Disease relevance of Adipoq

• Cardiac function gradually declined over the course of high-fat feeding, and after 20 weeks of high-fat diet, cardiac dysfunction was associated with mild hyperglycemia, hyperleptinemia, and reduced circulating adiponectin levels [1].
• We confirmed that t10,c12-CLA daily gavage performed in mice reduces white adipose tissue (WAT) mass and adiponectin and leptin serum levels and provokes hyperinsulinemia [2].
• CLINICAL IMPLICATIONS: The data suggest that adiponectin might play a role in the relationship between obesity and asthma [3].
• CONCLUSION: Our results indicate that serum adiponectin is reduced during pulmonary allergic reactions and that adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice [3].
• We are reporting that PRL deficiency does not affect the rate of weight gain, body composition, serum lipids, or adiponectin levels in either sex on any diet [4].
• APN KO mice are protected from chemically induced colitis; administration of APN restores inflammation [5].
• Pathologic analyses revealed reduced vascularization of APN null tumors along with increased hypoxia and apoptosis [6].
• Our observations indicate that CR can promote revascularization in response to tissue ischemia via an AMPK-eNOS-dependent mechanism that is mediated by adiponectin [7].

Psychiatry related information on Adipoq

• On the contrary, chronic renal failure, type 1 diabetes and anorexia nervosa are associated with increased plasma adiponectin levels [8].

High impact information on Adipoq

• We observed increased leptin sensitivity and increased serum adiponectin levels in Crebbp+/- mice [9].
• In cultured cardiac cells, adiponectin inhibited apoptosis and TNF-alpha production [10].
• Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms [10].
• These data suggest that adiponectin protects the heart from ischemia-reperfusion injury through both AMPK- and COX-2-dependent mechanisms [10].
• Ischemia-reperfusion in adiponectin-deficient (APN-KO) mice resulted in increased myocardial infarct size, myocardial apoptosis and tumor necrosis factor (TNF)-alpha expression compared with wild-type mice [10].

Chemical compound and disease context of Adipoq

• Our objectives were to compare: 1) weight gain, 2) body composition, 3) serum lipid profile, 4) circulating leptin and adiponectin levels, and 5) glucose tolerance in PRL knockout, heterozygous, and wild-type mice maintained on standard chow, high-fat, or low-fat diets [4].
• Adiponectin Expression is Paradoxically Increased in Gold-thioglucose-induced Obesity [11].
• Targeted deletion of PPARgamma in adipose tissue resulted in marked adipocyte hypocellularity and hypertrophy, elevated levels of plasma free fatty acids and triglyceride, and decreased levels of plasma leptin and ACRP30 [12].
• Thiazolidinediones have been shown to up-regulate adiponectin expression in white adipose tissue and plasma adiponectin levels, and these up-regulations have been proposed to be a major mechanism of the thiazolidinedione-induced amelioration of insulin resistance linked to obesity [13].
• Hyperinsulinaemia triggered by dietary conjugated linoleic acid is associated with a decrease in leptin and adiponectin plasma levels and pancreatic beta cell hyperplasia in the mouse [14].
• We conclude that the balance between free fatty acids and adiponectin impacts muscle proteolysis in insulin-resistant conditions and suggest a role for adipose tissue-muscle cross talk in diabetes and obesity [15].

Biological context of Adipoq

• RESULTS: In spite of hypoadiponectinaemia, Adipoq mRNA levels were markedly increased in the skeletal muscle of ob/ob mice and correlated with systemic oxidative stress [16].
• Adipoq upregulation was shown in laser-microdissected myocytes of obese mice [16].
• Diet-induced insulin resistance in mice lacking adiponectin/ACRP30 [17].
• These data demonstrate induction of endothelial apoptosis as an unique mechanism of adiponectin-induced antiangiogenesis [18].
• Adiponectin induces a cascade activation of caspases-8, -9, and -3, which leads to cell death [18].

Anatomical context of Adipoq

• Pathological changes in epididymal adipose tissue, including increases in macrophage accumulation and Tnfa mRNA and reductions in Adipoq mRNA, were unaffected by the absence of MCP-1 [19].
• In vitro, adiponectin potently inhibits endothelial cell proliferation and migration [18].
• Adiponectin stimulated the differentiation of human umbilical vein endothelium cells (HUVECs) into capillary-like structures in vitro and functioned as a chemoattractant in migration assays [20].
• EPA/DHA increased plasma adiponectin levels, independent of food intake, reflecting the stimulation of Adipoq expression in adipocytes and the release of adiponectin from WAT, particularly from epididymal fat [21].
• In cultured C2C12 myotubes, a triglyceride mix and reactive oxygen species producers (H(2)O(2) or a lipoperoxidation end-product) upregulated Adipoq expression and adiponectin production [16].

Associations of Adipoq with chemical compounds

• When exposed to high fat diet, adiponectin null mice rapidly develop glucose intolerance [22].
• Food restriction decreased plasma triacylglycerols, glucose, insulin and leptin, but not adiponectin [21].
• We tested whether the anti-diabetic effects of EPA and DHA involve enhanced production of the endogenous insulin sensitiser, adiponectin [21].
• CONCLUSIONS/INTERPRETATION: Intake of diets rich in EPA and DHA leads to elevated systemic concentrations of adiponectin, largely independent of food intake or adiposity and explain, to some extent, their anti-diabetic effects [21].
• Adiponectin attenuates allergen-induced airway inflammation and hyperresponsiveness in mice [3].
• TNF-alpha, C-C motif chemokine receptor-2, and C-C motif chemokine ligand-2 were selectively elevated in mesenteric fat without altering glucose tolerance and adiponectin signaling [23].
• The above results indicate that adiponectin induces insulin secretion in vitro and in vivo [24].

Physical interactions of Adipoq

• Only eukaryotically expressed adiponectin bound to T-cadherin, implying that posttranslational modifications of adiponectin are critical for binding [25].
• Suppression of SIRT1 or activation of PPAR gamma enhances Ero1-L alpha expression and stimulates secretion of high-molecular-weight complexes of adiponectin in mature adipocytes [26].
• Adiponectin is covalently bound to the ER chaperone ERp44 [27].

Regulatory relationships of Adipoq

• Leptin also directly stimulated ApN mRNAs and secretion from 3T3-F442A adipocytes [28].
• In the present study, the mechanism by which adiponectin is regulated by TNF-alpha was investigated [29].
• Endothelin-1 inhibits adiponectin secretion through a phosphatidylinositol 4,5-bisphosphate/actin-dependent mechanism [30].
• We examined the role of PPAR gamma 2 and C/EBP alpha for adiponectin and aP2 gene activation in C/EBP alpha(-/-) fibroblasts by stably expressing PPAR gamma 2 or C/EBP alpha [31].
• METHODS AND RESULTS: Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal) [32].

Other interactions of Adipoq

• Because of the enhanced adipocyte differentiation, the ADSF-hFc transgenic mice show increased expression of leptin and adiponectin in adipose tissue [33].
• Mice lacking adiponectin show decreased hepatic insulin sensitivity and reduced responsiveness to peroxisome proliferator-activated receptor gamma agonists [22].
• Adiponectin and resistin, two recently identified adipocyte-specific secretory factors, are able to modulate insulin actions in target tissues [34].
• However, treatment with exogenous PIP(2):histone carrier complex and the actin depolymerizing agent latrunculin B (20 microM) did not reverse the ET-1-mediated decrease in adiponectin secretion [30].
• These observations suggest that "insulin-stimulated Akt activity in adipocytes" may play an important role in the regulation of adiponectin secretion [35].

Analytical, diagnostic and therapeutic context of Adipoq

• Plasma leptin levels were also increased by ovariectomy, whereas resistin and adiponectin levels were unchanged [36].
• Castration of male mice did not significantly change adipokine mRNA levels or plasma levels of resistin or leptin; however, adiponectin was significantly increased [36].
• Two weeks' oral administration of CL-316,243 led to decreased plasma levels of hemoglobin A1c, glucose, insulin, triglyceride and free fatty acid, and to an increased plasma adiponectin levels [37].
• Adiponectin mRNA expression was significantly higher in the CL-316,243-treatment group than in the control group in epididymal white adipose tissue but not in brown adipose tissue, soleus muscle or liver [37].
• 3T3-L1 adipocytes were treated with insulin (100 nM), ET-1 (100 nM), or the appropriate vehicle and adiponectin secretion into the media was determined by immunoblotting and densitometric analysis [38].

References