فبراير 3, 2017 - Glory Science العربية

An overview of adiponectin Adiponectin(ADPN) is an endogenous bioactive polypeptide or protein secreted by adipocytes. Adiponectin (ADPN) is an endogenous bioactive polypeptide or protein secreted by adipocytes. Adiponectin is an insulin-sensitizing hormone (An Insulin-sensitizing Hormone), can improve the mice's insulin resistance (Insulin resistance) and atherosclerosis; study found that the human body, adiponectin levels can predict type II diabetes And the development of coronary heart disease, and in clinical trials show anti-diabetic, anti-atherosclerotic and inflammatory potential. Biochemical characteristics of adiponectin Adiponectin is one of the most abundant proteins expressed in adipose tissue, which is found in a large number of blood proteins. In the human body in the concentration of 3-30ug/ml in circulating plasma. Adiponectin is also known as Acrp30, apM1, AdipoQ, GBP28, initially, Adiponectin in human subcutaneous adipose tissue, plasma and murine animal fat cells were found. Adiponectin from the body consists of 244 amino acids, molecular weight of 30KD. From the amino-terminal secretion signal sequence (aa 1-18), a specific sequence (aa19-41), a group of 22 amino acids consisting of collagen repeat (Aa 42-107), a segment of a spherical sequence (aa108-244). The globular region is a key site for the biological activity of adiponectin. Similar to the structure of TNF-α, Adiponectin is highly homologous to collagen Ⅷ, X and complement C1q. Adiponectin is a biologically active form or receptor affinity ligand that specifically binds to the G protein-coupled receptor type I or II adiponectin receptor on the skeletal muscle or liver cell membrane , Thereby regulating fatty acid oxidation and glucose metabolism. The biology of Adiponectin Adiponectin affects fat and carbohydrate metabolism Adiponectin as an insulin hypersensitizing hormone (An Insulin-sensitizing Hormone), can increase the promotion of skeletal muscle cell fatty acid oxidation and sugar absorption, significantly enhanced insulin inhibition of glycogenogenesis, inhibition of liver glucose production, is Lipid metabolism in the body and regulation of blood glucose homeostasis in the network of important regulatory factors. In the experimental atherosclerosis model, plasma adiponectin levels and triglycerides and low density lipoprotein negatively correlated with high density lipoprotein is positively correlated. Adiponectin treatment, significantly lower blood triglycerides and low density lipoprotein content, increase high-density lipoprotein levels, reduce atherosclerotic lesions. Effect of Adiponectin on the secretion of vascular endothelium Ouchi and so found that adiponectin can reduce the adhesion of monocytes, monocytes can make THP-1 cells arranged in human aortic endothelial line, and this adhesion occurs in early atherosclerotic lesions. Adiponectin also decreased the expression of VCAM-1, ICAM-1, and selectin-E in endothelial cells. NF-κB plays an important role in the transcriptional regulation of VCAM-1, ICAM-1, and selectin-E by TNF-α. Ouchi and Kihara and other reports, adiponectin may inhibit the NF-κB signaling pathway regulation of endothelial cell function. NF-κB-induced kinase (NIK) phosphorylates the IKB kinase (IKK) complex and activates NF-κB. TNF receptor binding factor 2 is the NIK and TNF-α signaling pathway connexin, which is a bifurcation point of TNF-α-induced activation of NIK-NF-κB and activation of JNK or p38 pathway. NIK is not involved in the activation of JNK and p38 kinase. It has been reported that cAMP-PKA signaling attenuates NF-κB activity by stabilizing IKB-α, although its precise mechanism has not been elucidated. Adiponectin specifically inhibits TNF-α-induced activation of the ΚκB-α-NF-κB pathway and does not affect the phosphorylation of JNK, p38 or Akt kinases, suggesting that adiponectin reduces the TNF-α level between NIK and ΙκB- Α induces NF-κB signal transduction. These results suggest that adiponectin does not depend on the effect of cAMP-PKA on TNF-alpha-induced expression of adhesion molecules. Effects of Adiponectin on the proliferation and migration of arterial smooth muscle cells Vascular smooth muscle proliferation induced by platelet-derived growth factor (PDGF) or heparin-binding epidermal growth factor (HB-EGF) plays an important role in vascular disease, and the physiological concentration of adiponectin is involved in PDGF-BB-induced vascular smooth muscle Proliferation and migration have an important inhibitory effect. The effect of Adiponectin on tumor necrosis factor (TNF) secretion Adiponectin can inhibit the formation and release of TNF, has a certain anti-inflammatory effect, alcoholic liver injury has important cytoprotective effect. Medical effects of Adiponectin Kondo and other extensive genome scan found that type 2 diabetes and metabolic syndrome susceptibility locus on chromosome 3q27, which is the site of adiponectin gene. They screened a subset of Japanese patients with type 2 diabetes and matched controls with age and body mass index, analyzed their adiponectin gene mutations, and identified four missense mutations in the globular region of adiponectin (R112C, I164T, R221S and H241P), which were present in heterozygous form. The frequencies of I164T mutations in patients with type 2 diabetes were significantly higher than those in the control group (P<0.01). Moreover, patients with I164T mutations had lower concentrations of Adiponectin than those without such mutations, and all patients with this mutation showed signs of metabolic syndrome, including hypertension, high blood pressure Lipidemia, diabetes, arteriosclerosis. Through enzyme-linked immunosorbent assay study found that I164T and R112C mutation and low plasma adiponectin concentrations and type 2 diabetes. The genetic polymorphism of the adiponectin gene leads to a decrease in the production and secretion of adiponectin, at least in part, explaining the pathophysiological characteristics of insulin resistance syndrome. The analysis and detection of Adiponectin genes are of great help in developing drugs that are specific to diabetes, including selecting the most effective treatment principles for each individual, as well as providing drugs specific to their genetic information. To further explore the relationship between adiponectin, obesity, insulin sensitivity, insulinemia and glucose tolerance, Weyer and other obese and type 2 diabetes tend to 23 Caucasian and 121 Indian plasma lipid The concentrations of Adiponectin, body fat, insulin sensitivity and glucose tolerance were measured. Confirming that obesity and type 2 diabetes are associated with low plasma adiponectin concentrations in different racial populations, suggesting that hypoadiponectinemia is more closely associated with obesity and glucose tolerance than insulin resistance and hyperinsulinemia. There is increasing evidence that adiponectin and its synthetic synergies are of value in the treatment of type 2 diabetes and metabolic syndrome associated with insulin resistance. Recent studies have reported that the rapid administration of cut-off Adiponectin in the body reduces postprandial plasma free fatty acids in mice fed a high-fat diet. If administered slowly, the mice will lose weight without affecting their food intake. Scherer and his associates have also demonstrated rapid injection of recombinant adiponectin, which will completely improve hyperglycemia in several animal models of diabetes, including ob/ob mice, nonobese diabetic mice, and streptozotocin-treated mouse.

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Pharmaceutical Research on Adiponectin

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