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PubMed2006

Adiponectin modulates carnitine palmitoyltransferase-1 through AMPK signaling cascade in rat cardiomyocytes.

Adiponectin, an adipocyte-derived polypeptide hormone, plays an important role in regulating fatty acid oxidation. beta-oxidation of fatty acids supplies most of the cardiac energy and carnitine palmitoyltransferase (CPT)-1 serves as a key regulator during this process. To characterize the potential effects of adiponectin on CPT-1, we incubated rat neonatal cardiomyocytes with globular adiponectin (gAd). Results showed that gAd promoted the activity and mRNA expression of CPT-1. The underlying signal pathway involved in this modulatory effect was further investigated. Inhibition of AMP-activated protein kinase (AMPK) with adenine 9-beta-d-arabinofuranoside (AraA) completely abrogated gAd-mediated AMPK and acetyl coenzyme A carboxylase (ACC) phosphorylation and suppressed the promotion of CPT-1 activity. gAd also induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and peroxisome proliferator-activated receptor (PPAR)-alpha, which was inhibited by AraA. SB202190, a p38MAPK inhibitor, blocked gAd-stimulated PPAR-alpha phosphorylation. When AMPK and/or p38MAPK was inhibited, gAd-enhanced mRNA expression of CPT-1 was partially reduced. In conclusion, our study suggests that the activation of AMPK signaling cascade participates in the promotion effect of gAd on CPT-1.

AMP-Activated Protein Kinases↗
PubMed2006

Exercise-induced alterations in plasma concentrations of ghrelin, adiponectin, leptin, glucose, insulin, and cortisol in horses.

Six Standardbred (STB) mares (11+/-2 years, 521+/-77 kg; means+/-SD) performed an exercise trial (EX) where they underwent an incremental exercise test (GXT) as well as a parallel control trial (CON) to test the hypothesis that short-term, high intensity exercise would alter plasma concentrations of glucose, leptin, adiponectin, ghrelin, insulin and cortisol. Plasma samples were taken before (0 min), during (last 10s at 6, 8m/s, and the velocity eliciting VO(2max)), and after exercise (2, 10, 30, 60 min; 12 and 24h post-GXT). A second set of blood samples was collected before and after an afternoon meal given at 1515 h (at 1500, 1514, 1530, and 1545 h). Data were analyzed using ANOVA for repeated measures and Tukey's test. During the GXT, there were no changes (P>0.05) in the plasma concentrations of glucose, leptin, adiponectin or ghrelin. However, there was a 29% increase (P<0.05) in mean plasma cortisol concentration and a 35% decrease (P<0.05) in mean plasma insulin concentration. Substantial increases (P<0.05) in the mean plasma concentrations of glucose and cortisol of 36% and 102%, respectively, were seen in the EX trial during the first 60 min post-GXT. Plasma leptin concentration, measured at the 24h post-GXT time point, was 20% lower (P<0.05) during the EX trial compared with the parallel time point in the standing control (CON) trial. Plasma ghrelin concentration was 37% lower (P<0.05) in the EX trial compared with CON before and after the afternoon meal, but was 43% higher (P<0.05) 12h post-GXT. There were no differences between EX and CON for plasma concentrations of insulin or adiponectin during recovery. It was concluded that short-term high intensity exercise alters plasma leptin and ghrelin concentrations in STB mares post-exercise, which may signal the exercised animals to alter energy intake.

Adiponectin↗
PubMed2004

Growth hormone is a positive regulator of adiponectin receptor 2 in 3T3-L1 adipocytes.

The fat-derived protein adiponectin is an important insulin-sensitizing adipocytokine which is downregulated in insulin resistance and obesity. Recently, two receptors of this adipose-expressed protein called adiponectin receptor 1 (AdipoR1) and 2 (AdipoR2) have been cloned. To clarify expression and regulation of these receptors in fat cells, AdipoR1 and AdipoR2 mRNA was measured by quantitative real-time reverse transcription-polymerase chain reaction during differentiation of 3T3-L1 adipocytes and after treatment with various hormones known to induce insulin resistance. Interestingly, AdipoR2 synthesis was significantly increased up to 4.8-fold during differentiation of 3T3-L1 preadipocytes, whereas AdipoR1 expression was only augmented up to 1.4-fold. Furthermore, growth hormone (GH) induced AdipoR2, but not AdipoR1 mRNA by up to 2.4-fold in a dose- and time-dependent fashion with significant stimulation detectable at concentrations as low as 5 ng/ml GH and as early as 2 h after effector addition. The positive effect of GH on AdipoR2 expression could be reversed by withdrawal of the hormone for 24 h. In contrast, other key hormones involved in the regulation of insulin resistance and energy metabolism such as insulin, isoproterenol, dexamethasone, triiodothyronine, angiotensin 2, tumor necrosis factor alpha, and interleukin-6 did not influence AdipoR1 and AdipoR2 synthesis in vitro. Taken together, our results suggest that AdipoR2 expression is differentiation-dependent and selectively regulated by GH implying a potential role of this hormone in adiponectin-associated alterations of insulin sensitivity and energy homeostasis.

3T3 Cells↗
PubMed2002

Adiponectin and development of type 2 diabetes in the Pima Indian population.

Adiponectin is a collagen-like circulating protein secreted by adipocytes that is proposed to mediate obesity-related resistance to insulin. In a case-control series, we assessed the role of adiponectin in later development of type 2 diabetes in 70 patients who later developed type 2 diabetes and 70 controls, matched for body-mass index, age, and sex. Cases and controls were taken from the longitudinal study of health in the Pima Indian population. At baseline, the concentration of adiponectin was lower in cases than in controls (p=0.01) and individuals with high concentrations of this protein were less likely to develop type 2 diabetes than those with low concentrations (incidence rate ratio 0.63 [95% CI 0.43-0.92]; p=0.02).

Adiponectin↗
PubMed2005

Adiponectin: a relevant player in PPARgamma-agonist-mediated improvements in hepatic insulin sensitivity?

The potent insulin-sensitizing effects of peroxisome proliferator-activated receptor gamma (PPARgamma) agonists are well established. However, it is still a matter of intense debate as to which tissue(s) represent the most critical sites of action for PPARgamma agonists, and what the relevant target genes are that ultimately mediate the improvements in insulin sensitivity. The cell type with the highest levels of PPARgamma is the adipocyte, and as such the adipocyte is an excellent candidate cell to look for critical mediators of PPARgamma agonist action. Adiponectin, an adipocyte-specific secretory protein, is upregulated in response to PPARgamma agonist exposure, and its serum levels consequently increase significantly. Genetic, pharmacological and clinical studies have demonstrated potent insulin-sensitizing effects of adiponectin. Here, we summarize the evidence that implicates adiponectin as a critical mediator of PPARgamma-agonist-mediated improvements in insulin sensitivity, particularly in the context of PPARgamma-agonist-mediated enhancements of hepatic insulin sensitivity.

Adiponectin↗
PubMed2003

Adipocytokines in anorexia nervosa: a review focusing on leptin and adiponectin.

Adipose tissue secretes a large number of physiologically active peptides that often share structural properties with cytokines, and are therefore collectively referred to as "adipocytokines". Some of these are almost exclusively secreted by adipose tissue. Leptin, adiponectin and resistin are specific fat-derived hormones that affect fuel homeostasis and insulin action, and may also be involved in hematopoiesis and immune functions. Anorexia nervosa is characterized by chronic self-starvation and severe weight loss, mainly at the expense of adipose tissue. Starvation-induced depletion of fat stores is accompanied by alterations of circulating adipocytokines. Plasma leptin and likely resistin levels are decreased in anorectic patients, while plasma adiponectin levels are increased. These alterations may have potential repercussions in the pathophysiology of anorexia nervosa. Thus, low leptin and high adiponectin may separately or in concert contribute to altered hematopoiesis and immunity, enhanced insulin sensitivity, neuroendocrine disturbances or osteopenia in anorexia nervosa.

Adipocytes↗
PubMed2006

Improved glycaemia in type 1 diabetes results in decreased levels of soluble adhesion molecules with no change in serum adiponectin or most acute phase proteins.

AIMS: To investigate how reduction of hyperglycaemia affects acute phase serum proteins in poorly controlled type 1 diabetic patients. METHODS: 24 patients (age 31.7 +/- 2.0 years, HbA1c 9.3 +/- 0.2%, BMI 24.2 +/- 0.7 kg/m2, diabetes duration 15.3 +/- 1.7 years) participated in the study. The treatment was optimised for 16 weeks. Blood samples were taken at baseline and at the end of the study. 16 healthy age- and BMI-matched subjects were chosen for a control group. RESULTS: At baseline, the patients had higher C-reactive protein (CRP) (1.09, median [range 0.24-18.82] mg/l vs. 0.66 [0.18-2.46] mg/l, p < 0.02), mean adiponectin (16.06 +/- 1.31 vs. 8.85 +/- 0.93 mg/l, p < 0.001), ceruloplasmin (306 +/- 16.1 vs. 205.4 +/- 5.5 mg/l, p < 0.001), fibrinogen (3.41 +/- 0.26 vs. 2.38 +/- 0.07 g/l, p < 0.001), soluble intercellular adhesion molecule-1 (sICAM-1) (255.4 +/- 10.3 vs. 194 +/- 10.6 microg/l, p < 0.001), soluble vascular adhesion molecule-1 (sVCAM-1) (533.4 +/- 21.8 vs. 422.9 +/- 20.7 microg/l, p < 0.01) and interleukin-6 (2.89 +/- 0.49 vs. 1.35 +/- 0.30 ng/l, p < 0.01) concentrations than the controls. During intensified treatment, HbA1c decreased (to 8.5 +/- 0.2%, p < 0.001). This resulted in reduced sE-selectin (from 44.6 +/- 2.6 to 38.8 +/- 2.6 microg/l, p < 0.01), alpha-1-acid-glycoprotein (A1GP) (from 622.9 +/- 47.9 to 525.7 +/- 27.9 mg/l, p < 0.01), sICAM-1 (from 255.4 +/- 10.3 to 240.8 +/- 9.1 microg/l, p < 0.05) and IL-6 (from 2.9 +/- 0.5 to 2.1 +/- 0.4 ng/l, p < 0.01). Serum amyloid A (SAA) and CRP did not change 12.00 (0.7-222.0) vs. 12.00 (1.6-277.0) mg/l for SAA and 1.09 (0.24-18.82) vs. 1.09 (0.18-23.08) mg/l for CRP, baseline vs. treatment, respectively. CONCLUSIONS: Poorly controlled type 1 diabetic patients have increased values of adiponectin, CRP, ceruloplasmin, fibrinogen, sICAM-1, sVCAM-1 and IL-6. Reduction of hyperglycaemia results in decreased sE-selectin, A1GP, sICAM-1 and IL6, while other inflammatory factors including CRP, SAA and adiponectin are not affected.

Acute-Phase Proteins↗
PubMed2006

Beta cell function, insulin resistance and plasma adiponectin concentrations are predictors for the change of postprandial glucose in non-diabetic subjects at risk for type 2 diabetes.

Insulin resistance, impaired insulin secretion, and low adiponectin levels have been shown to be predictors for type 2 diabetes. However, it is not yet clear whether these associations (1) are independent of changes in body weight, or (2) are valid for changes in glucose tolerance in the prediabetic state. Sixty-two non-diabetics (50 with normal glucose tolerance) aged 41 +/- 11 years, BMI 30.5 +/- 5.3 kg/m2 (mean +/- SD) were studied twice with a standard oral glucose tolerance test (oGTT, mean follow-up time 3.0 +/- 1.8 years (mean +/- SD) [range 0.5-6.5 years]). Insulin sensitivity and insulin secretion were estimated from oGTT using validated indices. Two-hour blood glucose during oGTT deteriorated over time (baseline 2 h glucose 6.32 +/- 0.21 VS. follow-up 2 h glucose 7.14 +/- 0.22 mM, p < 0.001) while the percentage body fat did not change (32.7 +/- 1.2 VS. 32.6 +/- 1.2%, p = 0.46). Follow-up 2 h blood glucose was predicted by adiponectin (p = 0.01), baseline insulin sensitivity (p = 0.02) and baseline insulin secretion relative to insulin sensitivity (p = 0.03) independent of sex, age, baseline 2 h blood glucose or change in percentage body fat. Our results suggest that low adiponectin levels, insulin resistance and low beta cell function predict the continuous deterioration of glucose tolerance in early prediabetic states, independent of changes in adiposity. Therefore, the early influence of these parameters should be the subject of future prevention programs to prevent deterioration of glucose tolerance.

Adiponectin↗
PubMed2005

Associations between two single nucleotide polymorphisms in the adiponectin gene and polycystic ovary syndrome.

In the present study we determined whether genetic variability in the gene encoding adiponectin is associated with polycystic ovary syndrome (PCOS). Altogether 143 Caucasian women with PCOS and 245 healthy controls were genotyped for two single nucleotide polymorphisms (SNPs) in exon 2 and intron 2 in the adiponectin gene. Single-point analysis was expanded to pair-of-loci haplotype analysis to examine the estimated haplotype frequencies of the two SNPs, of unknown phase, in the PCOS and control groups. Estimated haplotype frequencies were assessed using the maximum-likelihood method, employing an expectation-maximization algorithm. A significantly different allele distribution in intron 2 SNP was observed between the groups, with the T allele being significantly reduced in the PCOS group (25.9%) compared with the control group (32.7%) ( p = 0.047), at an odds ratio of 0.72 (95% confidence interval 0.52-0.99). Otherwise, the allele and genotype distributions in either SNP were not statistically different between the groups. In haplotype estimation analysis, there was a lower frequency of the haplotype T-T in the PCOS group (25.9%) than in the control group (32.7%) ( p = 0.058). We conclude that polymorphisms of the adiponectin gene may be implicated in individual susceptibility to PCOS.

Adiponectin↗
PubMed2003

A novel cellular marker of insulin resistance and early atherosclerosis in humans is related to impaired fat cell differentiation and low adiponectin.

The epidemic increase in type 2 diabetes can be prevented only if markers of risk can be identified and used for early intervention. We examined the clinical phenotype of individuals characterized by normal or low IRS-1 protein expression in fat cells as well as the potential molecular mechanisms related to the adipose tissue. Twenty-five non-obese individuals with low or normal IRS-1 expression in subcutaneous abdominal fat cells were extensively characterized and the results compared with 71 carefully matched subjects with or without a known genetic predisposition for type 2 diabetes. In contrast to the commonly used risk marker, known heredity for diabetes, low cellular IRS-1 identified individuals who were markedly insulin resistant, had high proinsulin and insulin levels, and exhibited evidence of early atherosclerosis measured as increased intima media thickness in the carotid artery bulb. Circulating levels of adiponectin were also significantly reduced. Gene analyses of fat cells in a parallel study showed attenuated expression of several genes related to fat cell differentiation (adiponectin, aP2, PPARgamma, and lipoprotein lipase) in the group of individuals characterized by a low IRS-1 expression and insulin resistance. A low IRS-1 expression in fat cells is a marker of insulin resistance and risk for type 2 diabetes and is associated with evidence of early vascular complications. Impaired adipocyte differentiation, including low gene expression and circulating levels of adiponectin, can provide a link between the cellular marker and the in vivo phenotype.

Adiponectin↗
PubMed2006

The effect of liposuction and diet on ghrelin, adiponectin, and leptin levels in obese Zucker rats.

BACKGROUND: The fat-regulating hormones, adiponectin, ghrelin, and leptin, have been studied extensively with the hope that some therapeutic modality might be gleaned from their augmentation or blockade. The authors studied levels of ghrelin, adiponectin, and leptin after liposuction in obese male Zucker rats. In addition, they altered the fat and carbohydrate content of the rats' postoperative diets to determine whether diet affects hormonal levels and/or liposuction outcome. METHODS: Thirty-five male, obese Zucker rats were divided into four experimental groups. Group I (n = 10) was fed a low-fat/low-carbohydrate diet; group II (n = 10) was fed a regular chow diet; and group III (n = 10) was fed a high-fat/high-carbohydrate diet. Five additional rats served as the baseline, unoperated group. The experimental rats underwent subcutaneous liposuction, and for 6 weeks they were then fed their experimental diets starting on day 0. Experimental rats were euthanized on day 42 and blood was sampled for hormonal, triglyceride, and cholesterol levels. RESULTS: Triglyceride levels were significantly higher in the high-fat/high-carbohydrate group compared with the regular chow and low-fat/low-carbohydrate groups, indicating an effect of diet on systemic circulation after liposuction. Ghrelin levels decreased significantly and leptin levels demonstrated an increasing trend after liposuction. Adiponectin levels did not demonstrate any change with alteration in diet or liposuction. CONCLUSIONS: Liposuction may prove to offer patients medically therapeutic benefits through hormonal alterations. After liposuction, diet plays an important role in weight gain.

Adipocytes↗
PubMed2004

Effect of dieting on plasma leptin, soluble leptin receptor, adiponectin and resistin levels in healthy volunteers.

OBJECTIVE: Recent findings demonstrating important effects of the adipokines on metabolism, energy homeostasis and body weight regulation have prompted research on the possible role of negative energy balance in altering adipocytokine regulation. The goal of this study was to evaluate the effects of a hypocaloric diet in healthy normal-weight volunteers. An additional goal was to help clarify the contribution of restricted caloric intake to altered plasma adipokine levels in the eating disorders anorexia nervosa and bulimia nervosa. DESIGN: Participants were studied before and after a 4-week reduced-calorie diet (1000-12000 kcal/day). patients Subjects included 15 healthy, normal-weight women (age 22 +/- 3 years). MEASUREMENTS: Plasma concentrations of leptin, soluble leptin receptor protein (sOB-R), adiponectin, resistin, thyroid hormones and beta-hydroxybutyrate were determined following overnight fast before and after the 4-week reduced-calorie diet. RESULTS: Subjects lost a mean of 3.4 +/- 2.1 kg in response to the reduced-calorie diet. The weight loss phase was associated with a 60.3% decrease in plasma leptin levels (P < 0.001), a 43.5% increase in sOB-R levels (P < 0.002) and a 16.2% decrease in plasma adiponectin levels (P < 0.04). There was no significant change in plasma resistin levels. CONCLUSIONS: These results demonstrate that a modest decrease in energy intake sustained over several weeks may play an important role in altering levels of plasma leptin and sOB-R. The findings also provide preliminary evidence that, in contrast to previous results in obese subjects, caloric restriction with accompanying weight loss in healthy, normal-weight volunteers may lead to decreased circulating adiponectin levels. Additional studies will be needed to clarify the contribution of altered energy intake to abnormalities in cytokine levels in the eating disorders.

3-Hydroxybutyric Acid↗
PubMed2005

Relationship of thyroid function with body mass index, leptin, insulin sensitivity and adiponectin in euthyroid obese women.

BACKGROUND: A possible relationship between thyroid hormones and adipose tissue metabolism in humans has been suggested. Aim of the study We sought to evaluate thyroid function and its possible relationship with body mass index (BMI), leptin, adiponectin and insulin sensitivity in euthyroid obese women. MATERIALS AND METHODS: Eighty-seven uncomplicated obese women (mean age 34.7 +/- 9 years, mean BMI 40.1 +/- 7 kg/m(2)) were studied. Levels of TSH, free thyroxine (FT4), free triiodothyronine (FT3), plasma adiponectin and leptin were evaluated. Insulin sensitivity was assessed by euglycaemic hyperinsulinaemic clamp (M index), fasting insulin and HOMA-IR. RESULTS: Uncomplicated obese women with BMI > 40 kg/m(2) showed higher serum TSH than obese subjects with BMI < 40 kg/m(2) (P < 0.01). TSH was correlated with BMI (r = 0.44, P = 0.01) leptin (r = 0.41, P = 0.01), leptin/BMI ratio (r = 0.33, P = 0.03), body surface area (r = 0.26, P = 0.05), HOMA-IR (r = 0.245, P = 0.05) and inversely with adiponectin (r = -0.25, P = 0.05) and M index (r = -0.223 P = 0.05). CONCLUSIONS: Our data show that, although thyroid function was normal in the studied obese population, TSH and BMI were positively related. TSH has been found to be correlated also with leptin adjusted for BMI. TSH could represent a marker of altered energy balance in severe, but uncomplicated obese women.

Adiponectin↗
PubMed2005

The relationship between serum resistin, leptin, adiponectin, ghrelin levels and bone mineral density in middle-aged men.

OBJECTIVE: Body weight is a significant predictor of bone mass. Hormonal factors such as sex hormones, insulin, leptin and adiponectin are thought to play a role in the mechanisms controlling the association of body weight and fat mass with bone mass. However, contradictory results have been reported for the association between serum adipocytokines and bone mineral density (BMD). We therefore examined whether the serum adipocytokine and ghrelin levels, markers of fat metabolism, are associated with BMD in male adults. PATIENTS AND MEASUREMENTS: For 80 male adults (average age 54.5 +/- 6.4 years; average body mass index (BMI) 24.4 +/- 2.5 kg/m2), the correlations between serum resistin, leptin, adiponectin and ghrelin levels with BMD were investigated. RESULTS: Among the adipocytokines, serum resistin levels were negatively correlated with lumbar spine BMD (r = -0.237, P = 0.05). After adjustment was made for age and BMI, log-transformed serum leptin showed a significant negative correlation with lumbar spine BMD, which was not seen on bivariate analysis (r = -0.237, P = 0.039). Femoral neck BMD was marginally associated only with serum adiponectin levels (r = -0.226, P = 0.062). In multiple regression analyses, among the adipokines, only resistin was a significant determinant of lumbar spine BMD, although the variance was small (R2 = 0.256). Serum ghrelin levels were not correlated with the BMD of either body site. CONCLUSIONS: Serum resistin level showed a significant negative correlation with lumbar spine BMD, although the variance was small. Further studies are needed to elucidate the role of adipocytokines in bone metabolism.

Adiponectin↗
PubMed2005

Effects of 17beta-oestradiol plus different doses of drospirenone on adipose tissue, adiponectin and atherogenic metabolites in postmenopausal women.

OBJECTIVE: To investigate how variation in the dose of the progestogen influence the impact of 17beta-oestradiol plus drospirenone (DRSP) treatment on adipose tissue and its secretor function with direct implications for atherogenic metabolites. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Primary care, single study site. SUBJECTS: A total of 240 healthy postmenopausal women 53-65 years old, 178 completer. INTERVENTION: Daily treatment with 1 mg 17beta-oestradiol plus 1, 2, or 3 mg DRSP, or placebo for 2 years. MAIN OUTCOME MEASURES: Absolute changes in central (CFM) and peripheral fat mass (PFM; dual-energy X-ray absorptiometry, DEXA), adipokines [interleukin (IL)-6 and adiponectin], atherogenic metabolites [triglycerides, high-density lipoprotein cholesterol (HDL-C), glucose] and blood pressure. RESULTS: Oestradiol plus 1 mg DRSP evoked significant decreases in CFM and the CFM/PFM ratio from baseline. These benefits virtually decreased with increasing dose of DRSP confounded by dose-dependent increases in CFM and PFM in smokers (P-value for trends <0.001), in whom the increases in bioavailable oestradiol were half of that in nonsmokers (P < 0.001). Treatment with 3 mg DRSP induced decreases in serum adiponectin by month 6 (P < 0.05), which persisted in nonsmokers only and led to significant increases in glucose and triglycerides and decreases in HDL-C (P < 0.05). Adiponectin in smokers normalized by the end of the study parallel with the increases in body fat mass. CONCLUSIONS: Interactions of the sex steroids with adipose tissue and its secretor function are important determinants of the overall impact of hormone therapy on cardiovascular risk. A DRSP dose up to 2 mg does not seem to exert adverse effects when combined with 1 mg 17beta-oestradiol.

Absorptiometry, Photon↗
PubMed2007

Common adiponectin gene variants show different effects on risk of cardiovascular disease and type 2 diabetes in European subjects.

Alterations in the secretion of adipokines may explain the link between obesity, type 2 diabetes (T2DM) and coronary artery disease (CAD). These conditions have been associated with variation in the adiponectin gene, although evidence for this relationship has been variable, with differences found even in similar samples. This study aims to clarify these inconsistencies by determining the impact of identified adiponectin gene (ADIPOQ) variants (-11391G>A,-1377C>G[promoter] and +45T>G[exon 2] and +276G>T[intron 2]) on the prospective risk of CAD and T2DM in healthy men, and on adverse metabolic markers, in myocardial infarct survivors and controls from different parts of Europe. The hazard ratio for cardiovascular disease varied across the -11391GG/GA/AA(p = 0.03) and -11371CC/CG/GG(p = 0.05) genotypes only. In contrast, only the +45T>G variant (3.80[1.76-8.24]) was associated with T2DM, while two haplotypes GCTT/GCGG (p < 0.05) and +276G>T(p = 0.01) increased risk in interaction with obesity. The variants were associated with a number of biomarkers in Southern but not Northern Europe (p = 0.01), despite no significant differences in allele or haplotype frequencies (p > 0.44). A risk haplotype could not be identified in either sample. Adiponectin gene variants are hence currently poor markers for the development of T2DM and CAD. Their influence on risk depends significantly on interactions that are not currently understood with either genetic variation elsewhere or the environment of the sample studied.

Adiponectin↗
PubMed2006

The evolving role of leptin and adiponectin in chronic liver diseases.

Leptin and adiponectin, the main metabolic products of adipose tissue, have been implicated in a wide spectrum of human diseases. Given the frequent presence of hepatic steatosis in several chronic liver diseases, there is currently increasing interest in the role of these adipokines in the development of hepatic steatosis and also in necroinflammation and fibrosis, mostly in patients with nonalcoholic fatty liver disease or chronic hepatitis C. According to experimental data, reduced adiponectin levels and increased leptin levels associated with leptin resistance, which are usually observed in obese patients with or without metabolic syndrome, may result in fat accumulation in the liver and in the enhancement of liver inflammation and mostly fibrogenesis. Increased leptin and decreased adiponectin serum levels have been detected initially in patients with nonalcoholic steatohepatitis and more recently in patients with chronic hepatitis C compared to healthy controls in most but not all studies, while the data on the associations between these adipokine levels and the severity of hepatic steatosis or fibrosis are still rather conflicting. However, several potential confounding parameters were not evaluated in all studies. Therefore, the associations between adipokines and liver histological lesions and their effects on liver cells should be evaluated further in prospective, carefully designed studies, including larger cohorts of patients with detailed assessment of metabolic and other potential confounding factors.

Adiponectin↗
PubMed2006

Fat-derived hormone adiponectin combined with FTY720 significantly improves small-for-size fatty liver graft survival.

Owing to the discrepancy between organ donation and the demand for liver transplantation, expanding the liver donor pool is of vital importance. However, marginal liver grafts, such as small-for-size and/or fatty grafts, were associated with primary graft nonfunction or poor function. Therefore, novel combination therapies to rescue small-for-size fatty liver grafts should be investigated. In this study, we applied a combination therapy using a fat-derived hormone adiponectin (anti-steatosis) plus immunomodulator FTY720 (anti-inflammatory) in a rat liver transplantation model using small-for-size fatty liver grafts, and investigated the underlying protective mechanism such as anti-steatosis, intra-graft energy metabolism, hepatic microcirculatory changes, cell signaling cascades for survival, apoptosis and inflammation. The current study demonstrated that even a single treatment of adiponectin or FTY720 improved the 7-day graft survival from 0% to 62.5% (p = 0.001). The combination therapy significantly increased the 7-day graft survival rate to 100% by remarkable attenuation of graft steatosis and acute phase inflammatory response, significant activation of cell survival Akt pathway and maintenance of intra-graft adenosine triphosphate metabolism and improvement of hepatic microcirculation. In conclusion, the fat-derived hormone adiponectin combined with FTY720 might be a novel combination drug therapy for prevention of small-for-size fatty liver graft injury.

Adiponectin↗