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PubMed2004

Lower plasma adiponectin concentration predicts the efficacy of pioglitazone in diabetic patients.

AIM: To investigate clinical efficacy of pioglitazone in association with plasma adiponectin concentration in type 2 diabetic patients. METHODS: Ten diabetic patients were treated with 15 or 30 mg of pioglitazone for 8 weeks, and association between plasma adiponectin concentration before treatment and decrease in glycated albumin levels was examined. RESULTS: Treatment with pioglitazone for 8 weeks lowered glycated albumin level (27.1 +/- 1.2 to 23.8 +/- 1.4%, p < 0.05), and inverse relationship between changes in glycated albumin and plasma adiponectin concentration before treatment was revealed (r = -0.66, p < 0.05). Plasma adiponectin concentrations of patients whose glycated albumin level reduced by more than 10% of the levels before treatment were significantly lower than those of patients whose glycaemic control was affected less (5.2 +/- 0.6 vs. 8.0 +/- 1.0 micro g/ml, p < 0.05). CONCLUSION: Lower plasma adiponectin concentration predicts the clinical efficacy of pioglitazone.

Adiponectin↗
PubMed2005

Inverse relationship between cord blood adiponectin concentrations and the number of cigarettes smoked during pregnancy.

BACKGROUND: Maternal smoking is linked with several neonatal metabolic disorders. Adiponectin is an adipose-specific hormone with anti-inflammatory and antiatherogenic properties. AIM: The aim of this study was to evaluate the effect of maternal smoking on cord blood adiponectin concentrations. METHODS: We evaluate the effect of maternal smoking on cord blood adiponectin concentrations comparing 14 full-term and seven preterm newborns born to mothers who smoked during pregnancy with 77 full-term and 10 preterm neonates born to non-smokers mothers. RESULTS: Maternal smoking during pregnancy was significantly associated with decreased adiponectin levels of preterm newborns (p < 0.05). CONCLUSIONS: Our findings also reveal a significant relationship between the reported number of cigarettes smoked during pregnancy and cord blood adiponectin concentrations (p = 0.01), suggesting that this association could have a causal relationship.

Adiponectin↗
PubMed2005

Genetic association study of adiponectin polymorphisms with risk of Type 2 diabetes mellitus in Korean population.

AIMS: To investigate any association between Type 2 diabetes mellitus and two single nucleotide polymorphisms (SNPs) in the adiponectin gene, T45G and G276T, in the Korean population. METHODS: We genotyped 427 non-diabetic controls and 493 Type 2 diabetic patients for SNPs T45G and G276T of adiponectin gene, measured plasma adiponectin concentrations, and examined clinical parameters in Koreans. RESULTS: There were no statistically significant differences in allele frequencies of SNPs 45 and 276 comparing control with Type 2 diabetic subjects (T frequency 68.3% vs. 71.6%, P=0.13 for SNP45, G frequency 72.2% vs. 68.9%, P=0.12 for SNP276). The genotype distributions of these SNPs had no association with the risk of Type 2 diabetes and metabolic parameters of insulin resistance. Plasma levels of adiponectin were not statistically different according to T45G and G276T either, in both control and Type 2 diabetic subjects. CONCLUSION: The T45G and G276T of the adiponectin gene may not be an important determinant of Type 2 diabetes or insulin resistance in Korean subjects.

Adiponectin↗
PubMed2006

A longitudinal study of serum adiponectin during normal pregnancy.

Adiponectin is secreted from adipose tissue. Serum adiponectin levels are inversely correlated with body mass index (BMI) and also insulin resistance, independent of the BMI. A role for adiponectin in the development of insulin resistance has been implied in pregnancy. However, no studies have been performed to describe the individual longitudinal course of adiponectin in normal pregnancies. Therefore, we measured serum adiponectin during and after normal pregnancy in 11 healthy women. Serum levels peaked in midpregnancy and the lowest levels were seen in late pregnancy. An inverse association with maternal BMI was observed.

Adiponectin↗
PubMed2006

Changes in plasma levels of fat-derived hormones adiponectin, leptin, resistin and visfatin in patients with rheumatoid arthritis.

BACKGROUND: Rheumatoid arthritis is a chronic autoimmune inflammatory condition characterised by polyarthritis and severe change in body mass and neuroendocrine environment. OBJECTIVES: To investigate plasma levels of adipocytokines (leptin, adiponectin, visfatin and resistin) in patients with rheumatoid arthritis and to compare them with levels in healthy controls. METHODS: Adiponectin, resistin, visfatin and leptin concentrations were measured in 31 patients with rheumatoid arthritis and 18 healthy controls by using specific enzyme-linked immunosorbent assays. RESULTS: Patients with rheumatoid arthritis showed considerably higher plasma levels of leptin, adiponectin and visfatin than healthy controls. No marked difference was observed in resistin levels between patients and controls. CONCLUSION: A marked increase in plasma levels of leptin, adiponectin and visfatin was noted in patients with rheumatoid arthritis, whereas resistin levels were similar to those observed in healthy controls. Coordinated roles for adiponectin, leptin and visfatin are suggested in the modulation of the inflammatory environment in patients with rheumatoid arthritis, whereas the lack of modulation in resistin levels is predictive of an irrelevant role for this peptide, suggesting that resistin level is probably not one of the main signals associated with the pathogenesis of this disease.

Adiponectin↗
PubMed2006

Pioglitazone increases secretion of high-molecular-weight adiponectin from adipocytes.

Adiponectin is an adipocyte-derived serum protein that plays important roles in energy homeostasis, obesity, and insulin sensitivity. Using sucrose gradients and Western blotting of nondenaturing gels, we examined the adiponectin isoforms secreted from human adipose tissue, human and mouse adipocytes, and cell lines in response to pioglitazone added in vitro. The predominant form secreted from adipose tissue in vitro was the high-molecular-weight (HMW) isoform, with small amounts of low-molecular-weight (LMW) forms present. The addition of pioglitazone (1-3 micromM) in vitro increased the secretion of the HMW isoform, with no significant effect on the other isoforms. Human adipose tissue was also examined for changes in adiponectin mRNA levels upon pioglitazone treatment. No difference was detected, suggesting that the effect of pioglitazone is not at the transcriptional level but, rather, at a posttranscriptional phase of the secretory pathway. Additional experiments were conducted to determine whether adiponectin expression was mechanistically similar in other adipose cells. Examination of primary human adipocytes revealed an increase in intracellular HMW isoform with a decline in LMW forms following pioglitazone treatment, with a corresponding increase in the secreted HMW form. Similar results were observed with primary mouse adipocytes, 3T3-F422A cells, and SGBS human adipocyte cells, although differences in the distribution of HMW and LMW isoforms were apparent between cell types. Although there are differences in isoforms between species, in all cases pioglitazone served to increase the secretion of the HMW form of adiponectin.

3T3 Cells↗
PubMed2003

Insulin resistance, intramyocellular lipid content, and plasma adiponectin in patients with type 1 diabetes.

Insulin resistance is a key pathogenic factor of type 2 diabetes (T2DM); in contrast, in type 1 diabetes (T1DM) it is considered a secondary alteration. Increased intramyocellular lipid (IMCL) content accumulation and reduced plasma adiponectin were suggested to be pathogenic events of insulin resistance in T2DM. This study was designed to assess whether IMCL content and plasma adiponectin were also associated with the severity of insulin resistance in T1DM. We studied 18 patients with T1DM, 7 older and overweight/obese patients with T2DM, and 15 nondiabetic, insulin-resistant offspring of T2DM parents (OFF) and 15 healthy individuals (NOR) as appropriate control groups matched for anthropometric features with T1DM patients by means of the euglycemic hyperinsulinemic clamp combined with the infusion of [6,6-2H2]glucose and 1H magnetic resonance spectroscopy of the calf muscles. T1DM and T2DM patients showed reduced insulin-stimulated glucose metabolic clearance rate (MCR: 5.1 +/- 0.6 and 3.2 +/- 0.8 ml x kg(-1) min(-1)) similar to OFF (5.3 +/- 0.4 ml x kg(-1) x min(-1)) compared with NOR (8.5 +/- 0.5 ml x kg(-1) min(-1), P < 0.001). Soleus IMCL content was increased in T1DM (112 +/- 15 AU), T2DM (108 +/- 10 AU) and OFF (82 +/- 13 AU) compared with NOR (52 +/- 7 AU, P < 0.05) and the result was inversely proportional to the MCR (R2 = 0.27, P < 0.001); an association between IMCL content and Hb A1c was found only in T1DM (R2 = 0.57, P < 0.001). Fasting plasma adiponectin was reduced in T2DM (7 +/- 1 microg/ml, P = 0.01) and OFF (11 +/- 1 microg/ml, P = 0.03) but not in T1DM (25 +/- 6 microg/ml), whose plasma level was increased with respect to both OFF (P = 0.03) and NOR (16 +/- 2 microg/ml, P = 0.05). In conclusion, in T1DM, T2DM, and OFF, IMCL content was associated with insulin resistance, demonstrating that IMCL accretion is a marker of insulin resistance common to both primary genetically determined and secondary metabolic (chronic hyperglycemia) alterations. The increased adiponectin levels in insulin-resistant patients with T1DM, in contrast to the reduced levels found in patients with T2DM and in OFF, demonstrated that the relationship of adiponectin to insulin resistance in humans is still unclear.

Adiponectin↗
PubMed2005

Association of visceral fat accumulation and plasma adiponectin with colorectal adenoma: evidence for participation of insulin resistance.

PURPOSE: Colorectal carcinogenesis is thought to be related to abdominal obesity and insulin resistance. To investigate whether visceral fat accumulation contributes to colorectal carcinogenesis, we examined its accumulation and the levels of the adipose tissue-derived hormone adiponectin in Japanese patients with colorectal adenoma. EXPERIMENTAL DESIGN: Fifty-one consecutive Japanese patients ages >/=40 years and with colorectal adenoma were subjected to measurement of visceral fat area by computed tomography scanning and plasma adiponectin concentration. The patients also underwent the 75-g oral glucose tolerance test. Insulin resistance was calculated by the homeostasis metabolic assessment (HOMA-IR) method. The controls were 52 Japanese subjects ages >/=40 years and without colorectal polyp. Cigarette smokers and subjects who consumed alcohol (>/=30 g ethanol/d) were excluded. RESULTS: The patients with colorectal adenoma showed significantly more visceral fat area and significantly less plasma adiponectin concentration in comparison with the controls [odds ratio (OR), 2.19; 95% confidence interval (95% CI), 1.47-3.28; P < 0.001 and OR, 0.24; 95% CI, 0.14-0.41; P < 0.001, respectively] by logistic regression analysis. HOMA-IR index was also associated with colorectal adenoma (OR 2.60; 95% CI, 1.20-5.64; P = 0.040). Visceral fat area and adiponectin were associated with adenoma number (1, 2, >/= 3), the size of the largest adenoma (<10 and >/=10 mm), and adenoma histology (tubular and tubulovillous/villous). CONCLUSIONS: These results suggest an association of visceral fat accumulation and decreased plasma adiponectin concentration with colorectal adenoma in Japanese patients. This study may offer a new insight to understanding the relationship of colorectal carcinogenesis with abdominal obesity and insulin resistance.

Adenoma↗
PubMed2005

Determinants of circulating adiponectin in women with polycystic ovary syndrome.

BACKGROUND AND AIM: Adiponectin is regarded as a possible link between adiposity and insulin resistance. Ghrelin and leptin are considered as signals of energy status. We evaluated the relationships between these peptides, androgens and insulin sensitivity in women affected by polycystic ovary syndrome. METHODS: Thirty-six women with PCOS were examined with euglycemic hyperinsulinemic clamp (to determine M/I, index of insulin sensitivity). Leptin, ghrelin, adiponectin, androgens, and SHBG were determined. Statistics was done using correlation analysis and backward stepwise multiple regression. RESULTS: The positive correlation of adiponectin with testosterone remains significant even after adjustment for BMI (p = 0.01), M/I (p = 0.009) and for both M/I and BMI (p = 0.02). In multiple regression with testosterone, M/I, leptin and ghrelin as independent variables, the model including testosterone (p = 0.03) and ghrelin (p = 0.002) explained 49% of the variability (p < 0.0012) of adiponectin. CONCLUSIONS: Both adiponectin and ghrelin can be involved in the pathophysiology of PCOS but their relation must be delineated further.

Adiponectin↗
PubMedDate not supplied

Adiponectin, T-cadherin and tumour necrosis factor-alpha in damaged cardiomyocytes from autopsy specimens.

This study determined the presence of adiponectin, T-cadherin (an adiponectin receptor) and tumour necrosis factor-alpha (TNF-alpha) in damaged myocytes from autopsied patients with acute or old myocardial infarction (MI) or dilated cardiomyopathy (DCM), using immunohistochemical staining. The enrolled patients included eight with acute MI, six with old MI and seven with DCM. Four autopsied individuals with no cardiac lesions were also enrolled as controls. Adiponectin and TNF-alpha were not observed in normal myocytes from control subjects, but T-cadherin was weakly detected. Immunoreactivity for adiponectin and T-cadherin was observed at the periphery of damaged myocytes from MI and DCM patients; intracellular reactivity for TNF-alpha was also seen. There were no statistically significant differences in the degree of reactivity for each molecule in the myocytes between the MI and DCM patients. These results suggest that the presence of adiponectin and TNF-alpha in damaged myocytes may contribute to the processes of myocardial injury occurring in MI and DCM.

Adiponectin↗
PubMed2006

Effect of gliclazide modified release on adiponectin, interleukin-6, and tumor necrosis factor-alpha plasma levels in individuals with type 2 diabetes mellitus.

OBJECTIVE: The aim of the study was to evaluate the effect of gliclazide modified release (MR) treatment on adiponectin, interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) plasma concentrations in type 2 diabetic patients. RESEARCH DESIGN AND METHODS: 24 randomly selected type 2 diabetic patients, aged 61.2 +/- 15.4 years, with poorly controlled glucose level (mean glycated hemoglobin [HbA1c] 7.6 +/- 1.1%) despite treatment with diet and/or oral hypoglycemic agents, were included in the study. All of the patients, after a 2-week run-in period, were given gliclazide MR for 12 weeks. At baseline, and after gliclazide MR treatment, HbA(1c) and plasma concentrations of IL-6, TNF-alpha, and adiponectin were measured. RESULTS: Gliclazide MR treatment produced significant reductions in fasting plasma glucose (from 7.6 +/- 1.4 to 6.6 +/- 1.2 mmol/L, p < 0.01), HbA(1c) (from 7.6 +/- 1.1 to 6.9 +/- 0.8%, p < 0.01), and plasma IL-6 concentrations (from 2.5 +/- 1.8 to 1.8 +/- 1.2 pg/mL, p < 0.05). A significant increase in plasma adiponectin level was noted (from 6.4 +/- 3.3 to 7.6 +/- 4.4 mug/mL, p < 0.05). Plasma TNF-alpha concentrations and homeostasis model assessment of insulin resistance (HOMA-IR) decreased after treatment, but these changes did not reach statistical significance. CONCLUSIONS: Gliclazide MR improves glycemic control and, in addition, has a positive influence on the plasma level of some inflammatory markers and adiponectin. Increased plasma adiponectin and decreased plasma IL-6, and TNF-alpha levels may explain, at least in part, the anti-atherogenic action of this drug reported elsewhere.

Adiponectin↗
PubMed2005

Regulation of T cell-mediated hepatic inflammation by adiponectin and leptin.

Concanavalin A-induced hepatotoxicity was compared in lipodystrophic aP2-nSREBP-1c transgenic mice (LD mice) lacking adipose tissue, obese leptin-deficient ob/ob mice, and lean wild-type (WT) mice. Serum leptin and adiponectin were low in LD mice, whereas ob/ob mice had undetectable leptin, but high adiponectin. Protection from hepatotoxicity was observed in ob/ob, but not in LD mice, despite low cytokine levels and reduced T cell activation and hepatic natural killer T cells in both groups. Administration of adiponectin protected LD mice from hepatotoxicity without altering cytokine levels. In contrast, administration of leptin heightened disease susceptibility by restoring cytokine production. Neutralization of TNF alpha protected LD mice from liver damage. Increased in vivo susceptibility to the hepatotoxic effect of TNF alpha was observed in LD mice. In vitro, adiponectin protected primary hepatocytes from TNF alpha-induced death, whereas leptin had no protective effect. In conclusion, although leptin increases susceptibility to hepatotoxicity by regulating cytokine production and T cell activation, adiponectin protects hepatocytes from TNF alpha-induced death.

Adiponectin↗
PubMed2003

Anorexia nervosa is characterized by increased adiponectin plasma levels and reduced nonoxidative glucose metabolism.

The aim of the present study was to examine the effects of anorexia nervosa (AN) on adipocytokines (leptin and adiponectin) plasma concentrations and insulin-stimulated glucose disposal in adolescent and young adult women. Adiponectin and leptin plasma levels, along with insulin-stimulated glucose disposal (as measured by the euglycemic-hyperinsulinemic glucose clamp) and oxidative and nonoxidative glucose metabolism (as measured by indirect calorimetry during the last 60 min of the insulin clamp), were measured in 11 anorectic patients and 26 normal-weight healthy female controls. Leptin levels were significantly lower in AN patients, according to the reduced body mass index and their respective fat mass. On the contrary, adiponectin plasma levels were significantly higher in AN patients than in control women. Likewise, insulin-stimulated glucose disposal and nonoxidative glucose metabolism were significantly lower in AN patients. In conclusion, our study shows that young women affected by AN have higher adiponectin plasma levels than healthy female controls of similar age, despite the presence of an impairment of insulin-stimulated glucose disposal, with a prevalent failure of nonoxidative glucose metabolism. Taken together, these data suggest that the reduction of fat mass may play the major role in the control of adiponectin release, with respect to changes in insulin sensitivity.

Adiponectin↗
PubMed2003

Adiponectin levels in women with polycystic ovary syndrome.

Serum adiponectin levels were evaluated in 60 women with polycystic ovary syndrome (PCOS), 30 normal-weighted and 30 obese women, and 60 healthy women age and body mass index (BMI) matched with the patients. The homeostasis model assessment (HOMA) score was also calculated. Both in PCOS and controls, serum adiponectin levels were significantly (P < 0.05) lower in obese than normal-weight women, without any difference between PCOS and controls. The HOMA score was significantly (P < 0.05) higher in obese than normal-weight women both in PCOS and controls; additionally, the HOMA score was significantly (P < 0.05) higher in normal-weight PCOS than normal-weight controls. Both in PCOS and controls, adiponectin levels were significantly correlated with BMI (r = -0.51, P < 0.01 in PCOS; r = -0.45, P < 0.01 in controls) and HOMA values (r = -0.39, P < 0.05 in PCOS; r = -0.35, P < 0.05 in controls); HOMA was correlated with BMI (r = 0.51, P < 0.01 in PCOS, r = 0.61, P < 0.001 in controls). In conclusion, our results confirm that adiponectin concentrations change according to variations of fat mass. They further suggest that insulin sensitivity per se probably does not play any pivotal role in the control of adiponectin levels in PCOS women.

Adiponectin↗
PubMed2004

Adiponectin in anorexia nervosa and bulimia nervosa.

To study the role of adiponectin, a novel adipocyte-specific secreted protein, on the pathophysiology of eating disorders, circulating levels of fasting adiponectin, leptin, insulin, and glucose were measured in 31 female patients with anorexia nervosa (AN) and in 11 with bulimia nervosa. Hormone levels were compared with 16 age-matched, normal body weight controls, six healthy constitutionally thin subjects, and nine obese subjects. Moreover, changes in levels were reevaluated after nutritional treatment and weight gain in 13 patients with AN. Serum adiponectin concentrations in AN and bulimia nervosa were significantly lower than those in normal-weight controls. These results were unexpected because the levels were high in constitutionally thin subjects and low in obese subjects, which provide a negative correlation with body mass index (BMI) and body fat mass. In contrast, serum leptin levels correlated very well with BMI and fat mass among all the patients and controls. The insulin resistance was significantly low in AN and high in obese subjects. The concentrations of adiponectin after weight recovery increased to the normal level despite a relatively small increase in BMI. These findings suggest that abnormal feeding behavior in the patients with eating disorders may reduce circulating adiponectin level, and weight recovery can restore it.

Adiponectin↗
PubMed2006

Possible role of adiponectin and insulin sensitivity in mediating the favorable effects of lower body fat mass on blood lipids.

AIMS: The objective of this study was to investigate the role of insulin sensitivity and serum adiponectin concentration as determinants, in middle-aged men, of the relationship between lower body fat and blood lipids after truncal fat has been accounted for. METHODS: Men (443) aged 39-65 yr, body mass index 18-43 kg/m(2), participated in the study. The following variables were measured: regional body fat distribution as assessed by dual-energy x-ray absorptiometry, maximal oxygen uptake, physical activity, fasting levels of serum adiponectin, triglycerides, and high-density lipoprotein- and total cholesterol. Plasma glucose and serum insulin were measured in the fasting state and after an oral glucose load. RESULTS: Lower body fat mass was inversely associated with serum triglycerides and total cholesterol and positively with serum high-density lipoprotein-cholesterol after adjustment for age, lean tissue mass, truncal fat mass, weight history, maximal oxygen uptake, and the level of physical activity (P < 0.0005). Serum adiponectin level and Matsudas insulin sensitivity index were positively intercorrelated, and both were positively correlated to lower body fat mass. When including adiponectin and insulin sensitivity in the analyses, the relationships between lower body fat mass and serum lipids were partly explained. CONCLUSION: For a given level of truncal fat mass, a large lower body fat mass is associated with an advantageous blood lipid profile, which may be partially mediated by the relationships to both insulin sensitivity and serum adiponectin level.

Absorptiometry, Photon↗
PubMed2006

Lower total fasting plasma adiponectin concentrations are associated with higher metabolic rates.

CONTEXT: The possible role of adiponectin, a protein uniquely produced by the adipose tissue and significantly reduced in obesity and other insulin-resistant states, in the regulation of energy expenditure (EE) is still poorly understood. OBJECTIVE: The objective of the study was to investigate the relationship between total fasting plasma adiponectin concentrations and the various components of EE measured in a metabolic chamber in Pima Indians and to test whether body fat distribution may have a role in this association. DESIGN: This was a cross-sectional study. SETTING: The study was an inpatient clinical research unit. PARTICIPANTS: Sixty nondiabetic Pima Indians (45 males and 15 females), aged 18-45 yr, spanning a wide range of adiposity (body mass index 19.6-46.2 kg/m(2)) participated in the study. MAIN OUTCOME MEASURES: Total fasting plasma adiponectin concentrations, EE (24-h respiratory chamber), insulin sensitivity (euglycemic-hyperisulinemic clamp), body composition (dual-energy x-ray absorptiometry), and body fat distribution (waist to thigh ratio) were the main outcome measures. RESULTS: Total fasting plasma adiponectin concentrations are negatively associated with sleep EE adjusted for sex, age, fat-free mass, and fat mass. This correlation is still significant, although attenuated, after inclusion of insulin-stimulated glucose disposal among the regressors and further attenuated when adjusted also for waist to thigh ratio. CONCLUSIONS: The decrease in total fasting plasma adiponectin concentrations that accompanies fat accumulation may be a mechanism to prevent further weight gain by decreasing insulin sensitivity and increasing energy expenditure.

Adiponectin↗
PubMed2001

The genetic basis of plasma variation in adiponectin, a global endophenotype for obesity and the metabolic syndrome.

Here we present the first genetic analysis of adiponectin levels, a newly identified adipocyte-derived protein. Recent work has suggested that adiponectin may play a role in mediating the effects of body weight as a risk factor for coronary artery disease. For this analysis we assayed serum levels of adiponectin in 1100 adults of predominantly northern European ancestry distributed across 170 families. Quantitative genetic analysis of adiponectin levels detected an additive genetic heritability of 46%. The maximum LOD score detected in a genome wide scan for adiponectin levels was 4.06 (P = 7.7 x 10(-6)), 35 cM from pter on chromosome 5. The second largest LOD score (LOD = 3.2; P = 6.2 x 10(-5)) was detected on chromosome 14, 29 cM from pter. The detection of a significant linkage with a quantitative trait locus on chromosome 5 provides strong evidence for a replication of a previously reported quantitative trait locus for obesity-related phenotypes. In addition, several secondary signals offer potential evidence of replications for additional previously reported obesity-related quantitative trait loci on chromosomes 2 and 10. Not only do these results identify quantitative trait loci with significant effects on a newly described, and potentially very important, adipocyte-derived protein, they also reveal the emergence of a consistent pattern of linkage results for obesity-related traits across a number of human populations.

Adiponectin↗