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Opposite changes in circulating adiponectin in women with bulimia nervosa or binge eating disorder.

Adiponectin is a recently discovered peripheral peptide that is secreted exclusively by differentiated adipocytes. It has been shown to enhance insulin sensitivity, control body weight, regulate lipid homeostasis, and prevent atherosclerosis. Dysregulation of both lipid and glucose metabolism and changes in body weight and body fat mass have been reported in bulimia nervosa (BN) and/or binge eating disorder (BED); hence, investigation of adiponectin secretion is of obvious interest in these eating disorders. To this purpose, we measured plasma levels of adiponectin, glucose, cholesterol, triglycerides, and thyroid hormones in 60 drug-free women, including 20 patients with BN, 20 patients with BED, and 20 healthy controls. Compared with healthy women, BN women exhibited significantly increased circulating adiponectin levels (P < 0.002) and cholesterol concentrations (P < 0.005), whereas BED women had significantly reduced plasma levels of adiponectin (P < 0.005) and increased concentrations of glucose (P < 0.01), cholesterol (P < 0.05), and triglycerides (P < 0.02). Moreover, plasma levels of adiponectin were significantly correlated to the frequency of binge/vomiting episodes (r = 0.65, P = 0.002) in bulimics but not to the frequency of bingeing in BED patients. Because we did not include a group of obese patients who did not binge eat, the specificity of our findings in the BED should be considered cautiously. However, on the basis of present results, it is tempting to speculate that the increased production of adiponectin in BN may represent a compensatory mechanism to counteract the possible development of insulin resistance, whereas the decreased secretion of adiponectin in individuals with BED may be a risk factor for the development of glucose intolerance.

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Plasma adiponectin concentrations in early pregnancy and subsequent risk of gestational diabetes mellitus.

Low plasma adiponectin has been identified as a risk factor for type 2 diabetes. Our objective was to determine the extent to which low maternal plasma adiponectin is predictive of gestational diabetes mellitus (GDM), a condition that is biochemically and epidemiologically similar to type 2 diabetes. We used a prospective, nested case-control study design to compare maternal plasma adiponectin concentrations in 41 cases with 70 controls. Subjects were selected from a population of 968 women who provided blood samples in early pregnancy. Plasma adiponectin was determined using an ELISA. Adiponectin concentrations were statistically significantly lower in women with GDM than controls (4.4 vs. 8.1 micro g/ml, P < 0.001). Approximately 73% of women with GDM, compared with 33% of controls, had adiponectin concentrations less than 6.4 micro g/ml. After adjusting for confounding, women with adiponectin concentrations less than 6.4 micro g/ml experienced a 4.6-fold increased risk of GDM, as compared with those with higher concentrations (95% confidence interval, 1.8-11.6). Our findings are consistent with other reports suggesting an association between hypoadiponectemia and risk of type 2 diabetes. Our findings extend the literature to include GDM. Studies designed to examine the effect of dietary and pharmacological mediators of adiponectin concentrations in pregnant and nonpregnant subjects are warranted.

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Association between circulating adiponectin and interleukin-10 levels in android obesity: effects of weight loss.

OBJECTIVE: Adiponectin inhibits vascular inflammation and increases IL-10 mRNA expression in human macrophages. Thus, we investigated the possible relationship between plasma adiponectin and IL-10 levels and the effects of a diet-induced moderate weight loss on both cytokines. PATIENTS AND STUDY DESIGN: Plasma adiponectin and IL-10 levels were analyzed in 64 android [body mass index (BMI), > 28 kg/m2; waist to hip ratio (WHR), > or = 0.86] and 20 gynoid [BMI, > 28 kg/m2; WHR, < 0.86] obese healthy women. Android obese women (49 +/- 14 yr) had a mean BMI of 37.1 +/- 5.3 kg/m2, similar to that of gynoid obese women (49 +/- 11 yr; BMI, 33.4 +/- 2.6 kg/m2). Twenty nonobese control women (46 +/- 11 yr; BMI, 25.2 +/- 2.2 kg/m2) were also studied. In 15 android obese women, measurements were repeated after a 12-wk diet period (1200 kcal/d). RESULTS: Median adiponectin [5.2 (range, 3.3-7.8) vs. 12.1 (9.7-13.9) vs. 15.0 (12.6-18.2) microg/ml; P < 0.0001] and IL-10 [1.8 (1.2-3.3) vs. 3.5 (2.9-4.3) and vs. 4.1 (3.5-4.8) pg/ml; P < 0.0001] levels were lower in android vs. gynoid vs. nonobese women. Among android obese women, low adiponectin levels were independently related (P < 0.0001) to decreased IL-10 levels, independently of BMI, WHR, or insulin resistance. No significant change in either median adiponectin or IL-10 levels was observed after body weight reduction (8 +/- 4 kg; P < 0.01), although percent changes in adiponectin paralleled those in IL-10 (P < 0.05). CONCLUSIONS: Android obesity is associated with a concomitant reduction of IL-10 and adiponectin levels. However, the antiinflammatory status of obesity might require prolonged periods of energy-restricted diets to revert to normal.

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Serum adiponectin and coronary heart disease risk in older Black and White Americans.

CONTEXT: Adiponectin may influence the risk of coronary heart disease (CHD) independently of traditional cardiovascular risk factors. OBJECTIVE: Because body composition and adiponectin levels vary by race, we examined the relationship of adiponectin with prevalent and incident CHD in a cohort of older Black and White adults. DESIGN AND SETTING: We conducted a cross-sectional and prospective cohort study at two U.S. clinical centers. PARTICIPANTS: Participants included 3075 well-functioning adults between ages 70 and 79 yr enrolled in the Health, Aging, and Body Composition study. MAIN OUTCOME MEASURES: Prevalent CHD was defined as history of myocardial infarction, coronary artery bypass graft, percutaneous coronary transluminal angioplasty, angina, or major electrocardiogram abnormalities. After excluding those with prevalent CHD, incident CHD was defined as hospitalized myocardial infarction or CHD death. RESULTS: At baseline, 602 participants (19.6%) had CHD. During 6 yr of follow-up, 262 (10.6%) incident CHD events occurred. Whites had higher median adiponectin than Blacks (12 vs. 8 microg/ml, P < 0.001). Race modified the effect of adiponectin (P for interaction was 0.002 for prevalent CHD, and P = 0.02 for incident CHD). Among Whites, an inverse association of adiponectin with CHD was explained by high-density lipoprotein and glucose. Among Blacks, a doubling of adiponectin was associated with a 40% higher risk of both prevalent CHD (odds ratio, 1.41; 95% confidence interval, 1.11-1.78) and incident CHD (hazards ratio, 1.37; 95% confidence interval, 1.01-1.87) after adjusting for explanatory variables. CONCLUSION: High circulating concentrations of adiponectin were associated with higher risk of CHD in older Blacks, even accounting for traditional CHD risk factors.

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Adiponectin in childhood and adolescent obesity and its association with inflammatory markers and components of the metabolic syndrome.

CONTEXT: Adiponectin levels are lower in obese children and adolescents, whereas markers of inflammation and proinflammatory cytokines are higher. Hypoadiponectinemia may contribute to the low-grade systemic chronic inflammatory state associated with childhood obesity. OBJECTIVE: We investigated whether C-reactive protein (CRP), the prototype of inflammation, is related to adiponectin levels independently of insulin resistance and adiposity. DESIGN, SETTING, PARTICIPANTS, AND MAIN OUTCOME MEASURES: In a multiethnic cohort of 589 obese children and adolescents, we administered a standard oral glucose tolerance test and obtained baseline measurements for adiponectin, plasma lipid profile, CRP, IL-6, and leptin. RESULTS: Stratifying the cohort into quartiles of adiponectin levels and adjusting for potential confounding variables, such as age, gender, ethnicity, body mass index z-score, pubertal status, and insulin sensitivity, the present study revealed that low levels of adiponectin are associated not only with higher CRP levels, but also with components of the metabolic syndrome, such as low high-density lipoprotein cholesterol and a high triglyceride-to-high-density-lipoprotein ratio. CONCLUSIONS: The link between adiponectin levels and a strong marker of inflammation, CRP, is independent of insulin resistance and adiposity in obese children and adolescents. Adiponectin may be one of the signals linking inflammation and obesity. Thus, adiponectin may function as a biomarker of the metabolic syndrome in childhood obesity.

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Effect of growth hormone therapy on serum adiponectin and resistin levels in short, small-for-gestational-age children and associations with cardiovascular risk parameters.

BACKGROUND: Adiponectin and resistin are fat cell-derived hormones, which are thought to be respectively protective and disadvantageous with regard to the development of cardiovascular disease and diabetes mellitus type 2. Low birth weight has been associated with increased risks for the development of these diseases. In short, small-for-gestational-age (SGA) children, GH therapy has several positive effects regarding cardiovascular risk factors. On the other hand, concern has been expressed about the effects of GH therapy on insulin sensitivity. METHODS: We measured adiponectin and resistin levels in 136 short prepubertal children born SGA and their association with cardiovascular risk parameters and growth factors. Also, we compared the levels with normal-statured controls. The effect of GH treatment was evaluated in 50 short SGA children vs. baseline and vs. an untreated sex- and age-matched SGA control group. RESULTS: Short SGA children had similar adiponectin and lower resistin levels, compared with normal-statured controls. In GH-treated SGA children, neither adiponectin nor resistin levels changed significantly during 2 yr of GH treatment. Compared with untreated sex- and age-matched SGA controls, GH-treated SGA children had similar adiponectin and lower resistin levels. Adiponectin correlated inversely with age but not any cardiovascular risk parameter or growth factor. Higher IGF-I levels in GH-treated children were associated with lower resistin levels. CONCLUSIONS: Compared with normal-statured controls, short prepubertal SGA children had similar adiponectin and lower resistin levels. Two years of GH treatment had no effect on their adiponectin and resistin levels.

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Adiponectin responses to continuous and progressively intense intermittent exercise.

PURPOSE: Adiponectin is a recently discovered adipocyte protein that is lower in patients with coronary artery disease and in Type II diabetics who have insulin resistance. Regular exercise is known to be a preventative factor in the development of atherosclerosis and Type II diabetes. Acute exercise increases insulin sensitivity; however, it also increases beta-adrenergic and glucocorticoid activities that may suppress adiponectin expression. Two experiments were conducted to determine whether acute exercise affects adiponectin concentrations. METHODS: In the first experiment, six healthy male subjects completed 30 min of heavy continuous running exercise at 79% of VO (2max). In the second experiment, well-trained runners completed strenuous intermittent exercise consisting of treadmill running at 60, 75, 90, and 100% VO (2max). A resting control trial for the second experiment was also conducted. RESULTS: Glucose and insulin were not altered significantly in the first experiment, but both increased significantly (P < 0.05) in the second experiment. A significant increase (P < 0.05) in adiponectin in the first experiment was no longer significant after correction for plasma volumes shifts. In the second experiment, there were significant (P < 0.05) changes in adiponectin concentrations over time but not a significant difference between adiponectin responses in exercise and control trials. CONCLUSIONS: The data suggest that 30 min of heavy continuous running or more strenuous intermittent running does not stimulate an increase in production and release of adiponectin, and small increases in adiponectin concentrations resulting from the exercise may be attributed to normal plasma volume shifts.

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Decrease in plasma adiponectin concentrations in patients with variant angina pectoris.

BACKGROUND: Plasma adiponectin is decreased in patients with coronary artery diseases, especially in patients with acute coronary syndrome (ACS). However, the correlation between plasma adiponectin and variant angina pectoris (VAP) has not been verified. Plasma adiponectin concentrations between VAP and other coronary artery diseases was compared in the present study. The association between plasma adiponectin concentration and VAP was also investigated. METHODS AND RESULTS: Plasma adiponectin concentrations in the VAP group (n=101) were compared with those of the ACS group (n=117), the stable angina pectoris group (n=108), and the normal coronary group (n=81). Plasma adiponectin concentrations in VAP and ACS were significantly lower than that of the normal coronary group (6.6+/-5.4 vs 5.2+/-4.0 vs 9.0 +/-6.2 microg/ml, p<0.001, respectively). Multivariate analysis indicated that plasma adiponectin (odds ratio (OR) 0.735, 95% confidence interval (CI) 0.621-0.855, p=0.011), smoking (OR 2.012, 95% CI 1.210-3.880, p=0.020), and age (OR 0.976, 95% CI 0.957-0.997, p=0.022) correlated independently with the development of VAP. CONCLUSIONS: Our results suggest that a decrease in plasma adiponectin concentration might be associated with the development of VAP.

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[The mechanisms by which PPARgamma and adiponectin regulate glucose and lipid metabolism].

Obesity, a state of increased adipose tissue mass, is a major cause for type 2 diabetes, hyperlipidemia, and hypertension, resulting in clustering of risk factors for atherosclerosis. Heterozygous PPARgamma knockout mice and KKA(y) mice administered with a PPARgamma antagonist were protected from high-fat diet-induced adipocyte hypertrophy and insulin resistance. Moderate reduction of PPARgamma activity prevented adipocyte hypertrophy, thereby diminution of TNFalpha, resistin, and FFA and upregulation of adiponectin and leptin. These alterations led to reduction of tissue TG content in muscle/liver, thereby ameliorating insulin resistance. Insulin resistance in the lipoatrophic mice and KKA(y) mice were ameliorated by replenishment of adiponectin. Moreover, adiponectin transgenic mice ameliorated insulin resistance and diabetes, but not the obesity of ob/ob mice. Furthermore, targeted disruption of the adiponectin gene caused moderate insulin resistance and glucose intolerance. In muscle, adiponectin activated AMP kinase and PPARgamma pathways, thereby increasing beta-oxidation of lipids, leading to decreased TG content, which ameliorated muscle insulin resistance. In the liver, adiponectin also activated AMPK, thereby downregulating PEPCK and G6Pase, leading to decreased glucose output from the liver. In conclusion, PPARgamma plays a central role in the regulation of adipocyte hypertrophy and insulin sensitivity. The upregulation of the adiponectin pathway by PPARgamma may play a role in the increased insulin sensitivity of heterozygous PPARgamma knockout mice, and activation of adiponectin pathway may provide novel therapeutic strategies for obesity-linked disorders such as type 2 diabetes and metabolic syndrome.

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Low adiponectin level in young normotensive men with a family history of essential hypertension.

Circulating level of adiponectin, an adipocyte-derived protein, is reduced in states of insulin resistance such as obesity and type 2 diabetes. We have previously shown that hypoadiponectinemia is related to insulin resistance in essential hypertension. Recent studies have shown that normotensive subjects with a positive family history of essential hypertension (FH+) have decreased insulin sensitivity compared to subjects with a negative family history of essential hypertension (FH-). We here examined the association between adiponectin concentration and insulin sensitivity in FH+ and FH-. Thirty young, non-obese and normotensive men without a family history of diabetes mellitus were enrolled. A total of 15 subjects were FH+, and the remaining 15 subjects were FH-. Insulin sensitivity index (ISI) was evaluated by the euglycemic hyperinsulinemic glucose clamp technique. Concentrations of adiponectin and other metabolic variables were measured. The FH+ group had significantly lower levels of ISI and adiponectin than did the FH- group. In all of the subjects, ISI was positively correlated with adiponectin concentration and high-density lipoprotein (HDL) cholesterol level and was negatively correlated with insulin level. Adiponectin concentration was the only independent determinant of ISI in a multiple regression analysis. Our results showed that adiponectin level was significantly decreased and that this was accompanied by reduced insulin sensitivity in young, nonobese and normotensive men with a family history of essential hypertension. Phenotype of reduced adiponectin level as an earlier penetrance may be especially useful in genetic analyses of insulin resistance and essential hypertension.

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The relationships of plasma adiponectin with a favorable lipid profile, decreased inflammation, and less ectopic fat accumulation depend on adiposity.

BACKGROUND: The metabolic effects of adiponectin, including insulin sensitivity, seem to become stronger with increasing adiposity. Adiposity may also affect the relationship of adiponectin concentrations with serum lipid profile; markers of inflammation, atherosclerosis, and endothelial function; and ectopic fat accumulation. METHODS: We measured plasma adiponectin concentrations, serum lipids, and serum markers of inflammation, atherosclerosis, and endothelial function in 242 Caucasians without type 2 diabetes. We also measured visceral adipose tissue with magnetic resonance tomography and liver and intramyocellular fat with (1)H magnetic resonance spectroscopy. RESULTS: We divided the study participants into 2 groups: lean [mean (SE) total body fat, 26% (0.6%); n = 119] and obese [36% (0.6%); n = 123]. In the obese group, plasma adiponectin concentrations showed a strong positive association with concentrations of HDL cholesterol (P <0.0001) and negative associations with LDL cholesterol, triglycerides, high-sensitivity C-reactive protein, interleukin 6, apolipoprotein B(100), soluble E-selectin, soluble vascular cellular adhesion molecule 1, plasminogen activator inhibitor 1, leukocyte count, and liver and intramyocellular fat (all P <0.03). In the lean group, adiponectin showed a less strong association with HDL cholesterol (P = 0.005) and liver fat (P = 0.03) and no significant associations with the other variables (all P >0.10). High visceral adipose tissue was a strong predictor of low adiponectin concentrations, particularly in the obese group, and attenuated many of the significant relationships. CONCLUSIONS: High adiponectin plasma concentrations are associated with favorable lipid profiles, decreased subclinical inflammation, decreased markers of atherosclerosis and endothelial function, and low ectopic fat accumulation, particularly in obese persons. Adiponectin may also have a concentration-related effect on the relationship between visceral adipose tissue and these metabolic characteristics, especially in obese persons.

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Adiponectin expression and adipose tissue lipolytic activity in lean and obese women.

BACKGROUND: The authors evaluated whether adipose adiponectin expression is related to adipose tissue lipolytic activity and fatty acid oxidation rate in lean and obese women. METHODS: The study consisted of 60 adult females distributed in a wide range of adiposity (BMI 24.0-53.4 kg/m2). Body composition was estimated by bioelectrical impedance. Respiratory quotient was measured by open-circuit indirect calorimetry. RT-PCR assays were performed to measure TNFalpha and adiponectin expression in subcutaneous adipose tissue biopsies. Lipolysis studies were performed in fresh tissue samples obtained from subcutaneous abdominal depots during bariatric surgery in 19 morbidly obese females or by an incisional biopsy or during abdominal elective surgery in normal weight and obese females. Glycerol release was measured with a colorimetric endpoint method. RESULTS: Patients with a higher degree of adiposity showed lower adipose tissue adiponectin expression and hormone-sensitive lipase (HSL) activity than women in the low range of adiposity. HSL activity was positively related to adiponectin expression. No relationship was observed between adiponectin and TNFalpha subcutaneous adipose tissue expression. The positive relationship between respiratory quotient and adiponectin expression was in the limit of statistical significance (P=0.05). Percentage of body fat and mRNA adiponectin explained 26% of the variance of the adipose tissue HSL activity. CONCLUSIONS: Low adipose tissue adiponectin expression observed in obese people may contribute to the progression of obesity and its co-morbidities by modulating hormone-sensitive lipase activity and fatty acid oxidation.

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Serum adiponectin, resistin levels and non-alcoholic fatty liver disease in obese children.

The objective is to investigate the relation between the levels of two serum adipocytokines (adiponectin and resistin) and non-alcoholic fatty liver disease (NAFLD) in obese children. In this study, 113 obese children were enrolled and divided into 3 groups. Obese group 1 was defined as obese children without any liver abnormality. Obese group 2 was defined as obese children just with fatty infiltration of the liver in ultrasonic appearance and obese group 3 was defined as obese children with liver function abnormality. The controls consisted of 37 nonobese children without endocrine, metabolic or kidney disease. The levels of serum adiponectin and resistin were measured by ELISA method. Insulin resistance by homeostasis model (HOMA-IR), area under curve of glucose (AUCG), serum total cholesterol, triglyceride, alanine aminotransferase, uric acid, HDL-cholesterol, LDL-cholesterol and body mass index (BMI) were measured as well. In obese children, NAFLD were found in 63 cases (55.75%). Serum adiponectin levels of obese children were significantly lower than that of controls (3.63 vs 5.79 microg/mL, P<0.001) while serum resistin levels were not different (P = 0.876). Moreover, serum adiponectin levels in obese group 1 were significantly higher than that of group 2 and 3 (4.24 vs 3.37 and 3.12 microg/mL, all P<0.05) and no difference was found between obese group 2 and obese group 3 (P>0.05). Serum resistin levels among the three obese groups were 4.37 ng/mL, 3.72 ng/mL and 4.24 ng/mL without significant difference (P = 0.592). NAFLD, BMI, gender and HDL-cholesterol were independent determinants of serum adiponectin levels in children analyzed by multiple regression analysis, which explained 33% of the variance. Serum adiponectin levels were inversely associated with BMI, gender and NAFLD (all P<0.05) and were positively associated with HDL-cholesterol levels (P = 0.033). These results suggest that adiponectin might be a protective factor in NAFLD occurrence in obese children, and that the measurement of adiponectin should be part of the standard evaluation of the obese child and may help to evaluate the occurrence of NAFLD.

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Inverse relationship between plasma adiponectin and leptin concentrations in normal-weight and obese women.

BACKGROUND: Adiponectin, a novel adipocyte-derived collagen-like protein, is the gene product of the adipose most-abundant gene transcript 1 (apM1), which has been considered to have anti-inflammatory and anti-atherogenic effects. OBJECTIVE: To characterize the relationship between adiponectin and leptin, the ob gene product, in normal-weight and obese women. DESIGN AND METHODS: In this cross-sectional study, we measured fasting plasma adiponectin by ELISA, leptin concentrations by RIA, and related parameters such as blood pressure, body mass index (BMI), body fat mass, lipids, fasting blood glucose and insulin in 353 non-diabetic adult women with a wide range of BMI values. RESULTS: Plasma adiponectin concentrations in women with the highest tertile of BMI (at least 25.0 kg/m(2)) were decreased compared with those in the middle (22.0-25.0 kg/m(2)) or lowest (<or=22.0 kg/m(2)) tertile of BMI (means+/-s.e.m.: 6.7+/-0.3 microg/ml compared with 8.6+/-0.4 microg/ml and 9.2+/-0.3 microg/ml; both P<0.0001). Serum leptin concentrations in women with the highest tertile of BMI were increased compared with those in women in the middle or lowest tertile of BMI (13.2+/-0.4 ng/ml compared with 8.1+/-0.2 ng/ml and 5.2+/-0.2 ng/ml; both P<0.0001). These relationships were similar after adjustment for BMI or body fat mass. Adiponectin was negatively correlated with serum leptin concentration, fasting immunoreactive insulin, calculated insulin resistance (homeostasis model assessment), BMI and body fat mass. These negative relationships became stronger after adjustment for BMI or body fat mass. In stepwise regression analyses, leptin was the significant independent variable for adiponectin, and adiponectin was also the significant independent variable for leptin before and after adjustment for BMI or body fat mass. CONCLUSIONS: In this study, we found an inverse correlation between adiponectin and leptin in vivo.

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Influence of gender, age and renal function on plasma adiponectin level: the Tanno and Sobetsu study.

DESIGN: The aim of this study was to determine the association between aging and adiponectin level from the aspect of the influence of renal function and sex hormones in humans. METHODS: Serum adiponectin and blood urea nitrogen (BUN) levels were measured in 964 subjects (372 males) aged 60.3+/-12.5 years. Testosterone and free testosterone levels were measured in 123 males, and estrone and estradiol levels were measured in 114 females. The subjects were divided into two age groups; 65 years of age or older (Age > or = 65 group) and less than 65 years of age (Age < 65 group). RESULTS: Adiponectin level increased linearly with aging in males, whereas it increased dramatically in females until their 50s. The patterns of changes in adiponectin were similar to those in BUN. In multiple- regression analysis using adiponectin as a dependent variable BUN was selected as a significant independent variable in all subjects and in subjects in the Age > or = 65 group, whereas bioactive sex hormones were not selected. CONCLUSIONS: A decrease in adiponectin clearance in the kidney may be the cause of high levels of adiponectin in the elderly. Adiponectin level seems to be influenced more strongly by BUN than by sex hormones and to be increased by a decline in renal function with aging.

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Association of plasma adiponectin concentrations with chronic lymphocytic leukemia and myeloproliferative diseases.

Adiponectin, an adipocyte-secreted hormone, is an important negative regulator in the immune system and hematopoiesis. In this study, we investigated the association of adiponectin levels with chronic lymphocytic leukemia (CLL) and myeloproliferative diseases (MPDs). We measured adiponectin levels in 19 patients with CLL and 30 patients with MPD (chronic myelogenous leukemia, 15; polycythemia vera, 9; myelofibrosis, 4; essential thrombocythemia, 2). The data were (chronic myelogenous leukemia, 15; polycythemia vera, 9; myelofibrosis, 4; essential thrombocythemia, 2). The data were compared with results from a control group of healthy volunteers who were matched according to age, sex, and body mass index. The adiponectin levels in patients with CLL were lower than in the controls (4.71 +/- 1.33 microg/mL versus 16.61 +/- 3.91 microg/mL; P <.001). They were also significantly lower in patients with MPD than in the controls (8.95 +/- 1.33 microg/mL versus 16.16 +/- 4.77 microg/mL; P <.001). In addition, we compared the adiponectin levels of MPD patients who were treated with interferon (IFN) to the levels of patients who were not treated with IFN. Adipnectin levels were significantly higher in IFN-treated patients (11.03 +/- 1.39 microg/mL versus 6.87 +/- 1.79 microg/mL; P <.001). These results suggest that lymphopoiesis and myelopoiesis negatively influence adiponectin levels. Adiponectin may be related to inflammatory cytokine release. IFN therapy appears to have a positive influence on adiponectin secretion by suppressing inflammatory cytokines. Future studies are needed to prove causality and to provide insight about this hormone's mechanism of action and its potential role regarding the etiology and progression of CLL and MPD.

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Predictive value of the adipocyte-derived plasma protein adiponectin for restenosis after elective coronary stenting.

The purpose of this study was to test the hypothesis that plasma levels of adiponectin can predict angiographic in-stent restenosis after coronary stenting. We prospectively examined adiponectin levels in 127 consecutive patients undergoing elective coronary stenting. Restenosis was defined as more than 50% stenosis at follow-up study by quantitative coronary angiography. There were no significant differences in the clinical characteristics or angiographical findings between the groups with restenosis and no restenosis. The levels of adiponectin did not differ between the restenosis group and the no restenosis group (5.7 +/- 2.8 vs 5.9 +/- 3.6 microg/mL, p = 0.72). The plasma levels of adiponectin were not related with the late loss index after coronary stenting (r = 0.01, p = 0.89). The levels of adiponectin were significantly lower in men than in women (5.5 +/- 3.2 vs 8.8 +/- 3.7 microg/ mL, p < 0.001), and negatively correlated with body mass index (r = -0.21, p = 0.01). We analyzed adiponectin levels in male, female, obese, non-obese, diabetes, and non-diabetes patients, however, there were no significant differences between the restenosis group and no restenosis group. This study has demonstrated that the measurement of adiponectin could not predict angiographic restenosis after elective coronary stenting, whereas the plasma levels of adiponectin were associated with some coronary risk factors in patients with coronary artery disease.

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Adiponectin and mortality in patients with chronic kidney disease.

Adiponectin is presumed to possess antiatherogenic and cardioprotective properties. Limited data exist on the relationship between adiponectin and mortality in the earlier stages of chronic kidney disease. The Modification of Diet in Renal Disease study was a randomized, controlled trial that was conducted between 1989 and 1993. Adiponectin was measured in frozen samples that were obtained at baseline (N = 820). Survival status and cause of death, up to December 31, 2000, were obtained from the National Death Index. Multivariable Cox models were used to examine the relationship of adiponectin with all-cause and cardiovascular mortality. Mean +/- SD age was 52 +/- 12 yr, and mean +/- SD glomerular filtration rate (GFR) rate was 33 +/- 12 ml/min per 1.73 m2. Eighty-five percent of participants were white, and 60% were male. Mean +/- SD adiponectin was 12.8 +/- 8.0 mug/ml. Triglycerides, insulin resistance, glucose, body mass index, GFR, C-reactive protein, and albumin were inversely related and proteinuria and HDL cholesterol were directly related to adiponectin. During the 10-year follow-up period, 201 (25%) participants died of any cause, and 122 (15%) from cardiovascular disease. In multivariable adjusted Cox models, a 1-mug/ml increase in adiponectin was associated with a 3% (hazard ratio 1.03; 95% confidence interval 1.01 to 1.05; P = 0.02) increased risk for all-cause and 6% (hazard ratio 1.06; 95% confidence interval 1.03 to 1.09; P < 0.001) increased risk for cardiovascular mortality. High, rather than low, adiponectin is associated with increased mortality in this cohort of patients with chronic kidney disease stages 3 to 4. Further studies are necessary to confirm this association and to elucidate the underlying mechanisms.

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