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At least 793 records · Page 44Linked to original sources
PubMed2003

Conjugated linoleic acid enhances plasma adiponectin level and alleviates hyperinsulinemia and hypertension in Zucker diabetic fatty (fa/fa) rats.

Adiponectin is a recently discovered hormone secreted by adipocytes that has been reported to enhance insulin sensitivity. Although insulin resistance and/or compensatory hyperinsulinemia are considered to be involved with hypertension in obese humans, the relationship between plasma adiponectin level and obesity-related hypertension has not been fully clarified. In this study, we investigated the effect of dietary conjugated linoleic acid (CLA), reported as an insulin sensitizer, on plasma adiponectin, plasma insulin, and blood pressure in Zucker diabetic fatty (ZDF) rats. During the onset of obesity, blood pressure increased in ZDF rats. The increase, however, was prevented by dietary CLA. After 8 weeks, accumulated plasma insulin and glucose were also attenuated by CLA feeding. Dietary CLA increased plasma adiponectin levels in ZDF rats and the increase was attributed to the enhanced mRNA expression in white adipose tissue. This study provides the first evidence that dietary CLA increases plasma adiponectin level through the enhancement of mRNA expression. We speculate that the increase alleviates hyperinsulinemia and prevents the onset of hypertension in CLA-fed ZDF rats.

Adiponectin↗
PubMed2004

AICAR stimulates adiponectin and inhibits cytokines in adipose tissue.

5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR) can be used as an experimental tool to activate 5'-AMP-activated protein kinase (AMPK) and has been shown to improve insulin sensitivity. In parallel adiponectin also seems to activate AMPK and to improve insulin sensitivity. We have investigated the effects of AICAR on the gene expression of adiponectin and on gene expression and release of cytokines in human adipose tissue in vitro. AICAR stimulated AMPK alpha1 activity 3-4-fold (p<0.001), and dose-dependently increased adiponectin mRNA levels with significant stimulation (2-4-fold) at AICAR concentrations of 0.5-2mM (p<0.05). The adipose tissue protein release of tumor necrosis factor-alpha (TNF- alpha) and interleukin-6 (IL-6) was decreased by AICAR (p<0.05). In conclusion, AICAR stimulated adipose tissue AMPK alpha1 activity and adiponectin gene expression, while attenuating the release of TNF-alpha and IL-6. Reduced concentrations of these cytokines and increased levels of adiponectin might play a role for the insulin sensitizing effects of AICAR.

AMP-Activated Protein Kinases↗
PubMed2005

Inhibition by adiponectin of IL-8 production by human macrophages upon coculturing with late apoptotic cells.

Adiponectin, an adipocyte-derived hormone, reportedly suppresses the production of TNF-alpha and IL-6 by LPS-stimulated human or porcine macrophages, and the phagocytosis of microbeads by human macrophages. In this study, we used a high molecular weight form of adiponectin purified from human plasma to examine its effects on the phagocytosis of late apoptotic cells by human macrophages and the subsequent IL-8 production. Adiponectin suppressed both the phagocytosis of apoptotic cells and the IL-8 production. In contrast, adiponectin augmented both the phagocytosis of apoptotic cells and the IL-8 production in the presence of LPS. These results suggest that adiponectin is not an anti-inflammatory hormone but rather a dual modulator of innate responses.

Adiponectin↗
PubMed2006

Adiponectin protects human neuroblastoma SH-SY5Y cells against MPP+-induced cytotoxicity.

1-Methyl-4-phenylpyridinium ion (MPP+), an inhibitor of mitochondrial complex I, has been widely used as a neurotoxin because it elicits a severe Parkinson's disease-like syndrome characterized by elevation of intracellular reactive oxygen species level and apoptotic death. Adiponectin, secreted from adipose tissue, mediates systemic insulin sensitivity with liver and muscle as target organs. Adiponectin can also suppress superoxide generation in endothelial cells. In the present study, we investigated the protective effects of adiponectin on MPP+-induced cytotoxicity in human neuroblastoma SH-SY5Y cells, as well as the underlying mechanism. Our results suggest that the protective effects of adiponectin on MPP+-induced apoptosis may be ascribed to its anti-oxidative properties, anti-apoptotic activity via inducing expression of SOD and catalase, and regulation of Bcl-2 and Bax expression. These data indicated that adiponectin might provide a useful therapeutic strategy for the treatment of progressive neurodegenerative diseases such as Parkinson's disease.

1-Methyl-4-phenylpyridinium↗
PubMed2004

Adiponectin, obesity, and cardiovascular disease.

Several adipocyte-secreted factors have been demonstrated to potentially link obesity, insulin resistance, and cardiovascular disease. Among those, adiponectin is an insulin-sensitizing and anti-inflammatory adipokine, concentrations of which are decreased in obesity-associated metabolic and vascular disorders. Recently, two adiponectin receptors (AdipoR) have been isolated and adenosine monophosphate kinase (AMPK), as well as acetyl coenzyme A carboxylase (ACC), appear to be critical downstream mediators for various effects of this adipokine. In addition to beneficial metabolic effects, adiponectin seems to be vasoprotective by interfering with various atherogenic processes. Of clinical interest, thiazolidinediones (TZDs) which are used in the treatment of type 2 diabetes stimulate adiponectin expression and secretion whereas several hormones dysregulated in insulin resistance and obesity downregulate this adipokine. The current knowledge on regulation and function of adiponectin in obesity, insulin resistance, and cardiovascular disease is summarized in this review and its clinical implications are discussed.

Acetyl-CoA Carboxylase↗
PubMed2006

Role of adipokines in the control of energy metabolism: focus on adiponectin.

Leptin and adiponectin are the major adipokines secreted by fat cells. Leptin effects energy homeostasis by decreasing food intake and by acting on lipogenesis and fatty acid oxidation. Elucidation of the mechanisms of action of adiponectin (Acrp30), a hormone considered to be a major insulin-sensitizing hormone, and leptin has been improved by the delineation of their impact on muscle and liver cells via regulation of AMP kinase function. A recent study has defined a human skeletal muscle pathway by which adiponectin increases mitochondrial number and function. In addition, adiponectin signaling pathways have recently been clarified by the discovery of a protein that interacts with adiponectin receptors.

AMP-Activated Protein Kinases↗
PubMedDate not supplied

Adiponectin and the systemic inflammatory response in weight-losing patients with non-small cell lung cancer.

The aim of the present study was to examine the relationship between adiponectin and the systemic inflammatory response in weight-losing patients with non-small cell lung cancer (NSCLC). Measurement of anthropometry, acute phase proteins, interleukin-6, leptin (total and free) and adiponectin were carried out on healthy subjects (n = 13) and non-small cell lung cancer patients with weight loss (n = 20). The groups were age and sex matched. Compared with the controls the cancer group had a lower BMI (p < 0.01), mid-upper arm circumference (p < 0.001), triceps skinfold thickness (p < 0.05) and circulating concentrations of albumin (p < 0.001), haemoglobin (p < 0.05), free and total leptin (p < 0.05) and adiponectin (p < 0.01). In contrast, the cancer group had elevated circulating concentrations of interleukin-6 and C-reactive protein concentrations (p < 0.001). In the cancer group circulating adiponectin concentrations were significantly inversely correlated with both free (rs = -0.675, p = 0.001) and total leptin concentrations (rs = -0.690, p = 0.001). However, neither weight loss, interleukin-6 or C-reactive protein concentrations were correlated with either adiponectin, free or total leptin concentrations in the cancer group. These results suggest that adipokine production is normal and is unlikely to play a major role in the abnormal fat metabolism in weight-losing cancer patients.

Adiponectin↗
PubMed2006

Resistin and adiponectin levels in subjects with coronary artery disease and type 2 diabetes.

BACKGROUND: Resistin and adiponectin are implicated in insulin resistance and atherosclerosis. The objective of this study was to evaluate the association between plasma resistin levels and the presence of coronary artery disease (CAD) or diabetes compared to the controls. In a cross-sectional study, we measured glucose, fasting lipid panel, resistin, adiponectin, insulin, C-reactive protein (CRP) and TNF-alpha in 57 subjects with CAD, 58 subjects with diabetes compared to 45 normal control subjects. RESULTS: Subjects with CAD compared to the control subjects had increased insulin resistance index (39+/-32 vs. 13.45+/-12.73 with p<0.0001), CRP levels (3.8+/-4.03 vs. 2.0+/-2.0 with p<0.05) and decreased levels of adiponectin (12.5+/-4.8 vs. 17.26+/-10.4 with p<0.0003). Subjects with diabetes compared to the controls had had increased insulin resistance index (69+/-19 vs. 13.45+/-12.73 with p<0.001), CRP levels (4.1+/-4.8 vs. 2.0+/-2.0 with p<0.01) and decreased levels of adiponectin (11.58+/-4.8 vs. 17.26+/-10.4 with p<0.001). Compared to the controls, there was no significant difference in the levels of resistin in subjects with CAD (4.92+/-3.2 vs. 4.1+/-2.4) as well as diabetes (4.92+/-3.2 vs. 4.6+/-2.6). Both CRP and resistin levels correlate with TNF-alpha (r=0.557, p<0.000001; r=0.84, p<0.000001). CONCLUSIONS: The present study shows decreased plasma adiponectin levels in subjects with diabetes as well as in subjects with CAD is similar to the literature. Plasma levels of resistin in subjects with CAD or diabetes are similar to the controls. However, there was a strong correlation of resistin levels with inflammatory markers. This suggests resistin as an inflammatory marker associated with CAD.

Adiponectin↗
PubMed2004

Sibutramine improves fat distribution and insulin resistance, and increases serum adiponectin levels in Korean obese nondiabetic premenopausal women.

The aim of this study was to evaluate the effects of sibutramine on body composition and fat distribution, insulin resistance, and serum adiponectin levels in obese women. A total of 28 obese, premenopausal women (mean age, 34.5 +/- 13.7 years; BMI, 31.00 +/- 4.10 kg/m2) was studied before and after 12-week-course of sibutramine (10mg/day). Sibutramine treatment reduced body mass index (P < 0.05) and total body fat (P < 0.05). Abdominal subcutaneous and visceral fat areas (ASFA and AVFA) and mid-thigh low density muscle areas (LDMA) measured by computed-tomography decreased significantly (all, P < 0.05). Insulin resistance (IR) calculated from the homeostasis model assessment (HOMA) method decreased (P < 0.05) and serum adiponectin levels increased significantly (P < 0.05). In our sequential data, the changes of fasting serum insulin levels and the HOMA-IR scores, serum free fatty acids and triglyceride levels, serum adiponectin levels and the mid-thigh LDMA preceded significant changes of body weight, total body fat, and abdominal fat distribution, suggesting sibutramine might improve insulin sensitivity directly by alterations of fatty acid metabolism or secondarily by increasing serum adiponectin levels. Conclusively, sibutramine improved fat distribution and insulin resistance, and increased serum adiponectin levels in Korean obese nondiabetic premenopausal women.

Adiponectin↗
PubMed2006

Serum adiponectin, interleukin-10 levels and inflammatory markers in the metabolic syndrome.

We examined the association between interleukin-10 (IL-10), adiponectin levels and inflammatory markers such as interleukin-6 (IL-6) and high-sensitive C-reactive protein (hsCRP). Furthermore, the association of these anti-/pro-inflammatory cytokine levels with the metabolic syndrome was investigated. The study subjects were composed of 312 Korean individuals without diabetes. Serum adiponectin level was associated with hsCRP (r=-0.21, P<0.001), IL-6 (r=-0.13, P<0.05) and IL-10 (r=-0.22, P<0.001) levels. Subjects without the metabolic syndrome showed higher adiponectin (17.03 microg/ml versus 13.85 microg/ml, P<0.001) and IL-10 (4.74 pg/ml versus 4.34 pg/ml, P=0.014) levels, and lower serum hsCRP (0.38 microg/ml versus 0.66 microg/ml, P=0.001) and IL-6 (0.94 pg/ml versus 1.32 pg/ml, P=0.009) levels compared to those with the metabolic syndrome. In multiple logistic regression analysis, the metabolic syndrome was associated with sex, age, waist circumference, systolic blood pressure, HDL cholesterol, triglyceride, fasting blood glucose and interleukin-10. Furthermore, serum adiponectin levels are associated with serum hsCRP, IL-6 and IL-10 levels. These results suggest that adiponectin might be associated with the metabolic syndrome through regulation of pro-/anti-inflammatory cytokines.

Adiponectin↗
PubMed2006

A novel index of insulin resistance determined from the homeostasis model assessment index and adiponectin levels in Japanese subjects.

Insulin resistance is the principal cause of glucose intolerance and type 2 diabetes and induces progression of severe atherosclerosis in these patients. Adiponectin, the adipose-specific proteins, is known to correlate negatively with insulin resistance in patients with obesity and type 2 diabetes. The purpose of this study was to evaluate the potential of using serum adiponectin levels as a marker of insulin resistance in various states of insulin resistance. Furthermore, we attempted to establish a modified index of the homeostasis model assessment index (HOMA-IR), calculated from the product of serum insulin and plasma glucose levels divided by serum adiponectin levels (HOMA-AD). We recruited 117 Japanese subjects with various degrees of glucose tolerance and determined serum adiponectin levels and insulin sensitivity (M-value) by using the euglycemic hyperinsulinemic clamp technique. M-value, the gold standard index of insulin resistance, correlates significantly and independently with fasting insulin (r=-0.313, P<0.001), glucose (r=-0.319, P<0.001), and adiponectin (r=0.241, P<0.002) levels. M-values were more significantly correlated with HOMA-AD (r=-0.643, P<0.001) than HOMA-IR values (r=-0.591, P<0.001). In subjects with moderate hyperglycemia (fasting glucose levels>8.0mmol/L, n=30), HOMA-AD showed a more significant correlation with the M-value than HOMA-IR (r=-0.535, P=0.005 versus r=-0.461, P=0.010). We would therefore like to propose a novel index, HOMA-AD, as a simple and adequate index for determining insulin resistance even in diabetic patients with overt hyperglycemia.

Adiponectin↗
PubMed2004

Resistin, but not adiponectin, inhibits dopamine and norepinephrine release in the hypothalamus.

Adiponectin (Adipocyte Complement-Related Protein of 30 kDa, ACRP30) and resistin are adipocyte-derived polypeptide hormones playing a role in metabolic homeostasis. Their plasma levels are inversely (adiponectin) or directly (resistin) correlated to obesity and they have opposite effects on insulin sensitivity. Adipose tissue hormones such as leptin have been shown to modulate neurotransmitters which control feeding in the hypothalamus. We have studied the effects of adiponectin and resistin on dopamine, norepinephrine and serotonin release from hypothalamic neuronal endings (synaptosomes) in vitro. We have found that adiponectin does not modify either basal or depolarization-induced amine release, while resistin inhibits the stimulated release of dopamine and norepinephrine, leaving unaffected serotonin release. We can conclude that, similarly to leptin, but differently from adiponectin, the adipose tissue hormone resistin could affect the central mechanisms of feeding by inhibiting catecholamine release in the hypothalamus.

Adiponectin↗
PubMed2005

Metformin reduces adiponectin protein expression and release in 3T3-L1 adipocytes involving activation of AMP activated protein kinase.

The drugs troglitazone and metformin are used to reduce the degree of insulin resistance in type 2 diabetes. Both compounds act through different mechanisms which might include opposing effects on the production of adiponectin, an insulin-sensitizer released by adipocytes. This study compared the effects of troglitazone and metformin on adiponectin production by 3T3-L1 adipocytes during 48 h culture. Troglitazone increased adiponectin mRNA and protein expression as well as release, whereas metformin did not affect transcription but reduced protein expression and release. The effect of metformin was also seen with phenformin, and with low-glucose culture, all conditions with a reduced mitochondrial activity and an activated AMP activated protein kinase (AMPK). Addition of the AMPK activator 5-aminoimidazole-4-carboxamide-riboside (AICAR) also caused a decrease in adiponectin protein expression. These data indicate that metformin and troglitazone exert opposing effects on adiponectin expression and release by differentiated 3T3-L1 adipocytes. The metformin-induced suppression involves an activation of AMP activated protein kinase.

3T3-L1 Cells↗
PubMed2006

Tetrahydrobiopterin prevents endothelial dysfunction and restores adiponectin levels in rats.

Oxidative stress induces endothelial dysfunction and hypoadiponectinemia. We previously reported that supplementation with tetrahydrobiopterin (BH4), one of the most potent naturally occurring reducing agents and an essential cofactor of enzymatic NO synthase (NOS), ameliorates endothelial dysfunction and reverses hypoadiponectinemia as a result of oxidative stress in rats. To further confirm this hypothesis, we investigated the effects of treatment with BH4 on endothelium-dependent relaxation and adiponectin levels during oxidative stress in fructose-fed rats, which provide an animal model for the metabolic syndrome. Ingestion of a fructose diet for 8 weeks significantly impaired endothelium-dependent arterial relaxation in aortic strips and decreased plasma adiponectin levels, as well as adiponectin mRNA levels within adipose tissue. However, oral supplementation with BH4 (10 mg/kg day) over the final 4 weeks leads to a significant partial reversal of impaired endothelium-dependent arterial relaxation, as well as normalization of plasma adiponectin and fat adiponectin mRNA levels. Moreover, BH4 treatment of the fructose-fed rats significantly reduced the lipid peroxidation content of aorta, heart, liver, and kidney tissues, which were increased in fructose-fed rats. This effect of BH4 treatment may be due to its function as a cofactor for eNOS, as well as its anti-oxidative effects. Thus, BH4 might show promise for the treatment of oxidative stress-induced disorders, including the metabolic syndrome.

Adiponectin↗
PubMed2004

Angiotensin II-induced apoptosis in human endothelial cells is inhibited by adiponectin through restoration of the association between endothelial nitric oxide synthase and heat shock protein 90.

Adiponectin can protect vessels from injury by promoting the activity of endothelial nitric oxide synthase (eNOS) with increased nitric oxide production. Recently, it was demonstrated that eNOS activity is highly regulated by heat shock protein 90 (HSP90). We tested the hypothesis that adiponectin can prevent endothelial cell injury produced by angiotensin II through promotion of the association between eNOS and HSP90. Cultured human umbilical vein endothelial cells (HUVECs) were treated with angiotensin II (2 microM) to induce apoptosis. In the presence of globular adiponectin, apoptosis was inhibited in a dose-response manner. Angiotensin II-induced apoptosis was also inhibited by treatment with an NO donor and by combined treatment with both angiotensin II type 1 and type 2 receptor blockers. Western blotting and immunoprecipitation of the lysates from the treated cells showed that globular adiponectin could restore the association between eNOS and HSP90 and enhance the phosphorylation of eNOS. In conclusion, angiotensin II-induced human endothelial cell apoptosis can be prevented by adiponectin through promotion and stabilization of the association between eNOS and HSP90.

Adiponectin↗
PubMed2004

Reduced adipose tissue mass and hypoleptinemia in iNOS deficient mice: effect of LPS on plasma leptin and adiponectin concentrations.

The aim of this study was to evaluate the impact of the lack of inducible NO synthase (iNOS) on body weight and adipose tissue mass as well as on plasma leptin and adiponectin in basal conditions and 6 h after lipopolysaccharide (LPS) administration in mice. Body weight was not different among male, six-week-old wild-type (WT) and iNOS-/- animals. However, the amount of epididymal white adipose tissue (EWAT) in iNOS-/- mice was significantly reduced (P<0.05). Circulating leptin and leptin mRNA in EWAT were decreased in iNOS-/- mice (P<0.05 and P<0.01, respectively). Plasma adiponectin and adiponectin mRNA were unchanged. LPS administration increased plasma leptin in both genotypes (P<0.05). Neither genotype nor treatment changed plasma adiponectin. In summary, iNOS-/- mice exhibited normal body weight but reduced adipose mass accompanied by hypoleptinemia. Leptin responsiveness to LPS in iNOS-/- mutants is preserved, showing that the LPS-induced rise in leptin is independent of the presence of functional iNOS. In addition, iNOS deficiency or LPS does not influence expression and circulating levels of adiponectin.

Adiponectin↗
PubMed2005

Changes in insulin sensitivity induced by short-term growth hormone (GH) and insulin-like growth factor I (IGF-I) treatment in GH-deficient adults are not associated with changes in adiponectin levels.

To test potential effects of altered insulin sensitivity on circulating adiponectin levels, we studied patients with GH deficiency (GHD) undergoing high dose GH and IGF-I treatment in a well-defined short-term setting. This design allowed to exclude confounding effects of GH and IGF-I treatment on body composition. Six patients (three women and three men) with acquired GHD were treated in a randomised cross-over trial with GH (subcutaneous injections of GH 0.03 IU/kg/daily) or IGF-I (continuous subcutaneous infusion of 5 microg/kg/h recombinant IGF-I) for 5 days. Median age of patients was 60 (range 25-72) years, BMI 24.7 (20.7-30.7) kg/m(2), and baseline IGF-I concentration 60 (30-83) microg/L. HOMA scores (to assess insulin sensitivity) at baseline were 0.8 (0.3-11.7) and adiponectin concentrations were 7.0 (2.5-14.8) mg/L. HOMA scores increased rapidly and significantly up to a maximum of 2.7-fold (from baseline) at day 5 of GH treatment and returned promptly to baseline when GH was stopped, while adiponectin serum levels remained within the baseline range throughout the study period. HOMA scores dropped to a nadir of 0.66 from baseline at day 2 of IGF-I treatment whereas adiponectin levels remained within the baseline range. These data suggest that changes in insulin sensitivity (induced by high dose and short-term GH and IGF-I treatment) in patients with GHD are not associated with changes in adiponectin levels.

Adiponectin↗
PubMed2006

Non-viral adiponectin gene therapy into obese type 2 diabetic mice ameliorates insulin resistance.

Synthetic polymer vectors are attractive for gene delivery due to their potential safety and versatility. However, due to the low efficiency, most of the successful applications of polymeric vectors are focused on the therapeutic genes whose products have biological effects at low concentrations. Adiponectin is one of the abundant circulating proteins and possesses diverse effects including anti-hyperglycemic and anti-atherogenic properties. In this study, we performed the adiponectin gene delivery using a mini-circle DNA complexed with a polymeric carrier, polyethylenimine, into diet induced obese C57BL/6J mice. The mini-circle DNA showed much higher adiponectin expression than the conventional plasmid in vitro and in vivo. This strategy achieved a sufficient blood level of adiponectin and the parameters related with insulin resistance were normalized. The mini-circle DNA will be useful for the increased efficiency of polymeric vectors and adiponectin gene therapy which is applicable to the treatment of type 2 diabetes.

AMP-Activated Protein Kinases↗