| Background: The pathological mechanisms of both type 1 and type 2 diabetes are due to the attenuation of insulin actions by decreased insulin secretion, diminished insulin signal transduction or insulin resistance, which result in metabolic disorder, especially in glucose and lipid metabolism. The purpose of this article was to investigate the molecular mechanism for rosiglitazone and aerobic exercise interfering in glucose and lipid metabolism, in view of the facts that rosiglitazone and exercise being used in diabetic treatment are both aimed to regulate glucose and lipid metabolism. The peroxisome proliferator-activated receptor gamma isoforms(PPAR ) is a ligand-depend transcription factor that regulate transcription of the genes involving glucose and lipid metabolism. It has therefore been suggested that this receptor play a central role in modulating glucose and lipid metabolism. Glucose transporter 4(GLUT4) is found in muscle and adipose cells and plays an important role in taking up and utilizing glucose in these tissues. Fatty acid-binding proteins(FABPs) distribut in varied tissues widely and form a group of at least nine distinct protein types. The FABPs distributed in liver, muscle and adipose tissues are L-FABP, H-FABP and A-FABP respectively. They exert action in fatty acid(FA) uptake and transport and involve in the modulation of cellular signal transduction. GLUT4 express is influenced by PPAR agonists although its mechanism is unclear. PPAR y regulate directly A-FABP gene transcription and FABPs act as media of PPAR agonists signal transduction. There are functionalrelationship between FABPs and PPARs. Therefore, we hypothesize that rosiglitazone and aerobic exercise exert influence on glucose and lipid metabolism by improving PPAR express , which mediate GLUT4 and FABPs express, because rosiglitazone acts as a synthetic ligand and aerobic exercise mobilizes FAs as endogenesis ligands of PPAR . If thishypothesis is proved, at least in the three links of PPAR , GLUT4 and FABPs, we may unviel the molecular mechanism for antidiabetic agent and aerobic exercise interfering in glucose and lipid metabolism.Objective: To study that pharmaceutical and aerobic exercise interfere in glucose and lipid metabolism and their molecular mechanism.Methods: Firstly, to establish a model of laboratory rodents, 3-4 weeks old NOD mice were treated with rosiglitazone for 12 weeks, trained with treadmill exercise for 12 weeks,respectively. We observed appearance, body weight, blood glucose and belly fat weight to decid the difference between the treated mice and the control mice. Secondly, we viewed the pancreas tissue section by HE staining under the photic microscope to determine the degree of pancreatitis. We measured the concentration of serum insulin and some parameters in blood. Thirdly, the mRNA expression of PPAR , GLUT4 and FABPs was analyzed by RT-PCR to decide the effect of pharmaceutical and aerobic exercise on glucose and lipid metabolism in the molecular level.Result: Firstly, for the control NOD mice, the fur looked fade and dishevelled, body weight decreased, the level of blood glucose increased and fat withered. For the treated mice, the state of vigour is fine, body grew well, the level of blood glucose was stable and fat did not wither. There are marked difference between the treated mice and the control mice. These NOD mice can be used in the latter examination. Secondly, the pancreas tissue section of the control mice showed various degrees of pancreatitis, whereas those of the treated mice showed either no pancreatitis or slight lymphocyte immersion. The level of serum insulin of the control mice was higher than that of the treated mice. Thirdly, the parameters in blood showed that the level of blood glucose of the control mice was significant higher than that of the treated mice, thestate of blood lipid of the control mice was bad, for the level of TC, TG and LDL higher and HDL lower than the treated mice. Fourthly, compared with the control, the mRNA expression of PP...
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