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PubMed2006

Serum adiponectin and leptin concentrations in HIV-infected children with fat redistribution syndrome.

Human immunodeficiency virus (HIV)-related lipodystrophy is characterized by adipose tissue redistribution, dyslipidemia, and insulin resistance. We hypothesized that fat redistribution and metabolic abnormalities in HIV-infected children are related to alterations in endocrine function of adipose tissue. A multicenter study was conducted in 130 HIV-infected children. Lipodystrophy definition was based on the central to peripheral skinfold ratio. Fasting adiponectin, leptin, insulin concentrations, glycemia, and lipid profile were measured in all children. Fat redistribution syndrome was apparent in 32 children: 14 with atrophic (LPDA) and 18 with hypertrophic lipodystrophy (LPDH). Mean serum adiponectin levels were significantly decreased in LPDA and LPDH groups compared with the group with no lipodystrophy (LPD-). Fasting insulin concentration was significantly higher in LPDA and LPDH groups versus LPD-. Mean serum leptin concentration was significantly increased only in LPDH compared with LPDA and LPD- groups. Triglyceride levels were significantly increased and high-density lipoprotein (HDL)-cholesterol concentration decreased in the LPDA versus LPD- group. Controlling for puberty stage, gender, percentage of total fat mass, serum lipids, HIV treatment, and disease severity, adiponectin was significantly and inversely associated with central obesity and insulin/glucose ratio. Fat redistribution had no significant effect on leptin concentration, which was directly related to the percentage of body fat, female gender, and insulin/glucose ratio. In conclusion, HIV-infected children with symptoms of fat redistribution have decreased levels of adiponectin, associated with insulin resistance and dyslipidemia.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Body composition and adiponectin serum concentrations in adult patients with cystic fibrosis.

CONTEXT: Cystic fibrosis (CF) is a disease characterized by weight loss and chronic low-grade inflammation. OBJECTIVE: The objective of the study was to assess changes in body composition and the serum concentrations of adiponectin, a marker of negative energy balance and insulin sensitivity, in adult patients with CF. DESIGN: This was a cross-sectional study. SETTING: The study was conducted at an outpatient clinic of the University Hospital of Basel, Switzerland. PARTICIPANTS: Twenty-four stable adult CF patients and 24 healthy controls, matched for body mass index, age, sex, and hormonal therapy in women participated in the study. MAIN OUTCOME MEASURES: Changes in body composition (assessed by dual x-ray absorptiometry) and serum adiponectin levels were measured. RESULTS: Body mass index, percent fat mass (in percentage of body weight), and percent lean body mass were similar in patients and controls, whereas central fat accumulation was increased [trunk to extremity fat ratio 1.2 (0.99-1.51) vs. 0.99 (0.81-1.25), P = 0.01] in patients with CF, compared with controls. Decreased lean mass and increased highly sensitive C-reactive protein levels were independently associated with worse lung function in CF patients. Despite similar insulin resistance (homeostasis model assessment) and similar SHBG serum concentrations, the serum concentrations of adiponectin were higher in CF patients, compared with controls, independent of other confounders (P = 0.01). CONCLUSIONS: Central fat accumulation is increased in patients with CF. It is postulated that the energy deficit-induced increase in serum adiponectin could explain the preservation of insulin sensitivity in these patients despite the increase in central fat and in highly sensitive C-reactive protein serum concentrations and could prevent a further deterioration of protein catabolism.

Adiponectin↗
PubMed2006

High molecular weight, rather than total, adiponectin levels better reflect metabolic abnormalities associated with childhood obesity.

CONTEXT: Japanese are prone to obesity-induced metabolic derangement, which is linked to serum adipocytokine profile even in children. OBJECTIVE: The objective of the study was to determine whether high molecular-weight adiponectin (H-Adn) more specifically relates to metabolic derangement in obese children than total adiponectin (T-Adn). DESIGN AND SETTING: A case (n = 59) control (n = 28) study was performed at the pediatric clinic of a university hospital. PATIENTS: Japanese obese children (38 boys and 21 girls) were consecutively enrolled. The ages ranged from 5 to 15 (10.3 +/- 0.3; mean +/- sem) yr. Nonobese children (15 boys and 13 girls) were assigned as age-matched controls. MAIN OUTCOME MEASURES: Serum adiponectin multimeric complexes were assayed by an ELISA kit. The relationship of adiponectin to metabolic abnormalities was evaluated. RESULTS: T-Adn (5.1 +/- 0.2 vs. 8.8 +/- 0.4 microg/ml), H-Adn (1.3 +/- 0.1 vs. 4.8 +/- 0.4 microg/ml), and medium molecular weight-Adn were significantly lower in obese than in control children. After adjustment for age and sex, both T- and H-Adn were inversely correlated with insulin and homeostasis model of assessment-insulin resistance, whereas H-Adn (but not T-Adn) inversely correlated with visceral fat area, as determined by computed tomography. Seven obese children were estimated to have metabolic syndrome and showed selective decrease in H-Adn and H/T-Adn. CONCLUSION: H-Adn reflects metabolic abnormalities due to obesity better than T-Adn in children. H-Adn is associated with the development of metabolic syndrome, even in childhood.

Adiponectin↗
PubMed2006

Plasma adiponectin levels and endometrial cancer risk in pre- and postmenopausal women.

BACKGROUND: Adiponectin, an adipocytokine secreted by adipose tissue, is decreased in obesity, insulin resistance, type 2 diabetes, and polycystic ovary syndrome, all of which are well-established risk factors for endometrial cancer. METHODS: We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition to examine the relation between prediagnostic plasma adiponectin levels and endometrial cancer risk. Among pre- and postmenopausal women who were not currently using exogenous hormones, 284 women developed incident endometrial cancer during an average of 5.1 yr of follow-up. Using risk set sampling, 548 control subjects were selected, matched on center, age, menopausal status, phase of menstrual cycle, time of blood draw, and fasting status. Conditional logistic regression models were used to estimate relative risks and 95% confidence intervals. RESULTS: Adiponectin levels were inversely associated with endometrial cancer risk [body mass index-adjusted relative risk for the top vs. bottom quartile = 0.56 (95% confidence interval 0.36-0.86), P(trend) = 0.006]. There was evidence of a stronger inverse association among obese women than among nonobese women (P(heterogeneity) = 0.03). The inverse association also appeared stronger for women who were postmenopausal or perimenopausal than premenopausal at baseline, but this was not statistically significantly heterogeneous (P(heterogeneity) = 0.51). The association remained statistically significant after separate adjustment for other obesity-related physiological risk factors such as C-peptide, IGF binding protein-1, IGF binding protein-2, SHBG, estrone, or free testosterone but only marginally statistically significant after simultaneous adjustment for these factors. CONCLUSIONS: High circulating adiponectin levels are associated with reduced endometrial cancer risk, largely independent of other obesity-related risk factors.

Adiponectin↗
PubMed2005

Effects of dietary protein of Korean foxtail millet on plasma adiponectin, HDL-cholesterol, and insulin levels in genetically type 2 diabetic mice.

We examined the effects of intake of Korean foxtail millet protein (FMP) on plasma levels of lipid, glucose, insulin, and adiponectin in genetically type 2 diabetic KK-Ay mice. When mice were fed a normal FMP diet or a high-fat-high-sucrose diet containing FMP for 3 weeks, in both experiments plasma concentrations of high-density lipoprotein cholesterol (HDL-cholesterol) and adiponectin increased remarkably in comparison with a casein diet group, whereas concentrations of insulin decreased greatly and that of plasma glucose was comparable to that in the casein diet group. Considering the role of adiponectin, insulin, and HDL-cholesterol in diabetes, atherosclerosis, and obesity, it appears likely that FMP may improve insulin sensitivity and cholesterol metabolism through an increase in adiponectin concentration. Therefore, FMP would serve as another beneficial food component in obesity-related diseases such as type 2 diabetes and cardiovascular diseases.

Adiponectin↗
PubMed2005

Adiponectin and other adipocytokines as predictors of markers of triglyceride-rich lipoprotein metabolism.

BACKGROUND: Adipocytokines are bioactive peptides that may play an important role in the regulation of glucose and lipid metabolism. In this study, we investigated the association of plasma adipocytokine concentrations with markers of triglyceride-rich lipoprotein (TRL) metabolism in men. METHODS: Fasting adiponectin, leptin, resistin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), apolipoprotein (apo) B-48, apo C-III, and remnant-like particle (RLP)-cholesterol concentrations were measured by immunoassays and insulin resistance by homeostasis assessment (HOMA) score in 41 nondiabetic men with a body mass index of 22-35 kg/m2. Visceral and subcutaneous adipose tissue masses (ATMs) were determined by magnetic resonance imaging and total ATM by bioelectrical impedance. RESULTS: In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated with plasma apoB-48, apoC-III, RLP-cholesterol, triglycerides, VLDL-apoB, and VLDL-triglycerides (P <0.05). Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables, except for a direct correction between apoC-III and IL-6 (P <0.05). In multivariate regression including HOMA, age, nonesterified fatty acids, and adipose tissue compartment, adiponectin was an independent predictor of plasma apoB-48 (beta coefficient = -0.354; P = 0.048), apoC-III (beta coefficient = -0.406; P = 0.012), RLP-cholesterol (beta coefficient = -0.377; P = 0.016), and triglycerides (beta coefficient = -0.374; P = 0.013). By contrast, leptin was not an independent predictor of these TRL markers. Plasma apoB-48, apoC-III, RLP-cholesterol, and triglycerides were all significantly and positively associated with plasma insulin, HOMA, and visceral, subcutaneous, and total ATMs (P <0.05). CONCLUSIONS: These data suggest that the plasma adiponectin concentration may not only link abdominal fat, insulin resistance, and dyslipidemia, but may also exert an independent role in regulating TRL metabolism.

Adiponectin↗
PubMed2005

Changes in insulin resistance following bariatric surgery and the adipoinsular axis: role of the adipocytokines, leptin, adiponectin and resistin.

The fat mass participates in the regulation of glucose and insulin metabolism through the release of adipocytokines in a mechanism called the adipoinsular axis. Putative adipocytokines include leptin, adiponectin and resistin. Obesity plays an important role in the pathogenesis of insulin resistance and type 2 diabetes mellitus (T2DM). Bariatric surgery for morbidly obese patients leads to rapid and prolonged improvement in insulin resistance and T2DM in the vast majority of patients. We have previously proposed that the rapid improvement in insulin resistance observed following bariatric surgery is mediated by changes in incretin levels of the entero-insular axis and that long-term improvement is modulated by fat mass loss and changes in adipocytokine levels of the adipoinsular axis. In this review, we examine the information that supports a role of leptin, adiponectin and resistin in the development of insulin resistance and T2DM. Increasing levels of leptin and decreasing levels of adiponectin correlate with worsening insulin resistance in obese individuals. We also explore the relationship between changes in adipocytokines following bariatric surgery and long-term improvement in insulin resistance and T2DM. Leptin levels drop and adiponectin levels rise following laparoscopic adjustable gastric banding, gastric bypass and biliopancreatic diversion. These changes correlate with weight loss and improvement in insulin. Although resistin may play an important role in explaining insulin resistance, animal and human studies currently show conflicting results.

Adiponectin↗
PubMed2004

Short-term effect of bezafibrate on the expression of adiponectin mRNA in the adipose tissues: a study in spontaneously type 2 diabetic rats with visceral obesity.

The effect of short-term bezafibrate (BF) administration over time on the expression of adiponectin mRNA in the tissues was examined in Otsuka Long Evans Tokushima Fatty (OLETF) rats. Eight-week-old rats were divided into the high-dose (100 mg/kg) BF group (n=15), the low-dose (10 mg/kg) BF group (n=15), or the control group (n=15) and followed up for 14 d. Tri-glyceride and free fatty acid levels significantly decreased in a dose-dependent manner in the high-dose BF group. The insulin levels increased with time, although they were significantly lower in the high-dose BF group on d 3 and 7 than the control group. Adiponectin levels significantly increased in the high-dose BF group. On d 14 of BF administration, the levels of VLDL and chy-lomicron were significantly lower in BF groups, and adiponectin mRNA expression in the white adipose tissue was significantly higher in the high-dose BF group. Findings from this study suggest that in type 2 diabetes with insulin resistance, hypertriglyceridemia is closely linked to adiponectin.

Adiponectin↗
PubMed2006

Plasma adiponectin and insulin resistance in new onset hypertension.

OBJECTIVE: The data related to association among hypertension, insulin resistance, and plasma adiponectin concentration is controversial. We aimed to evaluate the relationships among these factors in a young hypertensive group who had no confounding factors. DESIGN AND METHODS: Thirty newly diagnosed and formerly untreated hypertensive males (mean age 23.4 +/- 4.0 yr; body mass index: 24.9 +/- 2.2 kg/m2), and 60 healthy control subjects (mean age 22.5 +/- 3.2 yr; body mass index: 24.6 +/- 1.6 kg/m2) were enrolled. Insulin resistance was calculated by homeostasis model assessment (HOMA). RESULTS: The two groups were similar in terms of age, body mass index, fasting glucose, total cholesterol, HDL and LDL cholesterol, adiponectin, insulin, HOMA, and hsCRP levels. Mean triglyceride levels in hypertensive patients were significantly higher than the controls (p = 0.02). CONCLUSIONS: These results indicate that young, newly diagnosed, uncomplicated patients with hypertension have similar plasma adiponectin levels and insulin sensitivities when compared to healthy controls. We suggest that high blood pressure itself may not be associated with insulin resistance or low adiponectin levels in patients with new onset, uncomplicated hypertension.

Adiponectin↗
PubMed2006

Relationship between plasma adiponectin levels and the metabolic syndrome among Korean people.

We investigated the relationship between plasma adiponectin levels and the parameters of the metabolic syndrome among Koreans. In 67 male and 115 female subjects, aged from 30 to 70 years, plasma adiponectin levels were positively correlated with HDL-cholesterol levels (r = 0.295, P<0.001), but negatively correlated with waist circumference (r = -0.140, P = 0.020), triglycerides (r = -0.174, P = 0.021), fasting plasma glucose (r = -0.159, P = 0.036), fasting plasma insulin (r = -0.172, P = 0.023) and HOMA-IR (r = -0.182, P<0.001), after adjustment for age, sex, and BMI. Stepwise multiple regression analyses revealed that HDL-cholesterol, sex, and HOMA-IR were the independent associated factors for plasma adiponectin levels. Multiple logistic analyses demonstrated that HOMA-IR, BMI, and age were the predominant independent factors associated with the metabolic syndrome, while plasma adiponectin levels exhibited a protective effect against the presence of the metabolic syndrome according to both NCEP ATP III criteria and IDF definition. Hypoadiponectinemia is associated with the phenotype of the metabolic syndrome as well as components of the metabolic syndrome.

Adiponectin↗
PubMed2006

Targeting adiponectin for cardioprotection.

Adiponectin is an adipose tissue-derived plasma protein which has a reduced concentration in subjects with obesity-related diseases. Adiponectin has antidiabetic and anti-inflammatory characteristics, which lead to beneficial actions on various obesity-linked complications. Recent experimental findings have shown that adiponectin contributes to protection against cardiac remodelling after pressure overload and cardiac injury following ischaemia-reperfusion. Thus, adiponectin could emerge as a potential cardioprotective agent for the treatment of several pathological heart conditions.

Adiponectin↗
PubMed2003

Absence of exercise-induced variations in adiponectin levels despite decreased abdominal adiposity and improved insulin sensitivity in type 2 diabetic men.

OBJECTIVE: We investigated the effect of an intensive training program on fasting leptin and adiponectin levels. METHODS: Sixteen middle-aged men with type 2 diabetes were randomly assigned to either a training or control group. The training program consisted of 8 weeks of supervised endurance exercise (75% VO(2peak), 45 min) twice a week, with intermittent exercise (five 2 min exercises at 85% VO(2peak) separated by 3 min exercises at 50% VO(2peak)) once a week, on an ergocycle. RESULTS: Training decreased abdominal fat by 44%, increased mid-thigh muscle cross-sectional area by 24%, and improved insulin sensitivity by 58% without significant change in body weight. Compared with controls, no significant variation in leptin or adiponectin levels was observed. However, in the trained group, change in adiponectin correlated with change in body weight (Spearman rank correlation, r(s):-0.76, P=0.03) but not with insulin sensitivity or abdominal adiposity variations. CONCLUSIONS: An 8 week intensive training program inducing a marked reduction in abdominal fat and increase in insulin sensitivity does not affect adiponectin and leptin levels in men with type 2 diabetes.

Abdomen↗
PubMed2006

Effect of rosiglitazone on plasma adiponectin levels and arterial stiffness in subjects with prediabetes or non-diabetic metabolic syndrome.

OBJECTIVE: Thiazolidinediones have favorable influences on surrogate markers of atherosclerosis such as adiponectin, and arterial stiffness in diabetic patients. However, it is not well known whether these beneficial effects occur in subjects without diabetes, such as prediabetes or the non-diabetic metabolic syndrome (MetS). The present study was therefore designed to evaluate the effectiveness of the insulin-sensitizing agent rosiglitazone on circulating adipocytokine levels and brachial-ankle pulse wave velocity (baPWV) in non-diabetics. DESIGN AND METHODS: Ninety-nine subjects with prediabetes or non-diabetic MetS were randomly assigned to either rosiglitazone or an untreated control group (50 and 49 subjects respectively). The rosiglitazone group was treated daily for 12 weeks with 4 mg rosiglitazone. All subjects received a 75 g oral glucose test (OGTT) before and after treatment. In addition, baPWV, together with the levels of adiponectin, resistin, and high sensitivity C-reactive protein (hsCRP) were determined. RESULTS: Rosiglitazone treatment significantly increased circulating adiponectin levels (P < 0.001) relative to the control group (P = 0.21). Plasma resistin levels were unchanged in both the rosiglitazone-treated and -untreated groups, but baPWV and hsCRP were significantly decreased (P < 0.001 and P = 0.003 respectively) in the rosiglitazone group only. Multiple linear regression analysis showed that changes in plasma adiponectin and baPWV were significantly affected by rosiglitazone treatment. CONCLUSIONS: These data suggest that rosiglitazone may have an anti-atherogenic effect in subjects with prediabetes or non-diabetic MetS.

Adiponectin↗
PubMed2006

Normative data for adiponectin, resistin, interleukin 6, and leptin/receptor ratio in a healthy Spanish pediatric population: relationship with sex steroids.

OBJECTIVES: To investigate the circulating levels of adiponectin, resistin, interleukin 6 (IL-6), and leptin/receptor ratio in healthy Spanish children throughout the different stages of pubertal development. To analyze the relationship between adipokines and sex steroid level changes during puberty. STUDY DESIGN: Serum adiponectin, resistin, IL-6 levels, and leptin/receptor ratio were studied in 160 healthy Spanish children grouped according to their pubertal stage (Tanner I, 23 girls and 22 boys; Tanner II, 19 girls and 16 boys; Tanners III and IV, 21 girls and 20 boys; and Tanner V, 20 girls and 19 boys). In addition, circulating levels of sex hormone-binding globulin (SHBG) were determined in every subject, and testosterone and estradiol levels in boys and girls respectively. RESULTS: Adiponectin levels decreased in boys from mid puberty (P < 0.05) to become significantly lower than in girls (P < 0.001), whereas IL-6 decreased in both sexes (P < 0.05). Resistin levels and leptin/receptor ratio showed no differences between sexes or according to pubertal stage, except in adult females, who had the highest levels of both parameters (P < 0.001). Serum IL-6 levels correlated significantly (P < 0.05) with testosterone and estradiol levels (r=-0.37 and -0.42 respectively), whereas estradiol, but not testosterone, correlated with leptin/receptor ratio (r=0.59; P < 0.001). Furthermore, a positive relationship was found between SHBG and adiponectin and IL-6 (P < 0.001 and P < 0.05 respectively). In addition, a direct correlation between leptin/receptor and body mass index was found in both sexes (P < 0.001). CONCLUSION: Variations in adipokine profiles throughout pubertal development appear to be related with progression of gonadal function.

Adiponectin↗
PubMed2006

Relationship between adiponectin levels, acylated ghrelin levels, and short-term body mass index changes in children with diabetes mellitus type 1 at diagnosis and after insulin therapy.

OBJECTIVE: To determine the effect of the initial metabolic imbalance and its restoration after insulin therapy on adiponectin and acylated ghrelin levels in children with type 1 diabetes mellitus (T1DM). STUDY DESIGN: Twenty prepubertal children with newly diagnosed T1DM were prospectively studied at diagnosis and after 1 and 4 months of therapy. Body mass index (BMI) and serum levels of adiponectin, resistin, total and acylated ghrelin, leptin, tumor necrosis factor alpha (TNF-alpha), and interleukin-6 (IL-6) were determined. The control group comprised 40 healthy prepubertal children. RESULTS: BMI was decreased at diagnosis, normalized at 1 month, and remained so thereafter. Adiponectin levels at diagnosis were similar to controls, increasing significantly after 1 month and normalizing at 4 months. Acylated ghrelin levels were lower at diagnosis, with a significant increase at 1 month and normalizing at 4 months. Resistin levels were normal at all time points. Leptin levels were decreased, while TNF-alpha and IL-6 were increased at diagnosis and normalized at 1 month. CONCLUSIONS: These findings suggest that BMI is not the main predictor of acylated ghrelin or adiponectin levels in newly diagnosed T1DM subjects and that these peptides may play an important role in the metabolic adaptation in this disease.

Acylation↗
PubMed2003

Ratio of leptin to adiponectin as an obesity index of cynomolgus monkeys (Macaca fascicularis).

Obesity is responsible for inducing various metabolic diseases. Laboratory-bred cynomolgus monkeys exhibit spontaneous onset of obesity. However, to date, no blood chemistry index to identify the state of obesity in cynomolgus monkeys has been determined. In the present study, to determine such an index, we measured the serum levels of two adipocyte-derived hormones, leptin and adiponectin, and evaluated the relationship between these hormones and other serum energy metabolic factors (i.e. insulin, total protein, glucose, total cholesterol and triglyceride) as well as the percentage of body fat (%Fat) in mature cynomolgus monkeys. Both in females and males, leptin was positively correlated with insulin and %Fat, and adiponectin was negatively correlated with insulin and %Fat. In female cynomolgus monkeys, leptin, adiponectin, and glucose were selected as the most important determinants for %Fat in multiple regression analysis, and in male cynomolgus monkeys, leptin was selected. The ratio of leptin to adiponectin (L/A ratio) was significantly elevated in the animals with %Fat over 40 (P < 0.01). The results indicate that L/A ratio is a potential index for comprehensively identifying obesity in cynomolgus monkeys.

Absorptiometry, Photon↗
PubMed2002

A haplotype at the adiponectin locus is associated with obesity and other features of the insulin resistance syndrome.

Adiponectin is a protein secreted by adipocytes that modulates insulin action. To assess whether variants of this gene contribute to the prevalence of insulin resistance in Caucasians, we genotyped 413 nondiabetic individuals for two single nucleotide polymorphisms (SNPs) at this locus. The two SNPs (45T-->G and 276G-->T) were chosen because of their association with type 2 diabetes in Japanese. Whereas each polymorphism was significantly associated with some correlate of insulin resistance, the haplotype defined by the two together was strongly associated with many components of the insulin resistance syndrome. Homozygotes for the risk haplotype had higher body weight (P = 0.03), waist circumference (P = 0.004), systolic (P = 0.01) and diastolic (P = 0.003) blood pressure, fasting glucose (P = 0.02) and insulin (P = 0.005) levels, homeostasis model assessment (HOMA) for insulin resistance (P = 0.003), and total to HDL cholesterol ratio (P = 0.01). Homozygotes also had significantly lower plasma levels of adiponectin (P = 0.03), independent of sex, age, and body weight. In an independent study group of 614 Caucasians, including 310 with type 2 diabetes, the risk haplotype was confirmed to be associated with increased body weight (P = 0.03) but not with type 2 diabetes per se. We conclude that variability at the adiponectin locus is associated with obesity and other features of the insulin resistance syndrome, but given the nature of the two SNPs, the risk haplotype is most probably a marker in linkage disequilibrium with an as yet unidentified polymorphism that affects plasma adiponectin levels and insulin sensitivity.

Adiponectin↗
PubMed2004

Adiponectin and the development of type 2 diabetes: the atherosclerosis risk in communities study.

Adipocyte-derived secretory proteins have been increasingly linked to diabetes. To investigate whether adiponectin, a major adipocyte secretory protein, predicts diabetes, we conducted a case-cohort study representing the approximately 9-year experience of the 10,275 middle-aged, U.S. African-American and white participants of the Atherosclerosis Risk in Communities (ARIC) study. Adiponectin was measured on stored plasma of 581 incident diabetes case subjects and 572 noncase subjects. Overall hazard ratios (95% CIs) for developing diabetes, for those in the second, third, and fourth (versus the first) quartile of adiponectin were 0.57 (0.41-0.78), 0.39 (0.27-0.56), and 0.18 (0.11-0.27), respectively, after adjustment for age, sex, ethnicity, study center, parental history of diabetes, and hypertension and 0.72 (0.48-1.09), 0.67 (0.43-1.04), and 0.58 (0.34-0.99), respectively, after additional adjustment for BMI, waist-to-hip ratio, fasting glucose, insulin, and a score composed of six inflammation markers. The association was of similar magnitude in men and women and in whites and African Americans, but was absent in smokers and in those with a greater inflammation score (interaction P < 0.01 for each). In conclusion, in this community-based sample of U.S. adults, higher adiponectin levels were associated with a lower incidence of diabetes.

Adiponectin↗