| BackgroundsAdipose tissue is now regarded as an important endocrine organ, secreting kinds of adipocytokines, such as leptin, TNF-a, IL-6, resistin and adiponectin. Adiponectin is the most abundant protein in adipose tissue, as plasma levels high up to 5 to 15 mg/L on average in human. Adiponectin has been determined to have important role in insulin sensitizing, antiatherogenesis and antiinflammation. The expression of adiponectin decreases in obesity and insulin resistance, and becomes lower when diabetes complicated with macroangiopathy. Plasma levels of adiponectin have positive correlation with insulin sensitivity and negative with fasting insulin concentration. And these correlations are stronger than that of the protein and obesity or glycemia. Otherwise, hyperglycemia, glucocorticoid, p-adrenergic receptor agonists, IL-6 and TNF-a, et al. can downregulate adiponectin expression; on the contrary, weight loss, thiazolidinedione (TZDs), Ikappa B kinase beta(IKKbeta) inhibitor and insulin-like growth factor-1(IGF-1) , et al. can upregulate it. When treated with adiponectin, the insulin sensitivity was ameliorated in the adiponectin knock-out mice (KO mice). Severalresearches were performed on KO mice. Kubota et al. drew a conclusion that the decrease of adiponectin may act as an important role in the pathogenesis of insulin resistance. The research of Matsuzawa et al. showed that the absence of adiponectin didn't initiate insulin resistance without permanent high caloric food intake. But in the research of Ma et al., the insulin sensitivity of KO mice didn't show any significance difference from that of wild type mice, with or without permanent high caloric food intake. So which is the original factor, hypoadiponectinemia or insulin resistance, remains controversial.Ginsenoside Rgl has been clarified to be antidiabetic among several ginsenosides. Rgl improved glycemia in diabetic mice in a dose-dependent manner, and presented more effective in chronic treatment than acute treatment. Up to date, Rgl is considered to achieve the hypoglycemic effect through stimulating the islet to release insulin and improving insulin sensitivity in liver. Rgl could directly stimulate p cells to release insulin, and as the glucose concentration went up, the insulin released more. Rgl stimulated the hepatic cells to take glucose to synthesize glycogen, accelerated glucose metabolism and oxidative phosphorylation, thus improved insulin sensitivity in liver. There are no reports about Rgl as insulin sensitizor in other peripheral tissues, such as skeletal muscle or adipose tissue.To explore the effect of insulin on expression of adiponectin, and whether the insulin sensitizing effect of Rgl is achieved through improving the expression of adiponectin or not, we treated the 3T3-L1 adipocytes with different concentration of insulin only and with both of insulin and Rgl.Materials and MethodsThe murine 3T3-L1 preadipocyte cell line was grown in DMEM containing 25mmol/L glucose as normal anchoring cell. Confluent preadipocytes were cultured for 2 days in culture medium further supplemented with l0μg/ml insulin, 0.5mmol/L isobutylmethylxanthine and 0.25μmol/L dexamethasone and 2 days in culture medium with 10μg/ml insulin. After additional 4 to 6 days in culture medium, more than 90% of the cells had accumulated fat droplets.Insulin and Rgl were diluted to desired concentrations with culture medium. The major working solution concentrations of insulin were Onmol/L, lnmol/L, l0nmol/L, l00nmol/L, l000nmol/L, and Rgl was 0mg/L,20mg/L and 40mg/L. The effecting time of both on 3T3-L1 adipocytes was 48 hours. Then adiponectin gene expressions were measured by semi-quantitative reverse transcription-PCR, normalized to those of β actin.ResultsAfter 3T3-L1 adipocytes had been treated with insulin for 48hours, adiponectin mRNA levies decreased as the concentration of insulin increasing. When insulin concentrations were more than lOOnmol/L, adiponectin expression decreased significantly (p<0.05). There was no c... |
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