Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Adiponectin”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2006

The adiponectin signaling pathway as a novel pharmacological target.

There appear to be compelling evidences presenting adiponectin as a key regulator of energy homeostasis. Over the past 10 years, much work has been done to identify the molecular mechanisms by which adiponectin functions in the body. We and other groups have demonstrated that adiponectin activates multiple signaling pathways, which mediate its anti-diabetic, anti-atherogenic and anti-inflammatory functions. Comprehensive analysis of the mechanism of adiponectin action may allow us to elucidate the etiology of metabolic syndrome associated diseases including diabetes and cardiovascular diseases, where dysfunction of adiponectin may contribute to pathogenesis of diseases. While regulation of adiponectin gene expression or secretion remains an interesting topic in studies of cell metabolism, further intensive studies are necessary to illustrate the molecular mechanisms. Importantly, identification of molecules in the adiponectin signaling pathways and in the regulation of adiponectin gene expression may provide novel targets for therapeutic drugs.

Adiponectin↗
PubMed2003

Circulating adiponectin levels are reduced in nonobese but insulin-resistant first-degree relatives of type 2 diabetic patients.

Adiponectin, one of the most abundant gene transcript proteins in human fat cells, has been shown to improve insulin action and is also suggested to exert antiatherogenic effects. We measured circulating adiponectin levels and risk factors for atherosclerosis in 45 healthy first-degree relatives of type 2 diabetic subjects (FDR) as well as 40 healthy control subjects (CON) without a known family history of diabetes. Insulin sensitivity (S(i)) was studied with the minimal model, and measurements of adiponectin, metabolic variables, inflammatory markers, and endothelial injury markers, as well as lipoprotein concentrations, were performed. FDR were insulin resistant (3.3 +/- 2.4 vs. 4.5 +/- 2.6 x 10(-4) x min(-1) per microU/ml [mean +/- SD], P < 0.01), and their circulating plasma adiponectin levels (6.6 +/- 1.8 vs. 8.1 +/- 3.0 microg/ml, P < 0.03) were decreased. After adjustments for age in FDR, adiponectin levels were negatively correlated with fasting proinsulin (r -0.64, P < 0.001), plasminogen activator inhibitor (PAI)-1 activity (r -0.56, P < 0.001), fasting insulin (r -0.55, P < 0.001), and acute insulin response (r -0.40, P < 0.05); they were positively related to HDL cholesterol (r 0.48, P < 0.01) and S(i) (r 0.41, P < 0.01). Furthermore, when adjusted for age, waist, and S(i), adiponectin was associated with HDL cholesterol and proinsulin, which explained 51% of the variation in adiponectin in multiple regression analyses in that group. In conclusion, circulating plasma adiponectin levels were decreased in nonobese but insulin-resistant FDR and, in addition, related to several facets of the insulin resistance syndrome (IRS). Thus, hypoadiponectinemia may be an important component of the association between cardiovascular disease and IRS.

Adiponectin↗
PubMed2003

Induction of adiponectin, a fat-derived antidiabetic and antiatherogenic factor, by nuclear receptors.

Adiponectin is a fat-derived hormone with antidiabetic and antiatherogenic properties. Hypoadiponectinemia seen in obesity is associated with insulin-resistant diabetes and atherosclerosis. Thiazolidinediones, peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists, have been shown to increase plasma adiponectin levels by the transcriptional induction in adipose tissues. However, the precise mechanism of such action is unknown. In this study, we have identified a functional PPAR-responsive element (PPRE) in human adiponectin promoter. PPAR-gamma/retinoid X receptor (RXR) heterodimer directly bound to the PPRE and increased the promoter activity in cells. In adipocytes, point mutation of the PPRE markedly reduced the basal transcriptional activity and completely blocked thiazolidinedione-induced transactivation of adiponectin promoter. We have also identified a responsive element of another orphan nuclear receptor, liver receptor homolog-1 (LRH-1), in adiponectin promoter. LRH-1 was expressed in 3T3-L1 cells and rat adipocytes. LRH-1 bound specifically to the identified responsive element (LRH-RE). LRH-1 augmented PPAR-gamma-induced transactivation of adiponectin promoter, and point mutation of the LRH-RE significantly decreased the basal and thiazolidinedione-induced activities of adiponectin promoter. Our results indicate that PPAR-gamma and LRH-1 play significant roles in the transcriptional activation of adiponectin gene via the PPRE and the LRH-RE in its promoter.

3T3 Cells↗
PubMed2003

Genome-wide linkage analysis of serum adiponectin in the Pima Indian population.

Adiponectin is a circulating protein secreted by adipocytes and is thought to have insulin-sensitizing effects. We present genetic analysis of adiponectin levels in 517 Pima Indians without diabetes (from 162 families, 750 sib-pairs). Adiponectin concentrations were heritable, with 39% of the variance of age- and sex-adjusted adiponectin potentially accounted for by additive genetic influences in this population. In genome-wide linkage analyses, suggestive linkage (logarithm of odds [LOD] = 3.0) of adiponectin adjusted for age and sex was found on chromosome 9p at 18 cM. Linkage was also present after inclusion of adiponectin concentrations of siblings with type 2 diabetes not treated pharmacologically (total siblings 582, 182 families, 860 sib-pairs: LOD = 3.5). Tentative evidence of linkage was also found on chromosomes 2 (LOD = 1.7 at 89 cM), 3 (LOD = 1.9 at 124 cM), and 10 (LOD = 1.7 at 70 cM), offering some support to findings of a previous genome-wide scan of adiponectin. Our data suggest that quantitative trait loci on chromosomes 2, 3, 9, and 10 may influence circulating adiponectin concentrations in the Pima population.

Adiponectin↗
PubMed2004

CCAAT/enhancer binding protein and nuclear factor-Y regulate adiponectin gene expression in adipose tissue.

Adiponectin is one of the adipokines secreted by adipocytes and regulates energy homeostasis associated with insulin sensitivity, suggesting a possibility of nutritional regulation of adiponectin gene expression. In this study, we showed that the transcription of adiponectin gene was induced 4-6 h after refeeding of mice. Also, differentiated 3T3-L1 adipocytes that were treated with high glucose expressed significantly increased adiponectin mRNA. Promoter analysis using nuclear extracts from white adipose tissue revealed that CCAAT/enhancer binding protein (C/EBP) and nuclear factor-Y (NF-Y) bound on the -117/-73 region of the adiponectin promoter. This region was critical for the activity of the adiponectin promoter as the deletion or mutation of this region markedly diminished the promoter activity to a basal level. Furthermore, the C/EBP binding increased in both refed animal and high glucose-treated 3T3-L1 adipocytes in an electrophoretic mobility shift assay, suggesting that C/EBP is responsible for the dietary response of the adiponectin gene expression. Chromatin immunoprecipitation studies demonstrated the binding of C/EBP and NF-Y in both mouse and differentiated 3T3-L1 adipocytes and also that C/EBP binding increased in response to high glucose. These findings demonstrated that C/EBP and NF-Y are critical for the regulation of the adiponectin expression in response to nutrients and in the course of adipocyte differentiation.

Adipocytes↗
PubMed2005

Common Polymorphisms in the Adiponectin Gene ACDC Are Not Associated With Diabetes in Pima Indians.

Adiponectin is an abundant adipose tissue-derived protein with important metabolic effects. Plasma adiponectin levels are decreased in obese individuals, and low adiponectin levels predict insulin resistance and type 2 diabetes. Two variants in the adiponectin gene ACDC have been previously associated with plasma adiponectin levels, obesity, insulin resistance, and type 2 diabetes. To determine the role of genetic variation in ACDC in susceptibility to obesity and type 2 diabetes in Pima Indians, we screened the promoter, exons, and exon-intron boundaries of the gene to identify allelic variants. We identified 17 informative polymorphisms that comprised four common (minor allele frequency >15%) linkage disequilibrium clusters consisting of 1-4 variants each. We genotyped one representative polymorphism from each cluster in 1,338 individuals and assessed genotypic association with type 2 diabetes, BMI, serum lipid levels, serum adiponectin levels, and measures of insulin sensitivity and secretion. None of the ACDC variants were associated with type 2 diabetes, BMI, or measures of insulin sensitivity or secretion. One variant, single nucleotide polymorphism (SNP)-12823, was associated with serum adiponectin levels (P = 0.002), but this association explained only 2% of the variance of serum adiponectin levels. Our findings suggest that these common ACDC polymorphisms do not play a major role in susceptibility to obesity or type 2 diabetes in this population.

Adiponectin↗
PubMed2005

C/EBPalpha regulates human adiponectin gene transcription through an intronic enhancer.

Adiponectin is an adipose-derived hormone that enhances insulin sensitivity and plays an important role in regulating energy homeostasis. Here, we demonstrate that the DNA encoding the first intron of the human adiponectin gene contains an intronic enhancer that regulates adiponectin gene expression in an adipose tissue-specific manner. Insertion of the DNA encoding the first intron into reporter constructs containing the proximal adiponectin promoter (Pro-Int1-Luc) resulted in a 20-fold increase in activity relative to the promoter alone in 3T3-L1 adipocytes. Coexpression of CCAAT/enhancer-binding protein (C/EBP)alpha increased luciferase activity of the Pro-Int1-Luc construct approximately 75-fold but had no effect on the constructs containing the proximal adiponectin promoter alone. At least eight potential C/EBPalpha response elements are located between +3000 to +10000 nucleotides within the DNA encoding the first intron, including a 34-bp core sequence for the intronic enhancer that contains three tandem C/EBPalpha response elements. However, the intronic enhancer is not conserved between human and mouse. Overexpression or siRNA-mediated knockdown of endogenous C/EBPalpha significantly increased or decreased, respectively, adiponectin mRNA levels in differentiated human Chub-S7 adipocytes, while neither C/EBPbeta nor C/EBPdelta significantly affected adiponectin expression in mature adipocytes. Thus, C/EBPalpha is a key transcription factor for full activation of human adiponectin gene transcription in mature adipocytes through interaction with response elements in the intronic enhancer.

Adipocytes↗
PubMed2004

Adiponectin concentrations in sera from patients with type 2 diabetes are negatively associated with sympathovagal balance as evaluated by power spectral analysis of heart rate variation.

OBJECTIVE: To investigate whether cardiac autonomic activity, particularly sympathovagal balance as estimated by power spectral analysis (PSA) of heart rate variation (HRV), is associated with serum adiponectin concentrations in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: We studied 105 patients with type 2 diabetes (51 women and 54 men). Serum adiponectin concentrations were measured by sandwich enzyme-linked immunosorbent assay. HRV was determined automatically every 5 min over 24 h using Holter electrocardiographic recording. PSA of R-R intervals was performed using fast Fourier transformation. Low-frequency (both sympathetic and parasympathetic activities), high- frequency (pure parasympathetic activity), and the ratio of low-frequency-to-high-frequency power (LF-to-HF ratio), an index of sympathovagal balance, were used as indexes of cardiac autonomic activity. RESULTS: We found no significant correlation between serum adiponectin and low-frequency or high-frequency power in patients with diabetes. Serum adiponectin concentration correlated negatively with the 24-h LF-to-HF ratio (r = -0.343, P = 0.0009) and creatinine clearance (r = -0.411, P < 0.0001). Serum adiponectin concentrations were significantly higher in patients with overt albuminuria than in those with normoalbuminuria or microalbuminuria. In multivariate analysis controlling for sex, BMI, glycemic control, lipid profile, and renal function, serum adiponectin concentration showed an independent negative association with 24-h LF-to-HF ratio (beta = -0.332, P = 0.020). Furthermore, sex, HDL cholesterol, and renal function retained significant influence on the serum adiponectin concentration in patients with diabetes. CONCLUSIONS: Sympathovagal balance favoring relative sympathetic activation was associated with low serum concentrations of adiponectin in patients with type 2 diabetes.

Adiponectin↗
PubMed2005

Low plasma adiponectin levels are associated with increased hepatic lipase activity in vivo.

OBJECTIVE: Hepatic lipase plays a key role in hydrolyzing triglycerides and phospholipids present in circulating plasma lipoproteins. Plasma hepatic lipase activity is known to be regulated by several hormonal and metabolic factors, but hepatic lipase responsiveness to insulin is still controversial. Hypoadiponectinemia is known to be associated with insulin resistance, diabetes, and obesity. These conditions are often characterized by high plasma triglyceride and low HDL cholesterol levels, and they have been shown to be associated with high plasma hepatic lipase activity. We therefore raised the question whether adiponectin may be associated with plasma hepatic lipase activity in vivo. RESEARCH DESIGN AND METHODS: We measured plasma adiponectin and postheparin hepatic lipase activity in 206 nondiabetic men and in a second group of 110 patients with type 2 diabetes. The correlation of these parameters with markers of insulin resistance and systemic inflammation was investigated. RESULTS: In nondiabetic patients, adiponectin levels were significantly inversely correlated with plasma hepatic lipase activity (r = -0.4, P < 0.01). These results were confirmed in the group of patients with type 2 diabetes (r = -0.32, P = 0.004). Multivariate analysis revealed that adiponectin was the strongest factor influencing hepatic lipase activity. The association was independent of age, sex, BMI, plasma triglycerides, insulin, HDL cholesterol, and high-sensitivity C-reactive protein and accounted for approximately 10 and 12% of the variation in hepatic lipase activity in the two different patient cohorts, respectively. CONCLUSIONS: These results demonstrate for the first time a significant inverse association between adiponectin and postheparin plasma hepatic lipase activity that is independent of other factors such as markers of insulin resistance or inflammation. Therefore, adiponectin, rather than insulin, may represent an important factor contributing to the regulation of hepatic lipase activity in both nondiabetic individuals and patients with type 2 diabetes. The effect of adiponectin on hepatic lipase activity may also help to explain the HDL cholesterol-elevating action of adiponectin.

Adiponectin↗
PubMed2004

[Adiponectin levels and coronary risk factors in the elderly].

AIM: To determine the relationship between adiponectin level and coronary risk factors in men. METHODS: The subjects were 395 elderly men in two rural communities (Tanno, Sobetsu) in Japan. Blood pressure in the sitting position (SBP/DBP), after overnight fasting, plasma glucose level (FPG), total cholesterol (TC), triglyceride (TG), HDL cholesterol (HDL) and serum adiponectin were measured. The subjects were divided into two adiponectin level groups, a high adiponectin level (> or = 7.94 microg/ml) group (H-Adipo group) and a normal adiponectin level (< 7.94 microg/ml) group (N-Adipo group), and into two age groups, 70 years of age or older (70 or older group) and less than 70 years of age (under 70 group). RESULTS: Adiponectin showed negative correlations with BMI, FPG, TC and TG and positive correlations with age, SBP and HDL. In multiple regression analysis using adiponectin as a dependent variable. BMI, SBP, FPG, TG and HDL were selected as independent variables. Age and HDL in the H-Adipo group were significantly higher than those in the N-Adipo group, and BMI, FPG, TC and TG in the H-Adipo group were significantly lower than those in the N-Adipo group. In the 70 or older group. SBP and adiponectin were significantly higher and BMI, DBP, FPG, TC and TG were significantly lower than those in the under 70 group. The mean number of total coronary risk factors in the 70 or older group (1.71) was significantly lower than that in the under 70 group (2.06). CONCLUSIONS: Coronary risk factors other than systolic blood pressure were significantly reduced in the older subjects.

Adiponectin↗
PubMed2004

[Serum adiponectin levels in patients with obstructive sleep apnea-hypopnea syndrome].

OBJECTIVE: To explore the changes of serum adiponectin levels in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). METHODS: Polysomnography was performed in 71 obese OSAHS patients (obese OSAHS group), 21 OSAHS patients without obesity (non-obese OSAHS group), 26 obese controls (obese group) and 22 normal healthy adults (control group). In both the obese OSAHS group and obese group, the body mass index (BMI) was higher than 25 and there was no significant difference in BMI. Serum adiponectin levels were measured by radioimmunoassay. RESULTS: The serum adiponectin level in the control group [(8.9 +/- 0.6) mg/L] was significantly higher than those in the obese group [(7.1 +/- 1.3) mg/L, P < 0.05], the non-obese OSAHS group [(5.4 +/- 0.6) mg/L, P < 0.01] and the obese OSAHS group [(5.0 +/- 1.0) mg/L, P < 0.01] respectively. The serum adiponectin level was significantly lower in both the obese OSAHS group and the non-obese OSAHS group (all P < 0.05). The serum adiponectin levels between the obese OSAHS group and the non-obese OSAHS group showed no statistical difference (P > 0.05). In the obese OSAHS patients and the obese patients serum adiponectin levels were negatively correlated with AHI (r = -0.78, P < 0.01), BMI (r = -0.21, P < 0.05), waist circumference (r = -0.36, P < 0.01), and neck circumference (r = -0.42, P < 0.01), but positively correlated with minimal pulse oxygen saturation (r = 0.48, P < 0.01). CONCLUSIONS: Serum adiponectin levels were significantly lower in OSAHS patients than in the normal control and the obese patients. In addition to increased waist and neck circumferences, OSAHS may contribute to the decreased serum adiponectin level.

Adiponectin↗
PubMed2005

Adiponectin, an adipocyte-derived protein.

Adipose tissue is a hormonally active tissue, producing adipocytokines which may influence activity of other tissues. Adiponectin, abundantly present in the plasma increases insulin sensitivity by stimulating fatty acid oxidation, decreases plasma triglycerides and improves glucose metabolism. Adiponectin levels are inversely related to the degree of adiposity. Anorexia nervosa and type 1 diabetes are associated with increased plasma adiponectin levels and higher insulin sensitivity. Decreased plasma adiponectin levels were reported in insulin-resistant states, such as obesity and type 2 diabetes and in patients with coronary artery disease. Activity of adiponectin is associated with leptin, resistin and with steroid and thyroid hormones, glucocorticoids, NO and others. Adiponectin suppresses expression of extracellular matrix adhesive proteins in endothelial cells and atherosclerosis potentiating cytokines. Anti-atherogenic and anti-inflammatory properties of adiponectin and the ability to stimulate insulin sensitivity have made adiponectin an important object for physiological and pathophysiological studies with the aim of potential therapeutic applications.

Adipocytes↗
PubMed2005

[Serum adiponectin concentration in relation to body fat distribution and tissue insulin sensitivity in the glucose clamp study].

OBJECTIVE: To study serum adiponectin level in relation to body fat distribution and tissue insulin sensitivity by using the extended hyperinsulinemic euglycemic clamp technique. METHODS: Extended hyperinsulinemic euglycemic clamp was performed in 44 Chinese individuals with normal glucose tolerance from Shanghai area, including 12 subjects with normal weight [body mass index (BMI) < 25 kg/m(2)], 19 with overweight (25 kg/m(2) < or = BMI < 30 kg/m(2)), and 13 with obesity (BMI > or = 30 kg/m(2)). The rate of insulin-mediated glucose disposal (Rd) during the steady state of glucose clamp was used to assess the peripheral tissue insulin sensitivity. Total body fat depots [BMI, percentage of body fat (FAT%), and body fat mass (FM)], regional body fat depots [waist circumference (W), hip circumference (H), W and H ratio (WHR), abdominal subcutaneous fat area (SA), intra-abdominal fat area (VA), and femoral subcutaneous fat area (FA)] were measured on all subjects. Fasting serum adiponectin level was determined by radioimmunoassay. RESULTS: (1) After the adjustment for age and sex, the serum adiponectin concentrations in the overweight and obesity groups were (8.7 +/- 4.8) mg/L and (6.7 +/- 0.8) mg/L, both significantly lower than that in the normal weight group [(15.7 +/- 1.8) mg/L, both P < 0.01]. (2) Serum adiponectin concentration was negatively correlated with BMI, W, WHR, FAT%, FM and VA, especially with W and VA (r = -0.46, P < 0.01, and r = -0.53, P < 0.01). (3) Serum adiponectin concentration was positively correlated with Rd (r = 0.52, P < 0.01) and the rate of glycogen synthesis (r = 0.36, P < 0.05), and was negatively correlated with free fatty acid level (r = -0.41, P < 0.05). (4) Stepwise regression analysis indicated that in addition to sex, BMI, WHR or VA and SA, serum adiponectin level was also the independent contributing factor for Rd, which explains 3.52% and 4.84% of the variance respectively (P all < 0.05). CONCLUSION: (1) The decrease in serum adiponectin level is associated with the increase of total body fat depot, especially the increase of total body fat depot in intra-abdominal fat area. (2) Serum adiponectin level is an independent contributing factor for insulin sensitivity.

Adiponectin↗
PubMed2005

Biological background and role of adiponectin as marker for insulin resistance and cardiovascular risk.

Adiponectin is a serum protein secreted by adipocytes and accounts for approximately 0.01% of total plasma protein. In healthy patient populations adiponectin can be found in concentrations of 7-12 mg/l. Unlike other adipocyte products, adiponectin correlates with decreased free fatty acid blood concentrations and reduced body mass index or body weight. Adiponectin protects from vascular diseases by inhibiting local proinflammatory signals, preventing preatherogenic plaque formation, and by impeding arterial wall thickening. Proinflammatory state and endothelial dysfunction are nominators of the metabolic syndrome, a complex set of risk factors including vascular and metabolic insulin resistance with hyperglycemia, hypertension, and dyslipidemia. Over the past years, thiazolidinediones, like rosiglitazone or pioglitazone, became known as a therapeutic option for patients suffering from the metabolic syndrome. It is considered that insulin sensitizers exert their benefit through indirect induction of adiponectin expression. Clinical studies have confirmed that treatment with thiazolidinediones may increase adiponectin concentrations in patients with type 2 diabetes independent from improvements in blood glucose control or parallel treatment with insulinotropic drugs. These findings suggest that adiponectin may have a diagnostic value and can be used especially for monitoring treatment success. This review summarizes recent biological and clinical data indicating that adiponectin may be the molecular link between obesity and insulin resistance and may serve as a biomarker for the metabolic syndrome.

Adiponectin↗
PubMedDate not supplied

[Serum leptin and adiponectin concentrations in patients infected with human immunodeficiency virus type 1 (HIV-1) on antiretroviral therapy].

UNLABELLED: The lipodystrophy syndrome with dyslipidaemia and insulin resistance is side-effect of combined antiretroviral therapy (CART). AIM OF THE STUDY: to describe the influence of CART on leptin and adiponectin concentration in connection with lipids levels in HIV-infected patients on antiretroviral therapy. BMI, serum leptin, adiponectin, triglycerides, total cholesterol, HDL- and LDL-cholesterol concentrations were measured in 56 HIV(+) patients before and on CART; average of treatment duration 38.4 +/-13.2 months. Significant increase of BMI (p=0.0268) of (22.6 +/- 3.3 before and 23.5 +/- 3.4 kg/m2 on therapy, respectively) and all analyzed lipids were found. Mean adiponectin concentration in treated patients was significantly (7.256 +/- 3.551 microg/ml) lower than mean value before treatment (8.395 +/- 3.568 microg/ml; p=0.0011). Mean values of leptin concentrations did not differ significantly (before therapy 3.721 +/- 0.347 log10; on therapy 3.1737 +/- 0.353 log10). Significant positive correlation between BMI and leptin concentrations was found before, as well as during CART (r=0.5333; p<0.0001), but negative correlation between adiponectin and leptin concentrations (r=-0.2677; p=0.042). Leptin and adiponectin concentrations did not revealed significant correlation with lipids levels before therapy. The decrease of adiponectin concentration on CART correlated negatively with total (r=-0.2912; p=0.0310) and LDL-cholesterol (r=-0.310; p=0.0225). CART lasting longer than 2 years resulted in the decrease of adiponectin concentration, with lack of influence on leptin concentration in analyzed group. The increase of total cholesterol and LDL-cholesterol in correlation with the decrease of adiponectin concentration confirms that CART induces metabolic disturbances related to higher risk of atherosclerosis and its sequel.

Adiponectin↗
PubMed2005

Inverse relationship between plasminogen activator inhibitor-I activity and adiponectin in overweight and obese women. Interrelationship with visceral adipose tissue, insulin resistance, HDL-chol and inflammation.

Adipose tissue is an active endocrine organ secreting different adipokines such as plasminogen activator inhibitor-1 (PAI-1) and adiponectin, among many others. In this study, we investigated the association between PAI-1 activity and serum adiponectin levels in a group of 444 overweight and obese women and assessed the interrelationship with visceral adipose tissue (VAT; CT-scan L4-L5), insulin resistance (HOMA-IR), HDL cholesterol (HDL-chol) and inflammation (hs-CRP). PAI-1 was inversely related to adiponectin (r = -0.25, p < 0.001; adjusted for age and BMI). After adjustment for age, VAT, HOMA-IR and hs-CRP, the relationship remained significant (r = -0.15; p = 0.001), but disappeared after additional adjustment for HDL-chol (r = -0.09; p = 0.067). Subjects were divided in two groups according to the median levels of adiponectin or PAI-1 levels. PAI-1 activity (19.1 +/- 11.4 vs. 15.8 +/- 8.6 AU/ml; p = 0.003) and adiponectin levels (9.8 +/- 4.6 vs. 8.4 +/- 4.0 microg/ml; p < 0.001) were significantly higher in the low adiponectin/PAI-1 groups. The difference in PAI-1 remained significant after adjustment for age and BMI (p = 0.001), became borderline significant after adjustment for age and VAT (p = 0.052), and disappeared after adjustment for age and HOMA-IR (p = 0.116) or age and HDL-chol (p = 0.443). The difference in adiponectin levels remained significant after adjustment for age, VAT, HOMA-IR and hs-CRP (p = 0.006), but disappeared after additional adjustment for HDL-chol (p = 0.089). Further analyses suggest a contribution of HOMA-IR and/or HDL-chol in the relationship between PAI-1 and adiponectin. HDL-chol was found to be the only factor independently determining both factors. In conclusion, in overweight and obese women, PAI-1 activity was inversely related to serum adiponectin, independent of visceral adipose tissue.

Adiponectin↗
PubMed2006

The relationship between adiponectin levels and metabolic status in centenarian, early elderly, young and obese women.

OBJECTIVES: Adipose tissue secretes proteins which regulate energy metabolism and insulin sensitivity. Adiponectin possesses anti-diabetic, anti-atherogenic and insulin-sensitizing properties. To assess the prognostic factors in prolonged survival and the potential protective role of adiponectin in aging, we examined the release of adiponectin in relation to the metabolic status of centenarians, compared with young, early elderly and obese subjects. MATERIAL AND METHODS: The study was carried out on 122 women: 22 centenarians aged 100-102 yrs, 45 younger women aged 20-43 yrs, 19 early elderly women aged 64-67 yrs, and 36 obese women aged 26-54 yrs. Anthropometric data, clinical features and blood samples were obtained. Plasma adiponectin and insulin concentrations were measured by RIA methods. Fasting plasma glucose levels, lipid profile and creatinine concentrations were determined using routine laboratory procedures. RESULTS: In centenarians we found that adiponectin concentrations were significantly increased, compared with young, early elderly and obese women. Insulin concentrations were lower than those in young and obese subjects. HOMA-IR was significantly lower than in obese women. Positive correlations were found between adiponectin and HDL, and negative correlations between adiponectin and HOMA-IR, total cholesterol, LDL, triglycerides, blood pressure and BMI. CONCLUSION: Our results indicate that adiponectin may play a protective role that contributes to longevity.

Adiponectin↗
PubMed2006

[Gender differences in adiponectin and leptin expression in epicardial and subcutaneous adipose tissue. Findings in patients undergoing cardiac surgery].

INTRODUCTION AND OBJECTIVES: The high level of metabolic activity present in visceral adipose tissue is associated with the development of atherothrombosis. Subcutaneous adipose tissue secretes larger quantities of the adipocytokines leptin and adiponectin than visceral adipose tissue. Epicardial adipose tissue secretes inflammatory mediators, and the resulting proinflammatory activity is greater than that associated with subcutaneous adipose tissue. The aim of this study was to compare adiponectin and leptin expression in human epicardial and subcutaneous adipose tissue. METHODS: Samples of both epicardial and subcutaneous adipose tissue were taken from 46 patients who were undergoing heart surgery, coronary artery bypass surgery, or aortic or mitral valve replacement. Levels of protein and gene expression of leptin and adiponectin were assessed immunohistochemically and by RT-PCR, respectively. Levels of mRNA expression in the 2 adipose tissue types were compared by real-time quantitative PCR. RESULTS: Significant differences were found between adiponectin and leptin mRNA expression in epicardial and subcutaneous adipose tissue, with epicardial adipose tissue exhibiting lower levels of adiponectin and leptin expression. Moreover, adiponectin and leptin mRNA expression in epicardial adipose tissue was higher in women than men. CONCLUSIONS: Adiponectin and leptin expression is lower in epicardial than in subcutaneous adipose tissue. Moreover, there are differences in adiponectin and leptin expression in epicardial adipose tissue between women and men.

Adiponectin↗