Adiponectin Concentrations In Patients Research Articles

Serum Concentrations of Adiponectin in Patients with Hyperthyroidism before and after Control of Thyroid Function

Thyroid hormone affects adipocyte function, which in turn influences lipid and carbohydrate metabolism. Adiponectin is one of the adipocytokines that regulates lipid and carbohydrate metabolism. The aim of our study was to evaluate circulating levels of adiponectin in patients with thyroid dysfunction before and after normalization of thyroid function with appropriate medication. One hundred and twenty patients with hyperthyroidism were recruited at the time of diagnosis. Measurements of free T4 (FT4), thyroid-stimulating hormone (TSH), thyrotropin binding inhibitor immunoglobulin (TBII), adiponectin, fasting blood glucose, fasting serum insulin, lipid profile, and body mass index (BMI) were taken before and after 6 months of medical treatment, at which point all patients were in a euthyroid state. Any change in BMI was strongly correlated with changes in serum-adiponectin levels (r = -0.789, p<0.001). Any change in serum FT4 was also correlated with changes in BMI and serum adiponectin levels (r = -0.254, p = 0.05 and r = 0.501, p = 0.029 respectively). After controlling for BMI changes, we found correlation also between serum FT4 and adiponectin (r = 0.29, p = 0.005). Multivariate-regression analysis still revealed BMI to be a statistically strong predictor for serum-adiponectin level (p<0.001). However, that analysis also revealed thyroid function level as another predictor (p = 0.029). Although BMI is the best predictor of adiponectin, that thyroid hormone might influence circulating levels of adiponectin.

Clinical Implication of Adiponectin

Adipose tissue is now considered as an active hormone-secreting organ, which secretes a number of biologically active adipokines such as free fatty acids, leptin, tumor necrosis factor alpha (TNFα), interleukin-6, plasminogen activator inhibitor-1, adiponectin and retinol binding protein 4 (RBP4). Among these, adiponectin has attracted considerable attention as an adipokin e that has important role in the development of type 2 diabetes, atherosclerosis and cardiovascular diseases. Adiponectin was discovered to be the most abundant adipose-specific transcript. Many epidemiological and clinical studies have demonstrated that serum levels of adiponectin are inversely associated with body weight, especially abdominal visceral fat accumulation. Studies among Japanese and Pima Indians have reported lower concentrations of adiponectin in patients with type 2 diabetes than in those with normal glucose tolerance. A low level of adiponectin was found to be a significant risk factor for the development of cardiovascular events in the Korean patients with type 2 diabetes. We recently published that exercise, having an insulin-sensitizing effect, could be a good therapy to prevent or delay diabetes and cardiovascular diseases in middle-aged women through the modification of adiponectin. These results suggest that the clinical implication of adiponectin. A number of studies have been conducted to clarify the biological role of adiponectin. Recent studies have showed that adiponectin has anti-inflammatory, anti-atherogenic, and glucos e-lowering properties. Taken together, it is conceivable that adiponectin plays as a backbone of metabolic syndrome. Finally, pleiotropic functions of adiponectin may possibly serve to prevent and treat atherosclerosis, type 2 diabetes and cardiovascular diseases. Furthermore, enhancement of adiponectin secretion or action may be a good therapeutic target for preventing type 2 diabetes or cardiovascular diseases. (KOREAN DIABETES J 32:85-97, 2008)

Plasma adiponectin concentration in patients after successful kidney transplantation – a single-center, observational study

Adiponectin is an anti-inflammatory protein secreted almost exclusively by adipocytes which improves insulin sensitivity and presents antiatherogenic properties. Plasma adiponectin concentration is almost 3 times higher in hemodialysis patients and markedly decreased after successful kidney transplantation. However, until now, there are no studies analyzing plasma adiponectin concentration in kidney transplant patients (KTx) during the long-term period after transplantation. Therefore, the aim of present study was to examine plasma adiponectin concentration in KTx patients during the wide range of time after transplantation. Single center, cross-sectional study including 228 KTx adult recipients (143 M and 85 F) with estimated glomerular filtration rate (eGFR) > or = 15 ml/min, 80 hemodialysis patients (34 M and 46 F) and 52 healthy subjects (33 M and 19 F). Plasma adiponectin concentration was estimated together with HOMA-IR (homeostasis model assessment insulin resistance index) and plasma lipid profile. In KTx patients plasma adiponectin concentration 14.0 (13.1-15.0) microg/ml was significantly (p < 0.001), lower than in hemodialysis ones 29.0 (24.7-33.3) microg/ml, however, significantly (p < 0.001) higher than in healthy subjects 10.1 (8.8-11.5) microg/ml. Among KTx patients the highest plasma adiponectin concentration was observed in the subgroup of patients surviving with the functioning graft more than 8 years after transplantation. In KTx patients, significant, negative correlations were found between plasma adiponectin concentration and BMI (p = 0.017), HOMA-IR (p = 0.02) and estimated GFR (p < 0.009), respectively. Multiple regression analysis performed in the group of KTx patients, with plasma adiponectin concentration as the dependent variable and BMI, age, gender, estimated GFR as independent variables showed that in this model (R2 = 0.09) plasma adiponectin concentration significantly depends on BMI (p = 0.035), gender (p = 0.004) and eGFR (p = 0.023). Patients with long-term renal graft survival are characterized by a higher plasma adiponectin concentration. Kidney graft function (assessed as estimated GFR) is an important factor influencing plasma adiponectin concentration.

Serum resistin and adiponectin concentrations in patients with overweight and obesity

Objective To explore the serum levels of resistin and adiponectin in patients with overweight and obesity. Methods Fifty-eight cases with normal weight and 24 patients with overweight and obesity have taken fasting blood samples for measurements of plasma glucose, plasma lipids, insulin, C-peptide, thyroid hormones, C-response protein, interleukin-6, TNF-α, leptin, adiponectin and resistin. Results The concentrations of resistin in cases with overweight and obesity were significant higher than those in the normal weight cases (16.01 ± 8.60 vs 11.63 ± 9.05 ng/ml, P = 0.047). Pearson relation analysis showed that serum resistin concentrations were positively correlated with age ( r = 0.476, P = 0.019), but negatively correlated with C-peptide ( r = −0.45, P = 0.024), and adiponectin concentrations were positively correlated with HDL-c ( r = 0.463, P = 0.023) and systolic blood pressure ( r = 0.409, P = 0.047) in overweight and obesity cases. Conclusion The concentrations of resistin in cases with over-weight and obesity are higher, and there is no correlation between resistin and blood glucose, blood lipids and insulin, while the serum adiponectin concentrations positively correlated with HDL-c and systolic blood pressure.

Hypoadiponectinemia

Hypertension is a public health challenge of increasing importance because of its high frequency and concomitant risk of cardiovascular and renal disease. It has been estimated that the worldwide prevalence of hypertension was 972 million in 2000, and this number will increase by 60% by the year 2025.1 A large body of evidence indicates that the increasing prevalence of hypertension is sustained by the escalation of overweight and obesity. Actually, most hypertensive patients are also overweight or obese,2 and this may contribute to further deteriorate their cardiovascular risk profile. Similar to hypertension, obesity is independently associated with numerous adverse cardiovascular outcomes, and, most importantly, adipose tissue expansion and hypertension have a synergistic negative impact on cardiovascular prognosis. Hence, the hypertension–obesity pandemic imposes today a considerable burden on societies and healthcare systems that one can reasonably expect to increase further in the next years. The importance of preventing hypertension underscores the critical role of a better understanding of the most common mechanisms underlying its development. The association between obesity and hypertension has been recognized for many decades,2 and an almost linear relation appears between body mass index and systolic and diastolic blood pressures, at least over a body mass index range from 16 to 31 kg/m2.3 Also, risk estimates from the Framingham Heart Study suggest that ≈78% of the hypertension cases in men and 65% in women can be directly attributed to obesity.4 Further evidence for a consistent link between adiposity and hypertension comes from studies showing that weight gain is almost invariably associated with an increase in blood pressure. The increase in blood pressure is closely related to the magnitude of weight gain, and even moderate weight gain is associated with an increased risk of developing hypertension.5 In addition, even modest weight …

Increase in serum adiponectin concentration in patients with heart failure and cachexia: relationship with leptin, other cytokines, and B-type natriuretic peptide

Adiponectin is a fat-derived hormone involved in the regulation of metabolism. Adiponectin concentration is inversely related to body weight and, in animals, causes weight loss. We, therefore, measured adiponectin concentration in patients with heart failure (HF) and cachexia. Serum adiponectin concentrations were measured in three groups of patients with coronary artery disease (CAD): (i) HF, reduced left ventricular systolic function, and cachexia (n = 10); (ii) HF, reduced systolic function but no cachexia (n = 20); (iii) HF-controls-patients with CAD, no HF, and preserved systolic function (n = 10); and in a healthy control group (n = 7). Patients with HF and cachexia had higher concentrations of adiponectin [23.8 (10.2-37.2) microg/mL] than all other groups: HF-no cachexia 8.1 (0.5-16.6) microg/mL; CAD-controls 7.1 (0.4-13.5) microg/mL; and healthy controls 8.7 (2.5-16.8) microg/mL) (P < 0.05 for each comparison). Adiponectin correlated negatively with body mass index, percentage of body fat, waist circumference and insulin resistance, and positively with B-type natriuretic peptide (BNP) and tumour necrosis factor-alpha. Cachexia in HF is associated with an increase in adiponectin concentration. This may represent preservation of the physiological response to change in body fat but might also suggest that adiponectin plays a role in the pathogenesis of cachexia. The correlation between BNP and adiponectin also raises the possibility that the former might increase the secretion of the latter.

Indapamide Decreases Plasma Adiponectin Concentration in Patients with Essential Hypertension

Background/Aim: Adiponectin is an adipose tissue-specific protein with antiatherogenic and insulin-sensitizing properties. In patients with essential hypertension, plasma adiponectin concentrations are lower than in healthy subjects. Antihypertensive drugs do not uniformly influence components of the metabolic syndrome. Therefore, the aim of this study was to evaluate the influence of 6 months’ monotherapy with different antihypertensive drugs on plasma adiponectin concentration in essential hypertension patients. Methods: Forty essential hypertension patients were randomized to receive enalapril, metoprolol, amlodipine or indapamide. Plasma concentrations of adiponectin, insulin, glucose and body fat content were estimated twice: before and after 6 months of antihypertensive monotherapy. Results: Plasma adiponectin concentration did not change significantly after enalapril (11.5 ± 4.8 vs. 11.1 ± 4.1 mg/l), metoprolol (10.2 ± 4.2 vs. 9.8 ± 4.5 mg/l), and amlodipine (9.0 ± 6.0 vs. 8.5 ± 5.4 mg/l) treatment. However, a significant decrease of plasma adiponectin concentration (from 11.6 ± 4.6 to 10.2 ± 4.2 mg/l, p = 0.047) was observed in patients treated with indapamide. Additionally in these patients, a significant increase of the HOMA-IR index was found (p = 0.021). Conclusion: Treatment with indapamide was followed by a significant decrease of plasma adiponectin concentration. This may participate in the pathogenesis of carbohydrate metabolism disturbances often found in patients treated with thiazide-type diuretics.

Elevated circulating adiponectin in type 1 diabetes is associated with long diabetes duration

To study circulating adiponectin concentrations in relation to diabetes duration and endogenous insulin secretion in patients with type 1 diabetes. Patients with haemoglobin A1c (HbA1c) < 6% (reference range 3.6-5.4%) were selected for the study. Twenty-two men and 24 women [age 41.3 +/- 13.8 years (mean +/- SD), diabetes duration 4 months to 52 years] participated. Healthy controls (15 women and nine men, age 41.3 +/- 13.0 years) were also included. Overnight fasting serum samples were analysed for adiponectin, HbA1c, C-peptide and lipoproteins. Significant positive associations were found between adiponectin concentrations and diabetes duration in univariate and multiple regression analyses. Serum adiponectin averaged 9.7 +/- 5.3 [median 8.1, interquartile range (IQR) 3.6] mg/l in patients with diabetes duration less than 10 years and 17.8 +/- 10.7 (median 14.7, IQR 7.5) mg/l in patients with longer duration (P = 0.0001). Among the patients, 24 were without detectable (< 100 pmol/l) and 22 with detectable C-peptide levels (185 +/- 91 pmol/l). C-peptide levels in controls averaged 492 +/- 177 pmol/l. HbA1c was 5.7 +/- 0.6% in patients without detectable C-peptide and 5.6 +/- 0.4% in patients with detectable C-peptide (ns). Serum adiponectin was higher in patients without detectable C-peptide than in patients with detectable C-peptide [17.3 +/- 11.1 vs. 10.6 +/- 5.8 mg/l (P < 0.005)] and in the controls [10.1 +/- 2.9 mg/l (P < 0.001 vs. patients without detectable C-peptide)]. The increase in circulating adiponectin concentrations in patients with type 1 diabetes appears to be strongly associated with long diabetes duration, irrespective of the metabolic control. Among other factors, a putative role for residual beta-cell function in the regulation of circulating adiponectin levels can be considered but we did not find sufficient evidence for this in the present study.

Steroid pulse therapy impaired endothelial function while increasing plasma high molecule adiponectin concentration in patients with IgA nephropathy

Decreased plasma adiponectin is associated with impaired endothelial function and, thereby, increased risk for cardiovascular events. Glucocorticoid (GC) affects vascular endothelial cells either favourably or harmfully depending upon the dosages and duration. We examined the effect of GC pulse therapy on vascular endothelial function. Fourteen young patients with IgA nephropathy were evaluated for flow-mediated vasodilation (FMD), plasma levels of adiponectin both in high molecular weight (HMW adiponectin) form and in single molecular form (total adiponectin), hepatocyte growth factor (HGF), asymmetric dimethylarginine (ADMA), and high-sensitive C-reactive protein, before and after a course of GC pulse therapy. GC pulse therapy significantly decreased FMD (from 7.2 +/- 2.6 to 5.7 +/- 2.5%, P < 0.01). Meanwhile, plasma adiponectin levels were significantly augmented (total adiponectin: from 10.2 +/- 4.0 to 12.1 +/- 6.3 microg/ml, P < 0.05; HMW: from 6.5 +/- 3.2 to 7.7 +/- 3.3 microg/ml, P < 0.05). In parallel, elevated concentrations of serum HGF (from 0.28 +/- 0.12 to 0.63 +/- 0.38 ng/ml, P < 0.01) and plasma ADMA (from 0.45 +/- 0.07 to 0.53 +/- 0.04 nmol/ml, P < 0.05) were observed. GC pulse therapy impaired endothelial function while increasing plasma adiponectin levels, which may in turn restore the endothelial function in patients with IgA nephropathy.

The effect of 6 months of treatment with pravastatin on serum adiponection concentrations in Japanese patients with coronary artery disease and hypercholesterolemia: A pilot study

Background: Pravastatin has been reported to reduce cardiovascular events and mortality in patients with coronary artery disease (CAD). Hypoadiponectinemia is a known risk factor for CAD Objective: This study analyzed the effects of shortterm pravastatin treatment on serum lipid and adiponectin concentrations in patients with CAD and hypercholesterolemia. Methods: This was a multicenter, observational pilot study of the effect of 6 months of treatment with pravastatin 10 to 20 mg/d on serum adiponection concentrations in patients with documented CAD and total cholesterol (TC) levels≥180 mg/dL. Patients from 13 medical centers in Japan were monitored at visits every 4 weeks for assessment of compliance and adverse effects. For the assessment of pravastatin's effects, patients were categorized according to baseline serum adiponectin concentrations: quartile 1 (Q1)=<4.83 μg/mL; quartile 2 (Q2)=4.83 to 7.20 μg/mL; (Q4)=>10.38 μg/mL. The primary end point of the study was the percent change from baseline in adiponectin nectin concentrations at 6 months. Secondary end points were changes in lipids, high-sensitivity C-reactive protein (hsCRP), and glycosylated hemoglobin (HbA 1c). Results: One hndred thirty consecutive patients were enrolled; 11 were excluded and 4 discontinued due to adverse events. Thus, 115 patients were included in the study analyses (83 men, 32 women; mean age, 68 years). No patient had a cardiac event during the 6-month follow-up period. After 6 months of pravastatin treatment, 74 (64.3%) patients had increases in serum adiponectin concentrations. Median (interquartile range) adiponectin concentrations increased significantly from 7.2 (4.8-10.4) μg/mL at baseline to 7.8 (5.4–11.2) μg/mL after 6 months of pravastatin treatment ( P<0.001); the mean percent increase from baseline was 16.3%. The percent increase from baseline in serum adiponection concentrations was significantly higher among patients in Q1 (39.3%) compared with those in Q3 (4.5%) and Q4 (6.3%) ( P<0.003 and P<0.005, respectively). The relative increase in adiponectin concentrations was significantly correlated with the relative increase in high-density lipoprotein cholesterol (HDL-C) ( f=0.47; P<0.001). After 6 months of pravastatin treatment, TC and lowdensity lipoprotein cholesterol levels had decreased, by 14.6% and 23.3%, respectively, and HDL-C levels had increased by 14.0% (all, P<0.001). The change in triglycerides (-13.3%) was not statistically significant. Serum hsCRP levels were significantly decreased from baseline after 6 months of pravastatin treatment ( P<0.001). HbA 1c did not change significantly. Conclusion: In this pilot study in Japanese patients with CAD and hypercholesterolemia, 6 months of treatment with pravastatin 10 to 20mg/d was associated with significant increases in serum adiponectin concentrations.

Comparison of Serum High–Molecular Weight (HMW) Adiponectin With Total Adiponectin Concentrations in Type 2 Diabetic Patients With Coronary Artery Disease Using a Novel Enzyme-Linked Immunosorbent Assay to Detect HMW Adiponectin

Adiponectin (Acrp30), an adipocyte-derived protein, exists in serum as a trimer, a hexamer, and a high-molecular weight (HMW) form, including 12-18 subunits. Because HMW adiponectin may be biologically active, we measured it in serum using a novel enzyme-linked immunosorbent assay (ELISA) confirmed by gel filtration chromatography that the ELISA detected mainly adiponectin with 12-18 subunits, and we compared HMW with total adiponectin concentration in patients with type 2 diabetes. We next investigated the relationship between serum HMW and coronary artery disease (CAD) in 280 consecutive type 2 diabetic patients, including 59 patients with angiographically confirmed CAD. Total adiponectin was measured in serum by a commercially available ELISA. Like serum total adiponectin, HMW adiponectin correlated positively with HDL cholesterol and negatively with triglyceride, insulin sensitivity, creatinine clearance, and circulating inflammatory markers. Total and HMW adiponectin were significantly higher in women than in men, as was the HMW-to-total adiponectin ratio. Serum HMW and the HMW-to-total adiponectin ratio were significantly lower in men with than without CAD (P < 0.05, respectively). In women, the ratio, but neither total nor HMW adiponectin, tended to be lower when CAD was present. In conclusion, determination of HMW adiponectin, especially relative to total serum adiponectin, is useful for evaluating CAD in type 2 diabetic patients.

Decrease in Plasma Adiponectin Concentrations in Patients with Vasospastic Angina

Background and Objectives:Plasma adiponectin, which decreases the progression of atherosclerosis and insulin resistance, as well as suppressing lipid accumulation in macrophages, is decreased in patients with acute myocardial infarction and unstable angina pectoris; however, the correlation between plasma adiponectin and vasospastic angina pectoris (VAP) remains to be verified. We compared the plasma adiponectin concentration between patients with VAP and other coronary artery diseases; moreover, we investigated the association between the plasma adiponectin concentration and VAP. Subjects and Methods:Following coronary angiography for the evaluation of chest pain, 395 subjects (180 women and 215 men) were divided into 4 groups: acute coronary syndrome (ACS)(n=117), VAP (n=94), stable angina pectoris (SAP)(n=108) and angiographically normal coronary artery (n=76). The acetylcholine provocation test was used to confirm VAP, and plasma adiponectin concentrations were measured in all participants. Results:The plasma adiponectin concentrations in patients with VAP and ACS were significantly lower than that of the normal coronary artery group (6.6±5.4 vs. 5.2±4.0 vs. 9.0±6.2 μg/mL, p<0.001, respectively). A multivariate analysis indicated that plasma adiponectin [odd ratio (OR) 0.744, 95% confidence interval (CI) 0.645 to 0.858, p=0.001], smoking (OR 2.054, 95% CI 1.027 to 4.106, p=0.042) and age (OR 0.966, 95% CI 0.935 to 0.997, p=0.031) were independently correlated in patients diagnosed with VAP. Conclusion:Our results suggest that a decreased plasma adiponectin concentration may be associated with VAP. (Korean Circulation J 2006;36:255-260)

Rilmenidine increases plasma adiponectin concentrations in patients with hypertension,

Rilmenidine increases plasma adiponectin concentrations in patients with hypertension,

Blockade of Sympathetic Nervous System Activity by Rilmenidine Increases Plasma Adiponectin Concentration in Patients With Essential Hypertension

Adiponectin is an adipose tissue-specific protein with antiatherogenic and insulin-sensitizing properties. In patients with essential hypertension plasma adiponectin levels are lower than in healthy subjects. It is hypothetized that low plasma adiponectin concentration may be involved in the pathogenesis of vascular complications in hypertension. The aim of the study was to evaluate the effect of 6 months of antihypertensive therapy with rilmenidine on plasma adiponectin concentration in patients with essential hypertension. In 20 patients with essential hypertension (mean age 39 +/- 14 years; 11 F, 9 M; mean duration of hypertension 8 +/- 9 years) plasma adiponectin concentration (ELISA; B-Bridge International, San Jose, CA), insulin sensitivity (metabolic clearance of glucose-M value and M/plasma insulin ratio) by the euglycemic-hyperinsulinemic glucose clamp technique, and body fat content (DEXA) were estimated twice, before and after 6 months of antihypertensive monotherapy with rilmenidine (daily dose 1 to 2 mg). The 6 months of treatment with rilmenidine resulted in a significant decrease of systolic (P = .007), diastolic (P = .002), and mean arterial blood pressure (P = .002), no significant change of body mass index (27.7 +/- 4.7 and 27.6 +/- 4.4 kg/m(2)), total body fat content (25.4 +/- 7.3 and 24.9 +/- 6.8 kg), and insulin sensitivity parameters (M value 6.0 +/- 2.5 and 5.8 +/- 4.3 mg/kg/min and M/plasma insulin ratio 7.4 +/- 5.0 and 6.9 +/- 4.3 mg/kg/min/mU/L). However after 6 months of treatment with rilmenidine a significant increase in plasma adiponectin concentration (from 12.5 +/- 6.1 to 16.9 +/- 11.1; P = .0002) was observed. Antihypertensive therapy with rilmenidine correlates with an increase of plasma adiponectin concentration without any significant changes of insulin sensitivity and body fat content in patients with essential hypertension.

Adiponectin. Spectator or Player?

Adiponectin. Spectator or Player?

Elevated plasma adiponectin concentrations in patients with liver cirrhosis correlate with plasma insulin levels

Adiponectin is a hormone secreted by adipocytes and has anti-diabetic and anti-atherogenic properties. Hypoadiponectinemia is associated with insulin-resistant diabetes and liver dysfunction. The aim of this study was to determine plasma adiponectin and insulin levels in patients with liver cirrhosis. Adiponectin and insulin levels were determined in 38 patients with cirrhosis and 30 healthy controls, and were correlated with various clinical and biochemical parameters. Patients included 21 with Child A, eight Child B, and nine with Child C liver cirrhosis. Log adiponectin and insulin levels were significantly elevated in patients with cirrhosis compared with the control. In liver cirrhosis, the level of adiponectin increased proportionately with the Child's classification score. In control subjects, plasma adiponectin correlated inversely with insulin levels. In contrast, plasma adiponectin correlated positively with insulin levels in patients with liver cirrhosis. Plasma adiponectin levels did not correlate with age, sex, body mass index, total bilirubin, aspartate aminotransferase, and fasting blood sugar levels in both groups, while alanine aminotransferase correlated negatively with adiponectin in control subjects as reported previously. Our results of high plasma adiponectin in patients with liver cirrhosis could reflect an imbalance between its production by adipocytes and metabolism in the liver.

Plasma Adiponectin Concentrations in Patients with Chronic Renal Failure: Relationship with Metabolic Risk Factors and Ischemic Heart Disease

To compare plasma adiponectin levels between healthy controls and patients with chronic renal failure and to examine for a relationship between plasma adiponectin levels and ischemic heart disease as well as aortic distensibility which is an early marker of atherosclerosis. We included 89 patients with CRF (45 on and 44 not on hemodialysis) and 70 controls in a cross-sectional study. Plasma adiponectin levels were measured by radioimmunoassay. Aortic distensibility was assessed by high-resolution ultrasonography. Plasma adiponectin levels were significantly almost twice as high in patients with renal failure compared to controls (9.7 +/- 1.1 vs. 5.4 +/- 0.6 microg/ml, p < 0.0001). No significant differences were found between renal patients on hemodialysis and not on hemodialysis (p = 0.71). Multivariate linear regression analysis in the renal patient group demonstrated a significant negative relationship between plasma adiponectin levels and ischemic heart disease (p = 0.02). The same analysis in the control subjects group showed a significant, negative relationship between plasma adiponectin levels and body mass index (p = 0.02) and a highly significant positive relationship with the high density lipoprotein cholesterol (p < 0.0001). In the total study population, glomerular filtration rate was the only independent predictor of plasma adiponectin concentrations. Aortic distensibility was lower in renal patients than in controls at a high level of significance (p < 0.0001). However, no significant relationship could be found between plasma adiponectin and aortic distensibility in either the controls or the renal patients. Plasma adiponectin levels are almost twice as high in patients with chronic renal failure in comparison with healthy controls, but not different between renal patients on and those not on hemodialysis. In addition, low plasma adiponectin levels are strongly associated with ischemic heart disease, but not with aortic distensibility in chronic renal failure.

Adiponectin may play a part in the pathogenesis of diabetic retinopathy.

To measure plasma adiponectin concentrations in patients with type 2 diabetes and to investigate any association with the severity of diabetic retinopathy, because adiponectin seems to be an important modulator for metabolic and vascular diseases. Seventy-four patients (mean age 46.8+/-5.1 years; body mass index (BMI), 26.8+/-2.10 kg/m(2)) and 54 healthy volunteers (mean age 46.8+/-5.4 years; BMI 26.47+/-2.33 kg/m(2)) were included. Adiponectin concentrations in the patients were significantly lower than those in controls (4.71+/-2.11 microg/ml for patients, n=74; 15.95+/-3.72 microg/ml for controls, n=54; P<0.001). In the patients group there was a significant negative correlation between adiponectin and homeostasis model assessment index (r=-0.318, P=0.006 respectively). Plasma adiponectin concentrations in patients with proliferative diabetic retinopathy (n=20; 3.16+/-1.83 microg/ml) or non-proliferative diabetic retinopathy (n=24; 3.97+/-1.47 microg/ml, P=0.014) were significantly lower than those in patients without diabetic retinopathy (n=30; 6.30+/-1.57 microg/ml, P=0.001). When the presence of diabetes was defined as the final variable in the conditional logistic regression model with the adiponectin concentration as the continuous variable, adiponectin was significantly involved in the model. The results show that adiponectin concentrations are lower in patients with type 2 diabetes and that the concentrations are associated with the severity of diabetic retinopathy. Our findings suggest that adiponectin may take part in the pathogenesis of diabetic retinopathy.

Blockade of the renin-angiotensin system increases adiponectin concentrations in patients with essential hypertension.

Adiponectin, an adipocyte-derived protein, has been suggested to play an important role in insulin sensitivity. We examined the association between insulin sensitivity (M value) evaluated by the euglycemic-hyperinsulinemic glucose clamp and adiponectin concentrations in 30 essential hypertensives (EHT) and 20 normotensives (NT) and investigated the effect of blockade of the renin-angiotensin system (RAS) on adiponectin concentrations. EHT were divided into 12 insulin-resistant EHT (EHT-R) and 18 non-insulin-resistant EHT (EHT-N) using mean-1 SD of the M value in NT. There were no intergroup differences in age, gender, and body mass index (BMI). EHT-R had significantly higher levels of insulin and triglyceride and lower levels of adiponectin than did NT and EHT-N. EHT-R had higher levels of free fatty acid and lower levels of high-density lipoprotein (HDL) cholesterol than did EHT-N. Adiponectin concentrations were positively correlated with M value and HDL cholesterol and negatively correlated with BMI, insulin, free fatty acid, and triglyceride but not with blood pressure. M value, BMI, and HDL cholesterol were independent determinants of adiponectin concentrations in multiple and stepwise regression analyses. Sixteen EHT were treated with an angiotensin-converting enzyme inhibitor (temocapril, 4 mg/d; n=9) or an angiotensin II receptor blocker (candesartan, 8 mg/d; n=7) for 2 weeks. Treatment with temocapril or candesartan significantly decreased blood pressure and increased M value and adiponectin concentrations but did not affect BMI and HDL cholesterol. These results suggest that hypoadiponectinemia is related to insulin resistance in essential hypertension and that RAS blockade increases adiponectin concentrations with improvement in insulin sensitivity.

Decreased plasma adiponectin concentration in patients with essential hypertension

Adipocytes secrete several biologically active substances that are presumed to be involved in obesity-related hypertension. There are no reports that deal with the relationship between plasma adiponectin concentration and blood pressure (BP).To evaluate the role of adiponectin in essential hypertension 33 patients with essential hypertensive (EHP) (12 women, 21 men) and 33 body mass index-matched normotensive healthy subjects (NHS) (13 women, 20 men) were studied.In EHP plasma adiponectin concentration was significantly lower than in NHS (9.1 ± 4.5 v 13.7 ± 5.2 μg/mL, respectively). In all subjects a significant negative correlation was found between plasma adiponectin concentration and mean, systolic, and diastolic BP, suggesting that adiponectin contributes to the clinical course of essential hypertension.