Lower Serum Adiponectin Concentrations Research Articles

Negative Correlation of Serum Adiponectin Level with Aortic Stiffness in Elderly Diabetic Persons.

Adiponectin has anti-inflammatory activity against atherosclerosis. Aortic stiffness is a common manifestation of atherosclerosis in diabetes mellitus and elderly persons. This study aimed to evaluate whether low serum adiponectin levels were associated with aortic stiffness in geriatric diabetic patients. Blood samples were obtained from 130 diabetic participants aged ≥ 65 years. We defined high aortic stiffness based on a carotid–femoral pulse wave velocity (cfPWV) of >10 m/s. Circulating adiponectin concentrations were examined using enzyme-linked immunosorbent assays. Sixty-six participants (50.8%) had aortic stiffness. Patients with aortic stiffness had lower serum adiponectin concentrations than those in the control group (p < 0.001). Multivariate logistic regression analysis showed that the adiponectin level (odds ratio: 0.939, 95% confidence interval: 0.898–0.981, p = 0.005) was an independent predictor of aortic stiffness in elderly diabetic persons. Multivariate forward stepwise linear regression analysis also demonstrated that the adiponectin level (β = −0.256, adjusted R2 change = 0.100, p = 0.003) was negatively associated with cfPWV values in older diabetic patients. In conclusion, serum adiponectin is negatively correlated with cfPWV and is an independent predictor of aortic stiffness in elderly diabetic persons.

Variation in insulin response to oral sugar test in a cohort of horses throughout the year and evaluation of risk factors for insulin dysregulation

BackgroundThe oral sugar test (OST) is commonly used to diagnose insulin dysregulation (ID) and equine metabolic syndrome; however, possible seasonal changes in OST results have not been evaluated.ObjectiveTo determine the possible variation in insulin response to OST throughout the year and risk factors associated with maximum insulin concentration (InsMax) and ID.Study designProspective, longitudinal cohort study.MethodsThe OST was performed on 29 Finnhorses every other month six times. Serum total adiponectin concentration and phenotypic variables related to obesity were also measured. Changes in InsMax, adiponectin, scale weight, body condition score, cresty neck score (CNS), and fasting glucose concentration were assessed. Risk factor analyses were performed on InsMax and ID status, and ID groups were compared with each other.ResultsFourteen horses were categorised with non‐ID each time and 15 as having ID at least once during the follow‐up period. The ID status of 12 horses varied throughout the year, but neither the insulin variables measured during the OST nor adiponectin expressed significant seasonal variation. Increasing age and CNS, and decreasing adiponectin were observed as risk factors for a high InsMax after OST. The risk of ID was higher in horses with no exercise compared to horses with exercise (OR 7.6, 95% CI 1.2‐49.3, P = .03). Horses with ID had lower serum adiponectin concentrations, longer neck circumference and larger height than horses in the non‐ID group.Main limitationsThe environmental conditions (feeding, exercise) were not constant for all horses throughout the study and only one breed was used.ConclusionsNeither OST results nor adiponectin varies with season; however, there were a substantial number of horses with variable ID status throughout the year, in which repeated OSTs may be beneficial. Lack of exercise was a risk factor for ID.

Interaction between Vascular Endothelial Growth Factor-A (rs2010963) Gene Polymorphisms and Dietary Diversity Score on Cardiovascular Risk Factors in Patients with Metabolic Syndrome

Background: The vascular endothelial growth factor-A (VEGFA) family of cytokines regulates proliferation, angiogenesis, and migration of endothelial cells, increases vascular permeability, and controls thrombogenicity. Recent studies have suggested that the VEGFA gene plays an important role in the pathogenesis of metabolic syndrome and its related disorders. Dietary diversity score (DDS) has also been shown to have potential favorable effects against features of metabolic syndrome. This study examined the interactions between +405 VEGFA C/G (rs2010963) polymorphism and DDS on the metabolic and biochemical profile of metabolic syndrome. Therefore, in the current study, we aimed to evaluate the interaction between DDS and VEGFA rs2010963 gene polymorphisms in modification of metabolic risk factors including serum lipids, blood pressure, serum adiponectin, and matrix metalloproteinase (MMP)-3 concentrations in patients with metabolic syndrome. Methods and Materials: In the current cross-sectional study, 254 patients with metabolic syndrome were recruited. Measurements of blood pressure, anthropometric parameters, and dietary intakes were performed and the DDS was calculated. Biochemical variables including serum adiponectin concentrations, lipid profile, serum glucose, and MMP-3 concentrations were measured by enzyme-linked immunosorbent assay method (ELISA) and enzymatic colorimetric methods. Determination of +405 C/G VEGFA gene polymorphisms was performed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: Patients in the lowest DDS quartile had higher insulin and homeostatic model assessment of insulin resistance (HOMA-IR), while patients in the highest DDS quartile had higher quantitative insulin check index (QUICKI; p < 0.05). Higher serum triglyceride and systolic blood pressure (SBP) values and lower serum adiponectin concentrations were also observed in lower DDS quartiles (p < 0.05). Patients with the CC genotype in the VEGFA rs2010963 polymorphism had significantly higher body mass index (BMI), fasting blood glucose, aspartate aminotransferase (AST), and alanine aminotransferase (ALT; p < 0.05) compared to patients with the other 2 genotypes. In lower quartiles of DDS, 30% of patients with metabolic syndrome had the GG genotype, while 30.4 and 30.8% of patients with metabolic syndrome in higher DDS quartiles had GC and CC genotypes, respectively (p = 0.04). Conclusion: Our study found lower insulin resistance, serum triglyceride, and SBP and higher adiponectin concentrations among patients with metabolic syndrome in highest quartiles of DDS. Moreover, patients with the CC genotype were more likely to have higher BMI, fasting blood glucose, AST, and ALT. This significant interaction gives a possible evidence of a VEGFA-DDS association that may be relevant to metabolic syndrome. Further studies are warranted to clarify the underlying mechanisms of these interactions.

Leptin/adiponectin ratio correlates with hepatic steatosis but not arterial stiffness in nonalcoholic fatty liver disease in Japanese population

Background and aimsCardiovascular disease (CVD) is a leading cause of mortality in nonalcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the relationship of leptin-to-adiponectin (L/A) ratio with hepatic steatosis and arterial stiffness in NAFLD. MethodsThe subjects were 871 Japanese adults who participated in a health survey. Dietary intake, body composition, lipid profile, serum interleukin-6 (IL-6), leptin, and adiponectin were analyzed. NAFLD was defined as fatty liver on ultrasonography in the absence of other causes of steatosis. Arterial stiffness was evaluated by the brachial-ankle pulse wave velocity (baPWV). ResultsThe subjects with NAFLD had a greater body mass index (BMI) and body fat percentage (BFP); a higher intake of daily energy (kcal) and carbohydrates; and a higher prevalence of hypertension, diabetes, and hyperlipidemia. The subjects with NAFLD had higher serum leptin and lower serum adiponectin concentrations and a higher L/A ratio than subjects without NAFLD. The L/A ratio increased with increasing severity of steatosis. The L/A ratio showed positive correlations with BMI and BFP, and a negative correlation with age. Women had higher L/A ratio and BFP levels than men regardless of the presence or absence of NAFLD. There was a weak positive correlation between baPWV and severity of steatosis. BaPWV was strongly correlated with age, while no relation was found between baPWV and L/A ratio. IL-6 level was correlated with baPVW and age, while the correlation between Il and 6 level and L/A ratio was very weak. The L/A ratio was correlated with triglycerides and the ratio of total cholesterol to high-density lipoprotein-cholesterol. ConclusionL/A ratio and arterial stiffness were associated with the severity of steatosis, whereas there was no correlation between L/A ratio and arterial stiffness in NAFLD. These findings suggest that not only leptin and adiponectin but also other factors might be involved in the pathogenesis for atherosclerosis in NAFLD.

Role of adipokines in obstructive airway disease and diabetes mellitus

This review summarizes the state of the current literature relating to the associations of lung disease and adipokines (proteins produced by adipose tissue) in humans. The mechanistic basis for these associations in humans is not established, although a possible role for adipokines has been invoked. Leptin, a pro-inflammatory adipokine, and adiponectin, an anti-inflammatory adipokine, are causally associated with asthma in mice. Although human studies are currently inconclusive, high-serum leptin and low-serum adiponectin concentrations predict asthma, independent of obesity, in select population groups, such as premenopausal women in the United States. In contradistinction, low-serum leptin and high-serum adiponectin concentrations are associated with stable COPD, although these associations are likely confounded by fat mass. Interestingly, leptin may promote systemic and airway inflammation in stable COPD patients. On the other hand, COPD may upregulate systemic and lung adiponectin expression. The precise mechanism and significance of the associations between these adipokines and lung disease at the current stage are confusing and frankly paradoxical in places. It is now known that adipose tissue is not an inert organ simply for energy storage, but regulates systemic inflammation via a variety of secreted proteins (called adipokines). While the associations of obesity and adipokines with cardiovascular, endocrine, and rheumatological diseases are well described, the respiratory effects of obesity and adipokines are less well known. This review will focus on the effect of obesity and adipokines on asthma and chronic obstructive pulmonary disease (COPD) in humans. This area of research needs additional study that may open up novel therapeutic strategies for these lung diseases.

Role of adipokines in obstructive airway disease and diabetes mellitus

This review summarizes the state of the current literature relating to the associations of lung disease and adipokines (proteins produced by adipose tissue) in humans. The mechanistic basis for these associations in humans is not established, although a possible role for adipokines has been invoked. Leptin, a pro-inflammatory adipokine, and adiponectin, an anti-inflammatory adipokine, are causally associated with asthma in mice. Although human studies are currently inconclusive, high-serum leptin and low-serum adiponectin concentrations predict asthma, independent of obesity, in select population groups, such as premenopausal women in the United States. In contradistinction, low-serum leptin and high-serum adiponectin concentrations are associated with stable COPD, although these associations are likely confounded by fat mass. Interestingly, leptin may promote systemic and airway inflammation in stable COPD patients. On the other hand, COPD may upregulate systemic and lung adiponectin expression. The precise mechanism and significance of the associations between these adipokines and lung disease at the current stage are confusing and frankly paradoxical in places. It is now known that adipose tissue is not an inert organ simply for energy storage, but regulates systemic inflammation via a variety of secreted proteins (called adipokines). While the associations of obesity and adipokines with cardiovascular, endocrine, and rheumatological diseases are well described, the respiratory effects of obesity and adipokines are less well known. This review will focus on the effect of obesity and adipokines on asthma and chronic obstructive pulmonary disease (COPD) in humans. This area of research needs additional study that may open up novel therapeutic strategies for these lung diseases.

Leptin and Adiponectin as markers for preeclampsia in obese pregnant women, a cohort study.

Preeclampsia (PE) is a serious complication of pregnancy, the pathogenesis of which is largely unknown. We hypothesize that adipocytokines may play a role in the pathogenesis of PE, particularly in obese women, and evaluate leptin and adiponectin as potential first trimester markers for predicting PE. A cohort of 2503 pregnancies, containing 93 PE pregnancies, was divided into women with normal weight, moderate, or severe obesity. All pregnancies had serum adiponectin and leptin measured in first trimester. Logistic regression was used to model PE with maternal characteristics and concentrations of the biomarkers. In obese women a lower concentration of adiponectin was found in PE pregnancies; the concentration was lowest in the severely obese (p = 0.005). No association was found in normal weight women (p = 0.72). Leptin concentration had no association with PE in normal weight and moderately obese (p = 0.175-0.072), however in women with severe obesity a lower level of leptin was found (p = 0.049). The AUC was 0.73 for the ROC curve of combined maternal characteristics and adiponectin. Using adiponectin in women with moderate to severe obesity the sensitivity was 72.9% and the specificity was 49%. In severely obese women, PE is associated with low serum adiponectin and leptin concentrations in first trimester. This indicates that the inability of adipokine regulation to adapt to severe obesity may play a role in the pathogenesis of PE. Adipocytokines may contribute in identification of risk pregnancies among severe obese.

The relationship between serum adiponectin and postpartum luteal activity in high-producing dairy cows

The aims of the present study were to initially determine the pattern of serum adiponectin concentrations during a normal estrous cycle in high-producing postpartum dairy cows and then evaluate the relationship between the serum concentrations of adiponectin and insulin with the commencement of postpartum luteal activity and ovarian activities in clinically healthy high-producing Holstein dairy cows. During a normal estrous cycle of cows (n = 6), serum adiponectin concentrations gradually decreased (P < 0.05) after ovulation by Day-17 estrous cycle and then increased before the next ovulation. Cows with higher peak of milk yield had lower serum adiponectin concentrations by week 7 postpartum (P = 0.01). Serum adiponectin and insulin concentrations in cows with different postpartum luteal activity (based on the progesterone profile) were evaluated using the following class of cows: normal (≤45 days, n = 11) and delayed (>45 days, n = 11) commencement of luteal activity (C-LA) and four different profiles of normal luteal activity (NLA, n = 5), prolonged luteal phase (n = 6), delayed first ovulation (n = 6), and anovulation (AOV, n = 5). Serum adiponectin concentrations decreased gradually by week 3 postpartum in NLA and then increased; whereas in AOV and delayed first ovulation, they were decreased after week 3 postpartum (P < 0.05). Moreover, serum adiponectin concentrations in NLA were more than AOV at weeks 5 and 7 postpartum (P = 0.05). The increase in the milk yield from weeks 1 to 7 postpartum in prolonged luteal phase (P = 0.05) and AOV (P = 0.04) cows was more than that of NLA cows. Insulin concentrations were almost maintained at a stable level in NLA cows (P > 0.05), whereas they increased in the other groups (P < 0.05). Moreover, adiponectin concentrations in cows with C-LA greater than 45 days decreased more than those with C-LA 45 days or less after week 3 postpartum (P = 0.002). Serum adiponectin concentrations at week 7 postpartum were lower in delayed C-LA (P = 0.01). Milk yield in cows with C-LA greater than 45 days increased more than cows with C-LA 45 days or less postpartum (P = 0.002). Insulin concentrations increased relatively in parallel from weeks 1 to 7 postpartum in cows either with C-LA greater than 45 or with C-LA 45 days or less. We showed for the first time the profile of serum adiponectin concentrations in a normal estrous cycle of dairy cows, and furthermore, it was found that high-producing dairy cows with higher postpartum serum adiponectin concentrations had NLA and earlier C-LA.

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.

Lack of any prognostic relationship between adiponectin receptor (Adipo R1/R2) expression for early/advanced stage gastric cancer.

Adiponectin (ApN) is a complement C1q-related protein, mainly secreted from adipose tissue, that signals through ApN receptor 1 (Adipo-R1) and ApN receptor 2 (Adipo-R2). Low serum ApN concentrations are associated with obesity-related malignancies. However, there are very few studies on any prognostic role of ApN receptors in gastric cancer. The aim of this study is to investigate the relationship between AdipoR1/R2 expression and early/advanced stage gastric cancer in terms of clinicopathologic characteristics and survival. Eighteen patients with early and 39 with advanced stage gastric cancer who underwent surgical gastric resection were included in this study. Adipo-R1 expression was low in 2 of the 18 patients with early stage gastric cancer (11.1%), while 4 had low Adipo-R2 expression (22.2%). In those with advanced stage gastric cancer, 7 of 39 had low Adipo-R1 expression (17.9%) and 16 had low Adipo-R2 expression (41%). Adipo-R2 expression was significantly higher (p=0.011) in moderately differentiated tumors when compared to well-differentiated tumors. While there was nearly a statistically significant relationship between TNM stage (T, tumor size; N, regional lymph node; M, whether distant metastases exist) and Adipo-R2 expression (p=0.054), there was no relationship between Adipo-R1/-R2 expression with tumor stage and survival. Adipo-R1/-R2 expression has no prognostic significance of in early/advanced stage gastric cancer.

Low serum adiponectin concentrations are associated with insulin sensitivity independent of obesity in Sudanese subjects with type 2 diabetes mellitus.

AimsPrevalence of Type 2 diabetes mellitus among Sudanese population was found to be 3.4% and associated with high rates of complications and obesity. Different adipocytokines are secreted from adipose tissues, among them adiponectin, which was shown to have insulins ensitizing properties and anti-inflammatory, anti-atherogenic effect. The aim of this study was to characterize type 2 diabetes in Sudanese diabetic subjects and controls in respect to hormones influencing or influenced by glucose metabolism.Methods104 type 2 diabetic patients (45 men and 59 women), and 75 matched control subjects (34 men and 41 women) were studied. Fasting serum samples were used to measure adiponectin, leptin, insulin, proinsulin, ghrelin and glucose. Body mass index, insulin/proinsulin ratio and (HOMA) insulin resistance and beta cell function were also calculated.ResultsAdiponectin serum concentrations were significantly lower in subjects with type 2 diabetes compared with controls subjects (P = 0.002), comparison between males and females did not reach significant levels in both diabetic (P = 0.06) or controls (P = 0.16) groups. In the diabetic group adiponectin correlated positively with serum glucose, negatively with serum proinsulin and HOMA beta cell function (P = 0.03) respectively and serum ghrelin (P = 0.003), but not with BMI, HOMA insulin resistance, insulin or leptin. In controls serum adiponectin correlated negatively with BMI (P = 0.002) but not with other variables.ConclusionsThe findings of this study suggest that, adiponectin concentrations independent on BMI as a measure of adiposity, were mostly linked to insulin sensitivity and not to insulin resistance in Sudanese type 2 diabetic subjects, where race specific regulation mechanisms or different type 2 diabetes phenotype suggested being a major contributory factor in clarification the findings of this study.

Übergewicht und Prostatakarzinom

Obesity is proposed as a possible risk factor for many tumors. The present review discusses the current knowledge on the clinical and biological impact of obesity on the development and progression of prostate cancer, the role of adipocyte-derived hormones (adipocytokines) in this scenario and the resulting clinical implications. In addition, the results of own experimental and clinical studies on the involvement of adipocytokines (e.g. leptin, adiponectin) in the pathophysiology of prostate cancer are presented. It was found that patients who were diagnosed with prostate cancer at this clinic had higher serum leptin and lower serum adiponectin concentrations. These investigations and other studies have further shown that higher serum levels of the adipocytokine leptin were associated with larger prostate cancer volumes, high-grade classification, biochemical recurrence, metastasis and progression of metastatic prostate tumors, as well as increased mortality. Moreover, there was a strong correlation between the serum level of leptin and serum levels of prostate specific antigen (PSA). Leptin stimulated in vitro the proliferation and inhibited the apoptosis of prostate cancer cells in a dose and time-dependent manner, however, androgen-resistant cell lines responded more strongly. At the molecular level, adipocytokines require the network of tyrosine kinases to accomplish the mitogenic and antiapoptotic effects in prostate cancer cells. Prominent members of the most important signal transduction cascades, such as MAPK, PI3-K and JAK/STAT are activated upon binding of leptin to its receptor on the cell membrane of prostate cancer cells. Adipocytokines such as leptin may serve as additional prognostic parameters for the evaluation of specific therapies for metastatic hormone refractory prostate cancer. The findings presented here are intended as a basis for further studies.

Association of PPAR‐γ gene polymorphisms with obesity and obesity‐associated phenotypes in north indian population

The worldwide increasing prevalence of obesity is considered as a major health problem. Peroxisome proliferator-activated receptor gamma (PPAR-γ) controls adipocyte differentiation and regulates a number of genes associated with energy homeostasis. In this study, we investigated the association of PPAR-γ gene Pro12Ala (rs1801282) and C1431T (rs3856806) polymorphisms with morbid obesity and related phenotypes, in north Indian population. A total of 6,42 subjects, 309, obese and 333 nonobese individuals were included in this case-control study. Insulin, adiponectin, glucose, and lipid levels were estimated using standard protocols. All subjects were genotyped by PCR restriction fragment length polymorphism (PCR-RFLP) method. The ProAla+AlaAla genotypes of PPAR-γ Pro12Ala were significantly associated with higher risk of obesity while C1431T polymorphism did not show any significant association. None of the haplotypes showed association with morbid obesity. However, a strong association of variant genotypes was observed with higher levels of insulin, HOMA-IR, and lower serum adiponectin concentrations. PPAR-γ gene polymorphisms influence obesity and obesity phenotype in a complex manner, probably involving insulin resistance in north Indian population.

P2-477 The association of adiponectin gene polymorphisms (+45T>G and +276G>T) with adiponectin levels but not with characteristics of the insulin resistance syndrome in Northern India

IntroductionAdiponectin, the major adipocyte secretary protein, improves insulin sensitivity and possesses anti-inflammatory and anti atherosclerotic properties. In the present study, we investigated the association of adiponectin gene (APM1) +45T>G (rs2241766)...

Single nucleotide polymorphisms at the ADIPOQ gene locus interact with age and dietary intake of fat to determine serum adiponectin in subjects at risk of the metabolic syndrome

Adiponectin gene expression is modulated by peroxisome proliferator-activated receptor γ, which is a transcription factor activated by unsaturated fatty acids. We investigated the effect of the interaction between variants at the ADIPOQ gene locus, age, sex, body mass index (BMI), ethnicity, and the replacement of dietary saturated fatty acids (SFAs) with monounsaturated fatty acids (MUFAs) or carbohydrates on serum adiponectin concentrations. The RISCK (Reading, Imperial, Surrey, Cambridge, and Kings) study is a parallel-design, randomized controlled trial. Serum adiponectin concentrations were measured after a 4-wk high-SFA (HS) diet and a 24-wk intervention with reference (HS), high-MUFA (HM), and low-fat (LF) diets. Single nucleotide polymorphisms at the ADIPOQ locus -11391 G/A (rs17300539), -10066 G/A (rs182052), -7734 A/C (rs16861209), and +276 G/T (rs1501299) were genotyped in 448 participants. In white Europeans, +276 T was associated with higher serum adiponectin concentrations (n = 340; P = 0.006) and -10066 A was associated with lower serum adiponectin concentrations (n = 360; P = 0.03), after adjustment for age, BMI, and sex. After the HM diet, -10066 G/G subjects showed a 3.8% increase (95% CI: -0.1%, 7.7%) and G/A+A/A subjects a 2.6% decrease (95% CI: -5.6%, 0.4%) in serum adiponectin (P = 0.006 for difference after adjustment for the change in BMI, age, and sex). In -10066 G/G homozygotes, serum adiponectin increased with age after the HM diet and decreased after the LF diet. In white -10066 G/G homozygotes, an HM diet may help to increase adiponectin concentrations with advancing age. This trial was registered at clinicaltrials.gov as ISRCTN29111298.

Relationship between adiponectin and testosterone in patients with type 2 diabetes

This study was designed to investigate the relationship between serum adiponectin and testosterone in patients with type 2 diabetes. Serum level of adiponectin and testosterone were prospectively measured in 65 patients with type 2 diabetes and in 20 healthy subjects. Testosterone was determined by the radio-immunoassay whereas adiponectin levels were determined by enzyme-linked immunosorbent assay (ELISA). The average serum testosterone did not differ between the diabetes and the control group, but the average adiponectin in the diabetes group was lower (14.6 (14.2-15.0) vs. 24.3 (24.05-24.55) ng/mL, P = 0.001). In the diabetes group, the serum adiponectin level in patients with renal dysfunction (22.3 (21.5-23.1) ng/mL) was higher than in patients with no complications (12.1 (11.45-12.75) ng/mL) and than in patients with coronary artery disease (11.2 (10.25-12.15) ng/mL) (P = 0.009). Univariate correlation analysis showed an inverse weak correlation between adiponectin and testosterone concentrations in male diabetic patients (r = -0.27, P = 0.009). There was no significant correlation between adiponectin and testosterone in female patients (r = -0.05, P = 0.167). We conclude that patients with type 2 diabetes have lower serum adiponectin concentration than healthy individuals, and that there is a weak inverse correlation between adiponectin and testosterone serum concentrations in male diabetics.

Serum adiponectin is positively associated with lung function in young adults, independent of obesity: The CARDIA study

RationaleAdipose tissue produces adiponectin, an anti-inflammatory protein. Adiponectin deficiency in mice is associated with abnormal post-natal alveolar development.ObjectiveWe hypothesized that lower serum adiponectin concentrations are associated with lower lung function in humans, independent of obesity. We explored mediation of this association by insulin resistance and systemic inflammation.Methods and MeasurementsSpirometry testing was conducted at years 10 and 20 follow-up evaluation visits in 2,056 eligible young adult participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study. Body mass index, serum adiponectin, serum C-reactive protein (a marker of systemic inflammation), and insulin resistance were assessed at year 15.Main ResultsAfter controlling for body mass index, years 10 and 20 forced vital capacity (FVC) were 81 ml and 82 ml lower respectively (p = 0.004 and 0.01 respectively) in the lowest vs. highest adiponectin quartiles. Similarly, years 10 and 20 forced expiratory volume in one second (FEV1) were 50 ml and 38 ml lower (p = 0.01 and 0.09, respectively) in the lowest vs. highest adiponectin quartiles. These associations were no longer significant after adjustment for insulin resistance and C-reactive protein. Serum adiponectin was not associated with FEV1/FVC or peak FEV1.ConclusionsIndependent of obesity, lower serum adiponectin concentrations are associated with lower lung function. The attenuation of this association after adjustment for insulin resistance and systemic inflammation suggests that these covariates are on a causal pathway linking adiponectin and lung function.

Serum glucocorticoids and adiponectin associate with insulin resistance in children born small for gestational age

Altered glucocorticoid activity is one possible mechanism linking fetal growth restriction with later insulin resistance (IR) and type 2 diabetes. We aimed to investigate whether serum glucocorticoid parameters are related to IR in children born small for gestational age (SGA). A total of 110 children (55 age- and gender-matched pairs born SGA or appropriate for gestational age (AGA) in a case-control setting) were studied at the mean age of 12.2 (s.d. 0.2) years. Serum cortisol, corticosteroid-binding globulin (CBG), free cortisol index (FCI=cortisol/CBG), and glucocorticoid bioactivity (GBA, transactivation assay) were analyzed and related to serum adiponectin and insulin-like growth factor-binding protein 1 (IGFBP1) concentrations and homeostasis model assessment for IR (HOMA-IR) and QUICKI indices. In the pooled study population, GBA correlated well with cortisol and FCI (r=0.681 and 0.586 respectively; P<0.001 for both). Serum cortisol, CBG, FCI, GBA, HOMA-IR, or QUICKI did not differ between the SGA and AGA subjects, but the SGA children had lower body mass index (P=0.005) and waist circumference (WC) (P=0.001). The mean GBA in the highest GBA quartile was higher among the SGA subjects than among the AGA subjects (138.6 vs 96.4 nmol/l cortisol equivalents, P<0.001). In the SGA children, GBA correlated positively with HOMA-IR (r=0.522, P<0.001) and inversely with adiponectin (r=-0.278, P=0.042) (WC/height ratio adjustments), and in logistic regression analysis, higher GBA (odds ratio (OR) 1.3; P=0.013), lower adiponectin (OR 1.4; P=0.038), and lower IGFBP1 (OR 1.9; P=0.010) associated independently with higher HOMA-IR. These findings suggest that increased glucocorticoid activity and low serum adiponectin concentrations associate with IR in SGA children.

Obesity, adipokines, and lung disease.

This review summarizes the state of the current literature relating to the associations of lung disease on obesity and adipokines (proteins produced by adipose tissue) in humans. Obesity is an independent risk factor for asthma. Recent studies suggest that obesity is also an independent risk factor for chronic airflow obstruction, as is seen with chronic obstructive pulmonary disease (COPD). The mechanistic basis for these associations in humans is not established, although a possible role for adipokines has been invoked. Leptin, a proinflammatory adipokine, and adiponectin, an anti-inflammatory adipokine, are causally associated with asthma in mice. Although human studies are currently inconclusive, high-serum leptin and low-serum adiponectin concentrations predict asthma, independent of obesity, in select population groups, such as premenopausal women in the United States. In contradistinction, low-serum leptin and high-serum adiponectin concentrations are associated with stable COPD, although these associations are likely confounded by fat mass. Interestingly, leptin may promote systemic and airway inflammation in stable COPD patients. On the other hand, COPD may upregulate systemic and lung adiponectin expression. The precise mechanism and significance of the associations between these adipokines and lung disease at the current stage is confusing and frankly paradoxical in places. This area of research needs additional study that may open up novel therapeutic strategies for these lung diseases.

Flaxseed supplementation of rats during lactation changes the adiposity and glucose homeostasis of their offspring

Aims The aim of this paper was to evaluate the effects of maternal dietary flaxseed during lactation on endocrine and metabolic factors in the adult offspring. Main methods Lactating rats were divided into: (1) Controls (C), diet containing 20% casein; (2) Flaxseed (F), diet with additional 25% of flaxseed, containing 18.9% protein (13.9% from casein and 5% from flaxseed). The treatment started at birth, day 0 (d0) of lactation, and ended at weaning (d21). After weaning, all pups received a standard laboratory diet until 180 days old. Only male offspring were studied and were sacrificed at 21 or 180 days of age. Body composition was evaluated by carcass analysis. Key findings Offspring from F mothers had higher body mass since lactation until adulthood. At 21 days old, they presented lower total and subcutaneous fat mass, higher leptinemia, lower total cholesterol, lower triacylglycerol and lower insulinemia ( p < 0.05). At 180 days, offspring from F mothers had lower glycemia, higher insulinemia and lower adiponectin ( p < 0.05) concentrations and they did not show any changes in body composition. Significance Maternal intake of flaxseed in the diet during lactation produces early insulin sensitivity and hyperleptinemia; these hormonal imprinting factors could program for selective insulin resistance, since the higher insulin serum concentration was not associated with higher adiposity. These findings, associated with lower serum adiponectin concentration in adulthood, could indicate an increased risk for later development of diabetes mellitus.