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 307 records · Page 17Linked to original sources
PubMed2005

Prostate cancer and adiponectin.

OBJECTIVES: To search for any relation between plasma adiponectin levels and the cellular differentiation or progression of prostate cancer (PCa). PCa is becoming an increasingly important public health problem, particularly for those countries with a trend toward an aging population. Because insulin resistance in the setting of obesity is associated with the development of PCa, we hypothesized that decreased adiponectin levels might underlie the association between PCa and obesity/insulin resistance. METHODS: In this study, we investigated plasma adiponectin levels in 30 patients with PCa, 41 subjects with benign prostatic obstruction, and 36 healthy individuals. The body mass index and age of the groups were similar. Patients with PCa were stratified into two groups according to the spread of the disease as organ-confined and advanced disease and into three groups according to grade (low, intermediate, and high grade determined by a Gleason sum of less than 5, between 5 and 7, and more than 7, respectively). RESULTS: Plasma adiponectin levels were significantly lower in the PCa group than in the benign prostatic obstruction group or controls (P < 0.001 for both). Additionally, the plasma adiponectin levels were significantly lower in the advanced disease group than in the organ-confined PCa group (P = 0.012). Significant negative associations were found between plasma adiponectin levels and prostate-specific antigen levels or biopsy Gleason scores in the PCa group. The plasma adiponectin levels of those with high-grade PCa were also significantly lower than those for both the low-grade and intermediate-grade groups (P < 0.001 for both). CONCLUSIONS: The results of the present study imply that plasma adiponectin levels are not only lower in patients with PCa but are also negatively associated with the histologic grade and disease stage. Future prospective studies are recommended to establish any causal relation between PCa and plasma adiponectin levels.

Adiponectin↗
PubMed2003

Adiponectin gene expression and secretion is inhibited by interleukin-6 in 3T3-L1 adipocytes.

Recently, it has been shown that adiponectin is an important insulin-sensitizing fat-derived protein which is downregulated in insulin resistance and obesity, and replenishment of which improves insulin sensitivity. In contrast, interleukin (IL)-6 appears as an adipocytokine serum concentrations of which are elevated in these states. However, it has not been determined whether IL-6 might impact on expression and secretion of adiponectin. To clarify this, 3T3-L1 adipocytes were treated with different concentrations of IL-6 for various periods of time. Adiponectin mRNA was measured by quantitative real-time reverse transcription-polymerase chain reaction and secretion was determined by radioimmunoassays. Interestingly, treatment of 3T3-L1 cells with 30 ng/ml IL-6 significantly decreased adiponectin secretion to 75% of control levels. Adiponectin secretion was also inhibited between 25% and 45% by chronic treatment with forskolin (50 microM), tumor necrosis factor alpha (100 ng/ml), and dexamethasone (100 nM). Furthermore, adiponectin mRNA expression was downregulated by up to 50% in a time- and dose-dependent manner, with significant inhibition detectable at concentrations as low as 3 ng/ml IL-6 and as early as 8h after effector addition. The inhibitory effect of IL-6 was partially reversed by pretreatment of 3T3-L1 cells with pharmacological inhibitors of a p44/42 mitogen-activated protein (MAP) kinase. Moreover, the negative effect of IL-6 on adiponectin mRNA expression could be reversed by withdrawal of the hormone for 24h. Taken together, our results suggest that adiponectin gene expression is reversibly downregulated by IL-6 and support the concept of adiponectin being an important selectively controlled modulator of insulin sensitivity.

3T3 Cells↗
PubMed2002

Plasma adiponectin levels in overweight and obese Asians.

OBJECTIVE: Hypoadiponectin has been documented in subjects with obesity, diabetes mellitus, or coronary heart disease, suggesting a potential use of plasma adiponectin in following the clinical progress in subjects with metabolic syndrome (MS). In this study, we investigated the plasma adiponectin levels in relation to the variables of MS among overweight/obese Asian subjects. RESEARCH METHODS AND PROCEDURES: The plasma adiponectin, anthropometric and biochemical measurements, oral glucose tolerance tests (OGTT), and modified insulin suppression tests were performed on 180 overweight/obese Asian subjects [body mass index (BMI) >or= 23 kg/m(2)], including 47 subjects with morbid obesity (BMI >or= 40 kg/m(2)). RESULTS: The plasma adiponectin levels negatively correlated with BMI, waist-to-hip ratio, fasting plasma glucose, insulin, triglyceride, uric acid levels, hyperinsulinemia, and glucose intolerance in OGTT, but positively with high-density lipoprotein-cholesterol. In contrast, they were not related to blood pressure and total cholesterol. Moreover, insulin sensitivity, measured by quantitative insulin sensitivity check index (QUICKI) or in insulin suppression tests, significantly correlated with the plasma adiponectin levels. Among morbidly obese subjects, only the waist-to-hip ratio correlated with the plasma adiponectin levels. Using multivariate linear regression models, the area under curve of plasma glucose in OGTT and high-density lipoprotein-cholesterol among the overweight/obese subjects and WHR among the morbidly obese subjects were significantly related to the plasma adiponectin levels after adjustment for other variables. DISCUSSION: In overweight/obese Asians, the plasma adiponectin levels significantly correlated with various indices of MS except hypertension. Whether the plasma adiponectin level could be a suitable biomarker for following the clinical progress of MS warrants further investigation.

Adiponectin↗
PubMed2004

Association of the human adiponectin gene and insulin resistance.

Adiponectin is an adipocyte-secreted protein that modulates insulin sensitivity and whose low circulating concentration is associated with insulin resistance. In the present study, we analysed the association between two single-nucleotide polymorphisms (SNPs) in the adiponectin gene and insulin resistance in 253 nondiabetic subjects. In addition, we investigated whether this association is modulated by body mass index (BMI) levels. The SNPs +45T>G and +276G>T in the human adiponectin gene were detected in real-time PCR with LightCycler. No association was found with the +45T>G SNP. The +276G>T SNP was associated with higher BMI (P<0.01), plasma insulin (P<0.02) and HOMA(IR) (P<0.02). To analyse the possible interaction between BMI and the adiponectin gene on insulin resistance, the study group was divided into two subgroups, according to the BMI below or above the median of 26.2 kg/m(2). In both subgroups, subjects carrying the +276G>T SNP had higher HOMA(IR); however, the difference was highly significant among leaner (P<0.001), but not among heavier individuals, indicating that BMI status and the adiponectin gene interact in modulating insulin resistance. Among individuals with BMI <26.2 kg/m(2), the relative risk of insulin resistance was 9.7 (CI: 1.32-87.7, P<0.035). In a subgroup of 67 subjects, carriers of the +276G>T SNP had significantly (P<0.05) lower mean serum adiponectin levels (25.7 ng/ml) compared to noncarriers (37.0 ng/ml), suggesting a possible influence of the +276G>T SNP on adiponectin levels. In summary, we observed an association between the +276G>T SNP in the adiponectin gene and insulin resistance. In particular, among leaner individuals, the adiponectin gene appears to determine an increased risk to develop insulin resistance.

Adiponectin↗
PubMed2006

Low serum adiponectin levels in subjects born small for gestational age: impact on insulin sensitivity.

OBJECTIVE: Increasing evidence point to the role of the adipose tissue on the insulin resistance associated with reduced fetal growth. Since adiponectin, exclusively produced by the adipose tissue, exerts an important insulin-sensitizing activity, it appears critical to investigate the effect of being born small for gestational age (SGA) on adiponectin production in adulthood and its relationship with insulin sensitivity. SUBJECTS AND METHODS: Serum adiponectin concentrations were measured in 486 young adults born SGA, precisely selected on birth data, who were compared to 573 age-matched subjects born appropriate for gestational age (AGA). The relationship between serum adiponectin levels and insulin-resistance indices measured under OGTT were tested and compared between the two groups. RESULTS: The SGA group demonstrated significantly reduced serum adiponectin levels than controls (12.6 +/- 6.9 vs 13.2 +/- 6.4 microg/ml, P = 0.02) and the difference remained significant when the key regulatory factors were taken into account (P = 0.008). In the AGA group, fasting I/G taken as an insulin-resistance index negatively correlated with serum adiponectin concentrations (P = 0.02), while the relationship followed a U-shape with increased fasting I/G ratio despite high concentrations of serum adiponectin in the SGA group (P = 0.12). CONCLUSION: Subjects born SGA demonstrated significantly reduced serum adiponectin levels, which were not related to insulin-resistance indices in comparison to what observed in age-matched subjects born AGA. Although this defect in adiponectin production and in its insulin-sensitizing action remains to be elucidated at the molecular level, it strengthens the critical contribution of the adipose tissue in the metabolic complications associated with reduced fetal growth.

Adiponectin↗
PubMed2006

Sex-specific determinants of serum adiponectin in older adults: the role of endogenous sex hormones.

OBJECTIVE: To assess the sex-specific association of adiponectin with multiple factors thought to influence its levels, with a special emphasis on endogenous sex hormones. DESIGN AND METHODS: A cross-sectional study of determinants of serum adiponectin in 873 men and 673 postmenopausal women, ages 50-92. Factors evaluated include age, body size, fat distribution, lifestyle (exercise, smoking, alcohol intake), insulin resistance, renal function and endogenous sex hormone levels (total and bioavailable testosterone and estradiol). RESULTS: Median serum adiponectin was 50% higher in women than men (P<0.001). In unadjusted analyses, adiponectin was positively related to age, alcohol intake, high-density lipoprotein (HDL) and testosterone, and negatively related to waist girth, body mass index, Homeostasis Model Assessment for Insulin Resistance (HOMA-IR), triglycerides and bioavailable estradiol in both sexes (all P<0.01). Adiponectin was positively related to blood urea nitrogen, a measure of renal function, in men only (P<0.001). Sex-specific multivariate linear regressions adjusting for HDL and triglycerides showed that only age, HOMA-IR and sex hormones independently predicted circulating adiponectin for both men and women. Higher levels of endogenous testosterone and lower bioavailable estradiol concentrations each predicted higher adiponectin; this was true for both sexes, and was not explained by differences in age, adiposity, alcohol intake, insulin resistance or lipoprotein levels. CONCLUSIONS: The association of adiponectin with the factors studied here is strikingly similar for men and women. Sex differences in circulating adiponectin levels in older adults cannot be explained by sex hormone regulation.

Adiponectin↗
PubMed2002

Correlation of the adipocyte-derived protein adiponectin with insulin resistance index and serum high-density lipoprotein-cholesterol, independent of body mass index, in the Japanese population.

Adiponectin, which is secreted specifically by adipose tissue, has been shown to act as an anti-atherosclerotic protein by direct effects on endothelial cells. Clinical studies have shown that adiponectin levels are lower in individuals with obesity, diabetes and coronary artery disease. The present study investigated relationships between serum adiponectin levels and body mass index (BMI), blood pressure, insulin resistance index, lipid profile, uric acid and high-sensitivity C-reactive protein levels in a large number of Japanese subjects not taking any medication for metabolic disease and without severe illness (705 men and 262 women; age 30-65 years; BMI 22.5+/-2.9 kg/m(2)). The serum adiponectin concentration was measured by ELISA, without a protein-denaturing step. The insulin resistance index was assessed by homoeostasis model assessment (HOMA-IR). The serum concentration of adiponectin in women (13.5+/-7.9 microg/ml) was significantly higher than that in men (7.2+/-4.6 microg/ml). The serum adiponectin level was negatively correlated with BMI, systolic blood pressure, diastolic blood pressure, fasting plasma glucose, insulin, HOMA-IR, total cholesterol, triacylglycerols, low-density lipoprotein (LDL)-cholesterol and uric acid, and positively correlated with high-density lipoprotein (HDL)-cholesterol. The correlations between serum adiponectin level and insulin, HOMA-IR, triacylglycerols, HDL-cholesterol, LDL-cholesterol and uric acid were significant even after adjustment for age, sex and BMI. Stepwise multiple regression analysis revealed that HDL-cholesterol, sex, BMI and HOMA-IR were independently correlated with the serum adiponectin level (R(2)=0.377). These findings suggest that the serum adiponectin level is negatively correlated with HOMA-IR and positively correlated with HDL-cholesterol, independent of age, sex and BMI, in the Japanese population.

Adiponectin↗
PubMed2003

Circulating adiponectin levels during human endotoxaemia.

Adiponectin, an adipocytokine secreted by fat tissue, may prevent development of diabetes type II, as high adiponectin levels are linked with insulin sensitivity. In contrast, tumour necrosis factor (TNF)-alpha, which is also produced by fat tissue, leads to insulin resistance and furthermore inhibits adiponectin mRNA production and secretion of the protein. However, adiponectin also negatively regulates TNF-alpha levels. Therefore, we set out to test whether an infusion of endotoxin would influence circulating adiponectin levels in healthy human subjects. Twenty-three healthy human subjects were injected with endotoxin (2 ng/kg body weight); eight of these subjects were also injected with saline and served as controls. Plasma levels of adiponectin, TNF-alpha and interleukin-6 were measured at 0, 1.5, 2, 4, 8 and 24 h. TNF-alpha and interleukin-6 levels peaked at 1.5 h and 2 h, respectively. Control subjects injected with saline showed a decrease in adiponectin plasma levels with time (P < 0.05) presumably owing to the effect of fasting or physical inactivity. However, there was no change in adiponectin plasma levels in endotoxin injected subjects, thus the effect of fasting was opposed. In conclusion, circulating adiponectin levels are reduced during a resting and fasting state, an effect reversed by endotoxin injection.

Adiponectin↗
PubMed2002

Adiponectin--its role in metabolism and beyond.

Adiponectin is a recently identified adipose tissue-derived protein (adipocytokine) with important metabolic effects. It is exclusively expressed in adipose tissue and released into the circulation. Adiponectin expression and/or secretion is increased by insulin like growth factor-1 and ionomycin, and decreased by tumor necrosis factor-alpha, glucocorticoids, beta-adrenergic agonists and cAMP. Data for insulin are somewhat inconclusive. Moreover, adiponectin expression and secretion are increased by activators of peroxisome proliferator-activated receptor (PPAR)-gamma. Besides inhibiting inflammatory pathways, recombinant adiponectin increases insulin sensitivity and improves glucose tolerance in various animal models. This insulin-sensitizing effect appears to be mostly attributable to enhanced suppression of glucose production, but beneficial effects on muscle cannot be excluded. In humans, plasma adiponectin concentrations exceed those of any other hormone by a thousand times; they decrease with obesity and are positively associated with whole-body insulin sensitivity. Therefore, low adiponectin may contribute to the decrease in whole-body insulin sensitivity that accompanies obesity. Furthermore, there is increasing evidence that genetic variants in the adiponectin gene itself and/or in genes encoding adiponectin-regulatory proteins--such as PPAR-gamma--may be associated with hypoadiponectinemia, insulin resistance and type 2 diabetes. This suggests that adiponectin may reflect PPAR-gamma activity in vivo. Finally, reversal or alleviation of hypoadiponectinemia may represent a target for development of drugs improving insulin sensitivity and glucose tolerance.

Adiponectin↗
PubMed2003

Plasma adiponectin levels in women with anorexia nervosa.

Adiponectin is a plasma protein exclusively secreted by adipose tissue, which plays a role in modulating lipid and glucose metabolism. The plasma adiponectin concentration shows an inverse correlation with the body mass index in normal and obese individuals, but it has not been investigated in subjects with an extremely low body weight and undernutrition such as anorexia nervosa patients. We investigated plasma adiponectin levels in 21 females with anorexia nervosa. Nineteen healthy females served as the lean control group. The subjects with anorexia nervosa had a significantly lower weight and showed a tendency towards higher adiponectin levels than the control group. No correlation between adiponectin and BMI was found in patients with anorexia nervosa, while a linear negative correlation was seen in lean controls. The patient who showed the lowest adiponectin level reached a life-threatening state and required intravenous feeding in hospital. In association with improved nutrition and weight gain, the adiponectin level increased gradually until the body mass index was about 16 and then decreased subsequently as would be expected in lean normal subjects. These observations suggest that adipose tissue secretes less adiponectin and the adiponectin levels do not show an inverse correlation simply with body mass index in some subjects with severe undernutrition.

Adiponectin↗
PubMed2006

Association of serum adiponectin concentration to lipid and glucose metabolism in healthy humans.

BACKGROUND: Adiponectin is a recently discovered plasma protein with many associations to glucose and lipid metabolism. Due to its central role in cardiovascular diseases and insulin resistance, we studied the relationship between serum adiponectin and factors reflecting glucose and lipid metabolism. METHODS AND RESULTS: Thirty healthy participants (20M/10F, age 32.0 +/- 2.1 years, BMI 25.8 +/- 0.9 kg/m (2) and HbA (1c) 5.2 +/- 0.1 %) were studied four times at approximately one week intervals. The effects of a 4-hour euglycemic hyperinsulinemia (40 mU/m (2)/min), saline infusion (control), oral glucose, and oral fat load on serum adiponectin were studied. No significant correlation was found between serum adiponectin and insulin sensitivity before (r = 0.25) or after adjustment for age, BMI and gender (r = 0.04). Adiponectin concentration correlated inversely with HbA (1c) (r = - 0.43, p < 0.05), insulin concentration (r = - 0.38, p < 0.05) and triglyceride concentration (r = - 0.42, p < 0.05) but positively with HDL cholesterol (r = 0.38, p < 0.05). Metabolic procedures had no effect on serum adiponectin. CONCLUSIONS: Our findings favor the interpretation that adiponectin is not causally related to insulin sensitivity in healthy participants. The strongest associations of adiponectin in healthy participants are to be found to lipid metabolism. Serum levels of adiponectin are very stable and not acutely affected by hyperinsulinemia, oral glucose or fat load.

Adiponectin↗
PubMed2004

Adiponectin-induced antiangiogenesis and antitumor activity involve caspase-mediated endothelial cell apoptosis.

Obesity is a risk factor for the development of many severe human diseases such as cardiovascular disorders, diabetes, and cancer, which are tightly linked to angiogenesis. The adipose tissue produces several growth factors/hormones including leptin, tumor necrosis factor alpha, and adiponectin. It has been found that adiponectin levels are reduced in obesity. Here, we report a unique function of adiponectin as a negative regulator of angiogenesis. In vitro, adiponectin potently inhibits endothelial cell proliferation and migration. In the chick chorioallantoic membrane and the mouse corneal angiogenesis assays, adiponectin remarkably prevents new blood vessel growth. Further, we demonstrate that the antiendothelial mechanisms involve activation of caspase-mediated endothelial cell apoptosis. Adiponectin induces a cascade activation of caspases-8, -9, and -3, which leads to cell death. In a mouse tumor model, adiponectin significantly inhibits primary tumor growth. Impaired tumor growth is associated with decreased neovascularization, leading to significantly increased tumor cell apoptosis. These data demonstrate induction of endothelial apoptosis as an unique mechanism of adiponectin-induced antiangiogenesis. Adiponectin, as a direct endogenous angiogenesis inhibitor, may have therapeutic implications in the treatment of angiogenesis-dependent diseases.

Adiponectin↗
PubMed2002

Role of adiponectin in preventing vascular stenosis. The missing link of adipo-vascular axis.

Obesity is more linked to vascular disease, including atherosclerosis and restenotic change, after balloon angioplasty. The precise mechanism linking obesity and vascular disease is still unclear. Previously we have demonstrated that the plasma levels of adiponectin, an adipose-derived hormone, decreases in obese subjects, and that hypoadiponectinemia is associated to ischemic heart disease. In current the study, we investigated the in vivo role of adiponectin on the neointimal thickening after artery injury using adiponectin-deficient mice and adiponectin-producing adenovirus. Adiponectin-deficient mice showed severe neointimal thickening and increased proliferation of vascular smooth muscle cells in mechanically injured arteries. Adenovirus-mediated supplement of adiponectin attenuated neointimal proliferation. In cultured smooth muscle cells, adiponectin attenuated DNA synthesis induced by growth factors including platelet-derived growth factor, heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF), basic fibroblast growth factor, and EGF and cell proliferation and migration induced by HB-EGF. In cultured endothelial cells, adiponectin attenuated HB-EGF expression stimulated by tumor necrosis factor alpha. The current study suggests an adipo-vascular axis, a direct link between fat and artery. A therapeutic strategy to increase plasma adiponectin should be useful in preventing vascular restenosis after angioplasty.

Adenoviridae↗
PubMed2004

Adiponectin stimulates angiogenesis in response to tissue ischemia through stimulation of amp-activated protein kinase signaling.

Obesity is a risk factor for the development of cardiovascular diseases that are associated with impaired angiogenesis. Adiponectin is an adipocyte-specific adipocytokine with anti-atherogenic and anti-diabetic properties, and its plasma levels are reduced in association with obesity-linked diseases. Here, we investigated whether adiponectin regulates angiogenesis in response to tissue ischemia using adiponectin knock-out (KO) mice. Angiogenic repair of ischemic hind limbs was impaired in adiponectin-KO mice compared with wild-type (WT) mice as evaluated by laser Doppler flow method and capillary density analyses. Adenovirus-mediated supplement of adiponectin accelerated angiogenic repair in both adiponectin-KO and WT mice. Intramuscular injection of an adenovirus encoding dominant-negative AMP-activated kinase diminished the improvement in limb perfusion seen in WT mice and abolished the adiponectin-induced enhancement of perfusion. These data indicate that adiponectin can function to stimulate angiogenesis in response to ischemic stress by promoting AMP-activated kinase signaling. Therefore, adiponectin may be useful in the treatment for obesity-related vascular deficiency diseases.

AMP-Activated Protein Kinases↗
PubMed2006

Can adiponectin predict gestational diabetes?

The aim of the present study was to evaluate whether adiponectin is a predictive factor for gestational diabetes mellitus (GDM) and is appropriate as a screening test for GDM. Three-hundred and fifty-nine women with singleton pregnancy and indications for GDM screening according to criteria of the American College of Obstetricians and Gynecologists were enrolled in the study between July 5, 2004 and March 11, 2005. After confirming gestational age (GA) and number of fetuses by ultrasound, all women underwent a 1-h glucose challenge test with 50 g glucose load (50-g GCT) between 21 and 27 weeks of GA. Blood samples for determination of adiponectin levels were also obtained on the same day. Subsequently, between 24 and 28 weeks of GA, the women underwent an oral glucose tolerance test with 100 g glucose load (100-g OGTT). The diagnosis of GDM was established when two or more of the following criteria were fulfilled: (1) fasting glucose >95 mg/dl; (2) 1-h glucose >180 mg/dl; (3) 2-h glucose >155 mg/dl; (4) 3-h glucose >140 mg/dl. Sixty women were diagnosed with GDM, a prevalence of 16.7%. There was no difference in age between the GDM and non-GDM groups. Pre-pregnancy and sampling-day body mass index (BMI), increase in weight and all blood glucose levels were greater in women with GDM than in those without (p < 0.05). Adiponectin concentrations were significantly negatively correlated with GA and plasma glucose levels of the GCT and each OGTT. Using logistic regression analyses, adiponectin, but not age, pre-pregnancy BMI and increase in weight, was demonstrated as an independent predictive factor for GDM. The area under the receiver-operator characteristic curve of adiponectin was significantly lower than that of the GCT [0.63 (95% confidence interval (CI) 0.53-0.67) vs. 0.73 (95% CI 0.71-0.80), p < 0.001]. At a cut-off value of 140 mg/dl of the 50-g GCT, the sensitivity and specificity of the test were 90% and 61%, respectively. The 50-g GCT could identify GDM in 54 (90%) out of 60 women. On the other hand, at an arbitrary cut-off value of 10 microg/ml for adiponectin, sensitivity of 91% and specificity of 31% were achieved. If this cut-off value was used for ruling in or out pregnant women for the GDM screening, 27% of all women could be eliminated from needing to perform an OGTT, with five women (8.3%) misclassified. In conclusion, this study demonstrated that adiponectin was an independent predictor for GDM. As for GDM screening, adiponectin was not as strong a predictor as GCT. However, with advantage of being less cumbersome, adiponectin could be used to rule out pregnant women at low risk of GDM.

Adiponectin↗
PubMed2006

Serum adiponectin levels and enzyme markers of liver dysfunction in diabetic and non-diabetic Caribbean subjects.

Low adiponectin levels are associated with elevated plasma alanine aminotransferase, a marker of reduced hepatic insulin sensitivity and a risk factor for type 2 diabetes. This study aims to determine the relationship between serum adiponectin level and alanine aminotransferase in diabetic and non-diabetic subjects. Fifty-six type 2 diabetic patients and 33 non-diabetic subjects participate in the study. Baseline plasma concentrations of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and glucose are measured on a chemistry analyser. Insulin and adiponectin are measured using enzyme-linked immunoassay techniques and insulin resistance is determined using the homeostatic model assessment method. Diabetic patients showed significantly lower levels of serum adiponectin than did the non-diabetic subjects, whereas levels of alanine aminotransferase and alkaline phosphatase were similar in both groups. While female non-diabetic subjects showed higher serum adiponectin levels than did female diabetic patients, alanine aminotransferase level did not differ (P>0.05). No significant relationship was seen between adiponectin and alanine aminotransferase in diabetic and non-diabetic subjects (P>0.05). Serum adiponectin levels were higher in non-diabetic subjects but there was no significant correlation between adiponectin and alanine aminotransferase in both groups of subjects. The data suggest that low serum adiponectin level may not be a suitable marker for impaired liver function in diabetic patients.

Adiponectin↗
PubMed2005

Resting metabolic rate is an important predictor of serum adiponectin concentrations: potential implications for obesity-related disorders.

BACKGROUND: Little is known about the regulation of adiponectin. Animal studies suggest local regulation by adipocytokines or alterations in energy expenditure, and studies in humans suggest regulation by alcohol intake and ethnicity. OBJECTIVE: To identify regulators of adiponectin in humans, we measured resting metabolic rate (RMR), serum adiponectin, glucose, insulin, triacylglycerol, alcohol intake, and anthropometric indexes in 457 white patients with overweight or obesity. DESIGN: A cross-sectional design was used, and multivariate regression analysis was performed with adiponectin as the dependent variable and potential predictors as independent variables. RESULTS: Simple linear analyses showed significant associations between adiponectin and sex, with a standardized coefficient of -0.38 (women compared with men) and an explanation of variation of the model (R(2)) of 14%; age (0.21; 4%); RMR (-0.52; 27%); fat-free mass (-0.40; 16%); fat mass (-0.16; 2%); visceral fat (-0.24; 6%; computed tomography at L4-L5); fasting triacylglycerol (-0.28; 8%); and insulin resistance (-0.38; 14%; homeostasis model assessment). Adiponectin and alcohol were not associated (-0.04; 0%). Multivariate analyses, which allowed adjustment for confounding, showed that RMR is the most important predictor of adiponectin (-0.31; 29%), followed successively by insulin resistance (-0.16; 31%; model containing RMR and insulin resistance), fat mass (0.20; 34%), age (0.34; 35%), visceral fat (-0.34; 40%), and fasting triacylglycerol (-0.12, 41%). CONCLUSIONS: Low resting metabolism (RMR) is associated with high serum adiponectin. We speculate that subjects with low RMR, who are theoretically at greater risk of obesity-related disorders, are especially protected by adiponectin.

Adiponectin↗
PubMed2005

Association between dietary factors and plasma adiponectin concentrations in men.

BACKGROUND: Adiponectin, an adipocyte-derived peptide, improves insulin sensitivity, has antiinflammatory and antiatherogenic effects, and is associated with a lower risk of ischemic heart disease (IHD) and type 2 diabetes. However, little is known about dietary predictors of plasma adiponectin concentrations in humans. OBJECTIVE: Our objective was to examine cross-sectionally the association between dietary factors and plasma adiponectin in men. DESIGN: Our study included 532 male participants of the Health Professionals Follow-Up Study who were selected as control subjects for an investigation of biological predictors of IHD. Diet, lifestyle, and anthropometric data were assessed by questionnaires. RESULTS: After multivariable adjustment, adiponectin was significantly inversely related to glycemic load (-1.3 mg/L per 1-SD increase; P = 0.02) and tended to be positively associated with total fat intake (0.7 mg/L per 0.5% of energy from fat instead of carbohydrates; P = 0.06). We also found a significant nonlinear association between plasma adiponectin concentrations and alcohol intake (P for quadratic trend = 0.01). Thus, whereas nondrinkers had mean plasma adiponectin concentrations of 16.48 mg/L, those who consumed 0.1-4.9, 5.0-14.9, 15.0-29.9, or >/=30 g alcohol/d had mean concentrations of 16.79 (P = 0.77 compared with nondrinkers), 18.97 (P = 0.02), 19.11 (P = 0.01), and 18.39 (P = 0.10) mg/L, respectively. CONCLUSIONS: Moderate alcohol intake is associated with higher adiponectin concentrations, whereas a carbohydrate-rich diet with a high glycemic load is associated with lower adiponectin concentrations in men with no history of cardiovascular disease. Although the strength of these associations was modest, our observations highlight the hypothesis that dietary factors may modulate plasma adiponectin concentrations-a potential mediator related to a reduced IHD risk.

Adiponectin↗