| Objective: Many researches have certificated that the pathogenesy of type 2 diabetes mellitus (T2DM)refer to two aspects, the insulin deficiency and insulin resistance. Insulin resistance is the most important agent of T2DM. The key peripheral target organs of insulin resistance are skeletal muscle, liver, and adipose tissue. Investigation of recent years found that Adiponectin which is the abundant adipocyte-derived hormone possess improving insulin sensitivity. Besides this well charactreised biological functions, it also possesses anti-diabetic, anti- hyperlipemia, anti- hypertension, anti-inflammatory and anti-atherogenic.Adiponectin receptors (AdipoR1/2) have been cloned by Yamanchi for the first time in 2003. AdipoR1 has a wide distribution throughout the organism, especially expressed in adipose tissue. Study has certificated that adiponectin produce a marked effect by binding with AdipoR, then activating peroxisome-proliferator-activated receptor(PPAR)and adenosine monophosphate kinase(AMPK). Rosiglitazone is one of thiazolidinediones(TZDS) which are insulin sensitizing agents. It can adjust the metabolism of glucose and triglycerides and enhances insulin sensitivity by selectively upregulating PPAR. In this study, T2DM rat model was copied. Then the content of serum adiponectin in experimental animals and the protein expression of AdipoR1 in different adipose tissue were detected in order to discuss the association between adiponectin, AdipoR1 and insulin resistance in different adipose tissue of T2DM rats. Furthermore, Rosiglitazone were given to experimental rats to explain the mechanism of the TZD improve insulin resistance in different adipose tissue of T2DM rats.Methods: 10 of 40 Sprague-Dawlay(SD) rats were taken out randomly to be normal control rats (group A) and the rest were taken for test rats. The control rats were fed with general diet while the test rats were fed with high-sugar-fat diet (mixed 2.5% cholesterin, 15% cooked lard, 20% cane sugar and general diet together). 4weeks later, insulin resistance was induced in test group, then STZ 30 mg/kg was injected into abdominal cavity to destroy pancreas. At the end of 6 weeks, the rats whose fasting blood glucose (FBG) was greater than 7.8 mmol/L and insulin sensitivity decreased were considered as T2DM rats. Divided them randomly into 2 groups: T2DM model rats (group B), T2DM model rats treated with Rosiglitazone (group C). The experiment lasted 18 weeks. At the end of 4 and 6 weeks, body weight, FBG, fasting insulin (FINS), insulin sensitivity index (ISI), serum triglyceride (TG) and total cholesterol (TC) in different group rats were measured. At the end of this experiment, FBG and TG, TC, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C) and Adiponectin (APN) were detected. The content of visceral adipose depots and the shape of cells originating from visceral and subcutaneous adipose were observed with light and electron microscopes. The protein expression of AdipoR1 in visceral and subcutaneous adipose was detected by immunohistochemical staining. These graphic results were analyzed with computer image-analysis system and the integral optical density (IOD) counts of AdipoR1 were calculated. All the data were dealt with SPSS11.5.Results1 Various indexes after 4 weeks: Been fed with high-sugar-fat diet for 4 weeks, test rats were heavier than normal control rats (P<0.05). FBG(6.33±0.65 mmol/L), FINS 30.19(29.05~31.65 mIU/L), TG, TC of test rats were all higher than those in control rats (all P<0.01). At the same time, ISI 0.0053(0.0050~0.0054) in test rats was lower than that in control rats (P<0.01).2 Various indexes after 6 weeks: 2 weeks after STZ injection, the FINS18.79(18.23~19.29 mIU/L)in test rats compared to the level in control rats was unstatistices distinction (P>0.05). Other featues were retained. Body weight and FBG(13.18±1.47 mmol/L), TG, TC in test rats were all higher and ISI 0.0048(0.0045~0.0053) was lower than those in control rats (all P<0.01). Thus far, the T2DM rat model was accomplished.3 Various biochemical indexes after 18 weeks: When the experiment was finished, FBG(12.43±1.48 mmol/L),FINS 20.95(19.81~22.11 mIU/L), TG, TC, LDL-C and VLDL-C in group B rats were all higher than those in group A rats. And foregoing items in group C rats were lower than those in group B rats. HDL-C and ISI in group B rats was lower than that in group A and C rats(all P<0.05).4 Body weight and visceral adipose wat weight after 18 weeks: BW(252.33±11.62)g in group B rats were lower than that ( 282.80±5.39 ) g in group A rats.And the BW(266.07±10.55) in group C was higher than that in group B(252.33±11.62)g rats (P<0.05). VAT(10.83±3.13)g in group B rats was higher than that(4.79±1.53) in group A rats. VAT( 6.45±1.89 ) in group C rats were lower than that (10.83±3.13)g in group B rats(P<0.05).5 The serum content of adiponectin: The content of adiponectin (1.01±0.27 ug/mL) in group B rats was lower than that(1.73±0.32 ug/mL) in group A rats. And the content(1.34±0.43 ug/mL) in group C was higher than that in group B rats (all P<0.05). Related analysis showed that the serum content of adiponectin had a negative correlation with FBG, FINS, and LDL-C (r=-0.656, -0.359 and -0.637, all P<0.01), a positive correlation with HDL-C and ISI (r=0.614, 0.615, both P<0.01) in experimental rats.6 The protein expression of AdipoR1 in visceral adipose: The IOD(1172.40±99.22) in group B respectively was 56% of that (2104.69±117.25) in group A rats (P<0.05). The IOD(1742.65±105.21) of AdipoR1 in group C rats was 1.49 times larger than that (1172.40±99.22) in group B rats. Related analysis showed that AdipoR1 expression level had a negative correlation with FBG, FINS, LDL-C (r=-0.752, -0.748 and -0.703, all P<0.01), a positive correlation with HDL-C, ISI, APN(r=0.706, 0.683 and 0.620, all P<0.01) in experimental rats. The protein expression of AdipoR1 in subcutaneous adipose: The IOD of AdipoR1 in groupA rats was 2569.23±132.00. The IOD of AdipoR1 in group B rats was 2391.44±123.68. The IOD of AdipoR1 in group C rats was 2461.59±129.98. Related analysis showed that AdipoR1 expression level in subcutaneous adipose had no correlation with those factors.7 Morphology: HE staining showed that visceral adipose cells of group A rats were small and homogeneous. While visceral adipose cells of group B rats were bigger and inhomogeneinous and their walls were not clear. The visceral adipose cells of group C rats is smaller and the cell shape assumes the polygon, withered.The fat drop reduces obviously, the obvious knot contracts the organization proliferation. The subcutaneous adipose cells of group A rats were small and homogeneous. While in T2DM model rats, subcutaneous adipose cells were bigger. The small adipose cells in group C rats are obviously more than that in group C rats.Conclusions 1 The type 2 diabetic rat model that was induced by high-sugar-fat diet and a low dose of STZ had some characteristics similar to human T2DM. It would be available to study T2DM and its complications.2 The serum adiponectin content of the T2DM rats and the protein expression of AdipoR1 in visceral adipose were decreased. It indicated that adiponectin and AdipoR1 have a negative correlation with the occurrence and development of T2DM and insulin resistance.3 Related analysis showed that the decrease of serum adiponectin content and AdipoR1 protein expression in visceral adipose had a tight association with hyperglycemia and hyperlipemia and insulin resistance. It illuminated that the study on adiponectin, AdipoR1 and its activator might afford new theory to prevent and theat the hyperglycemia and hyperlipemia and insulin resistance.4 Rosiglitazone could increase serum concentrations of adiponectin and AdipoR1 protein expression level in visceral adipose, so it was one of the important ways to improve insulin sensitivity.5 Insulin resistance in the key peripheral target organs such as visceral adipose tissue was principal pathologic foundations in T2DM.
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