production is affected by age, which is related to the morphology of sperm abnormalities and can affect fertility. The aim of this study was to evaluate the relationship between age and concentrations of testosterone and adiponectin with sperm abnormalities in Simmental bulls.Materials and Methods:The study used 11 bulls, separated into three groups. The first group consisted of five bulls aged 4-5 years, and the second and third groups each consisted of three bulls, aged 6-7 and 8-10 years, respectively. The average sperm motility of the animals ranged from 57.66±2.60% to 70.17±0.22%. Blood samples were obtained from the coccygeal region of the animals. Testosterone and adiponectin analysis was performed using the enzyme-linked immunosorbent assay method. Sperm morphology was evaluated using carbol fuchsin-eosin staining according to the Williams method. Finally, correlations between testosterone and adiponectin concentrations, age, and sperm abnormalities were analyzed using Pearson’s correlation analysis.Results:The findings revealed a significant correlation (p<0.01) between the concentrations of testosterone and adiponectin (−0.538), age (−0.588), and abnormal sperm morphology (−0.912). Moreover, they revealed that the concentration of testosterone in the bulls aged 8-10 years was lower, at 21.89±4.56 ng/mL, compared to that in the bulls aged 4-5 years, at 36.15±1.29 ng/mL, and 6-7 years, at 35.16±5.39 ng/mL. The findings also revealed a positive correlation between adiponectin concentration and age (0.529) and sperm abnormalities (0.506). The increase in testosterone concentration was inversely related to the adiponectin concentration (−0.538). Moreover, the mean amount of abnormal sperm increased with increasing age: 3.82±0.33% in the group aged 4-5 years, and 4.40±0.72% and 10.20±1.97% in the groups aged 6-7 years and 8-10 years, respectively.Conclusion:The study data indicate that there is a decrease in testosterone concentration, a high adiponectin concentration, and an increase in abnormal sperm with increasing age in bulls.

Plasma Adiponectin and Blood Pressure Progression in African Americans: The Jackson Heart Study.

Little is known on the association of plasma adiponectin with blood pressure (BP) changes in African Americans (AAs). We evaluated the associations between plasma adiponectin and BP progression among AAs. We analyzed data from 1,184 participants without hypertension at baseline (2000-2004) with ≥1 follow-up visits in the Jackson Heart Study. We used robust Poisson regression to generate risk ratios (RRs) for BP progression (an increase by ≥1 BP stage) and incident hypertension. Over a median of 7 years, 71% progressed to higher BP stage and 65% developed hypertension. We found evidence of interaction by sex (P-interaction = 0.088). Compared with those in the lowest quartile (Q1), male participants in the highest adiponectin quartile (Q4) had reduced risks of BP progression (RR 0.76 [95% confidence interval, CI, 0.60-0.96]) and incident hypertension (RR 0.74 [95% CI 0.56-0.97]). After accounting for body mass index, this relation persisted among obese men (RR for the highest [vs. lowest] adiponectin quartile: 0.59 [95% CI 0.36-0.97] for incident hypertension, and 0.69 [95% CI 0.45-1.06] for BP progression). Among women, adiponectin was not associated with BP outcomes (RR [95% CI] for Q4 vs. Q1: 1.03 [0.86-1.23] and 1.01 [0.83-1.23] for BP progression and incident hypertension, respectively). Our findings were consistent across both the American College of Cardiology (ACC)/American Heart Association (AHA) and Seventh Joint National Committee (JNC-7) BP categories. In a large, community-based sample of AAs, higher adiponectin concentrations were associated with lower risks of BP progression and incident hypertension in men, but no significant association was observed in women.

Associations Between Antioxidant Vitamin Status, Dietary Intake, and Retinol-binding Protein 4 Levels in Prepubertal Obese Children After 3-month Weight Loss Therapy

Objective:Adiposity is associated with increased oxidative stress, leading to changed fat-soluble vitamin concentrations. The aim of this study was to determine whether weight loss alters fat-soluble vitamin status and whether these alterations are associated with dietary intake, anthropometric parameters and adipokines in obese children.Methods:Vitamin A and E concentrations were measured using high-pressure liquid chromatography in 60 obese children before and after weight loss therapy. Retinol-binding protein 4 (RBP4), leptin, soluble leptin receptor (sOB-R), and high molecular weight adiponectin concentrations were determined by immunoenzymatic assays.Results:The intake of vitamin E was lower in obese children with weight loss after therapy (p=0.038). In this group, an increase was found in the vitamin A/lipids (p=0.022) and the vitamin E/lipids (p=0.008) ratios but due to the reduction in triglyceride levels. In the obese group, changes in vitamin E level were positively correlated with changes in dietary vitamin E (p=0.017) and the leptin/sOB-R ratio (p=0.046). Changes in vitamin A level were positively correlated with changes in dietary vitamin A (p=0.001) and RBP4 concentration (p=0.023). Associations between changes in RBP4 level with the changes in body mass index (BMI) (p=0.011) and total cholesterol concentration (p=0.023) but not with changes in vitamin A concentration were found in the obese after therapy.Conclusion:An increased risk of vitamin E deficiency may occur in children losing weight during lifestyle intervention. Changes in BMI value may influence changes in RBP4 concentrations and consequently the vitamin A status in obese children after therapy.

Maternal Obesity Is Associated With Higher Cord Blood Adipokines in Offspring Most Notably in Females.

Deleterious long-term effects in the offspring from women with pregravid obesity have been described; however, the evidence supporting early metabolic and inflammatory markers in the offspring at birth and gender differences are conflicting. The present study aimed to compare cord blood adipokines and cytokines concentrations and anthropometric characteristics of the offspring of women with maternal obesity (MO) and normal-weight mothers (NWM). Also, maternal and neonatal variables on the association of maternal body mass index (BMI) with cord blood adipokines were evaluated. A cross-sectional analysis of a subsample of mother-child dyads participating in a cohort study (n = 221) was assessed. Anthropometrics, cord blood adipokines (leptin and adiponectin) and cytokines (interleukin [IL]-1β, IL-4, IL-10, IL-12 p40, IL-12p70, IL-13, and tumor necrosis factor α) concentrations in the offspring of normal-weight women (BMI >18.5 and <24.9 kg/m2) and women with pregravid obesity (BMI > 30 kg/m2) without comorbidities was performed. Offspring from mothers with obesity had higher birth weight, a higher proportion of large for gestational age, higher ponderal index, and heavier placentae than offspring from normal-weight mothers (P < 0.05). Within the offspring from women with obesity, males had significantly higher weight, length, the proportion of large-for-gestational-age newborns, higher weight for length ratio. Males had more efficient placentas than females (P < 0.05). Higher adiponectin and leptin in both sexes and higher leptin in female offspring of mothers with obesity after adjusting for birth size (P < 0.05) were found. Higher IL-12p40 in the offspring of women with MO with no other differences in other cytokines among groups were evidenced. Maternal obesity associates with a higher concentration of adiponectin and leptin in their offspring at birth. There is a relevant effect on anthropometrics in male offspring and on leptin in female newborn. Further studies need to evaluate the extension of these effects in postnatal life. NCT02903134.

Adiponectin and Its Effects on Acute Leukemia Cells: An Experimental and Bioinformatics Approach.

Acute lymphoblastic leukemia (ALL) is the most common pediatric malignancy. It is known that deregulation of adipokine pathways is probably implicated in the ontogenesis of ALL. The present work aims at investigating the role of adiponectin and its effects on an ALL cell line. The CCRF-CEM cells were used as a model. Cells have been treated with adiponectin, with different concentrations up to 72h. Cytotoxicity and cell cycle distribution were investigated for all concentrations using flow cytometry. Selected concentrations were also used for additional microarray analysis, using a small gene set of cancer-related genes. Lower and higher adiponectin concentrations did not produce an inhibition of proliferation, as well as an increase in cell death. It was found that adiponectin regulated differentially genes, such as CD22, CDH1, IFNG, LCK, MSH2, SPINT2, and others. At the same time, it appeared that adiponectin-related gene expression was more active on chromosomes 18 and 1. Machine learning classification algorithms showed that several genes were grouped together indicating common regulatory mechanisms. The present study showed that adiponectin is able to induce gene differential expression in leukemic cells in vitro, suggesting a possible role in the progression of leukemia. It is also an indication that more studies are required in order to further understand the role of adiponectin and adipokines in general in the role of human neoplasms.

Leptin and Adiponectin Concentrations Independently Predict Future Accumulation of Visceral Fat in Nondiabetic Japanese Americans.

Whether leptin and adiponectin are independently associated with regional body fat distribution was investigated in a prospective study of Japanese Americans. Nondiabetic participants 39 to 79 years of age were followed for 5 years to assess change in body composition. Leptin and adiponectin concentrations were evaluated at baseline and by single-slice computed tomography measurements of intra-abdominal fat (IAF), abdominal subcutaneous fat (SCF), and thigh SCF cross-sectional areas at baseline and at 5 years. Ninety-six men and ninety-five women without diabetes had the following baseline mean (SD) values: age 45.7 (3.5) years and 46.4 (3.9) years, IAF 78.7 (38.6) cm2 and 62.1 (39.0) cm2 , leptin concentration 4.5 (2.3) μg/L and 10.2 (5.2) μg/L, and adiponectin concentration 7.4 (3.2) μg/mL and 10.8 (4.7) μg/mL, respectively. Baseline leptin (β = 1.7722, P = 0.014) and adiponectin concentrations (β = -0.4162, P < 0.001) were significantly associated with IAF change over 5 years in multivariable models adjusting for age, sex, diabetes family history, weight change over 5 years, and baseline measurements of BMI, IAF, abdominal SCF, waist circumference, thigh fat, and homeostatic model assessment of insulin resistance. In nondiabetic Japanese Americans, a higher concentration of leptin was associated with greater accumulation of IAF and a higher concentration of adiponectin with lesser accumulation of IAF over 5 years.

Does fetal leptin and adiponectin influence children's lung function and risk of wheeze?

Adipocytokines, which are secreted during fetal development by both mothers and fetuses, may influence fetal lung development, but little human data are available. We used data from the HOME Study to investigate the associations of cord blood adipocytokine concentrations with children's lung forced expiratory volume (FEV1; N=160) and their risk of wheeze (N = 281). We measured umbilical cord serum adipocytokine concentrations using enzyme-linked immunosorbent assays and FEV1 using a portable spirometer at ages 4 and 5 to calculate the percent predicted FEV1 (%FEV1). Parents completed standardized questionnaires of their child's wheeze symptoms every 6 months from birth to age 5, then again at ages 6 and 8. We used multivariable linear mixed models and modified Poisson regression with generalized estimating equations to estimate associations of adipocytokine concentrations (log2-transformed) with children's %FEV1 and the risk of wheeze, respectively, adjusting for sociodemographic, perinatal, and child factors. Cord serum leptin was not associated with children's %FEV1. Higher cord serum adiponectin concentrations were associated with higher %FEV1 in girls (β = 3.1, 95% confidence interval [CI]:0.6, 5.6), but not in boys (β=-1.3, 95%CI:-5.9, 3.3) (sex × adiponectin p-value = 0.05). Higher leptin was associated with lower risk of wheeze in girls (RR = 0.74, 95%CI:0.66, 0.84), but not boys (RR = 0.87, 95%CI:0.69, 1.11) (sex × leptin p-value = 0.01). In contrast, higher adiponectin concentrations were associated with lower risk of wheeze (RR = 0.84, 95%CI:0.73, 0.96) in both boys and girls. These data suggest that fetal adipocytokines may impact lung development and function in early childhood. Future studies are needed to confirm these findings and explore the mechanisms underlying these associations.