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Objective To explore the relation between serum TGF?1 and diabetic nephropathy(DN). Methods Forty-five cases of type 2 diabetes mellitus patients were divided into three groups according to urine albumium excretion rate (UAER): normoalbuminuria (NA)group; microalbuminuria (MA) group; macroalbuminuria group (overt DN). Serum TGF?1, fasting blood glucose (FBG), HbAlc.BUN. Cr. Ccr were detected in all cases. Microalbundnuria group and macroalbuminuria group were respectively divided into group.treated with captopril and regular treatment group. Results Serum TGF?1, had significantly differences in four groups(23. 95?8. 01ng/ml vs 35.02?6. 70ng/ml, 39.3i? 5. 35ng/ml vs 58. 58?9. 56ng/ml,P
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AIM: To explore the changes in serum TGF ? 1 in type 2 diabetes mellitus. METHODS: Forty-five cases type 2 diabetes mellitus patients were divided into three groups according to urine albumim excretion rate(UAER): normoalbuminuria(NA)group and microalbuminuria(MA) group and macroalbuminuria group (Overt DN). Serum TGF ? 1, fasting blood glucose(FBG), HbA 1c ,BUN,Cr,Ccr,lipidemia were detected in all cases. RESULTS: Serum TGF ? 1 in NA, MA and ODN groups [(35.02?6.70) ?g/L, (39.31?5.35) ?g/L, (58.58?9.56) ?g/L, respectively] was higher than that in control [(23.95?8.01) ?g/L, P
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Objective To determine whether the AT, All66C gene polymorphism is associated with CHD in type 2 diabetes patients. Methods Investigating the allele frequency and the genotype distribution of the AT1 All66C gene in the group of normal control (n= 73),simple diabetes (n= 80),diabetic CHD (n=43) by means of PCR-RFLP. Results The group of diabetic CHD had a significant higher frequency of C allele of the AT1 All66C gene than normal control (X2 = 6. 02,P＜0. 05) and diabetes (X2= 5. 71,P＜0. 05). Conclusion The result indicated that there was an association between the 1166C allele of the AT1 gene polymorphism and CHD in type 2 diabetes patients.
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0.05).Conclusion The elevation of GH involved in the pathogenesis of diabetic microangiopathy possibly by exacerbation of disorders of glucose and lipid metabolism.
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AIMTo develop a rat model of insulin resistanc e,and to study the effect of puerarin injection on expression of protein kinase B in insulin resistanc e rats. METHODS30 SD rats were randomly divded into two groups. The model group were given the high fat diets(0 30 pig fat, 0 10 sucrose, 0 0 3 cholesterol) for 8 weeks. Then 9 rats of the group had been choosen as the pu erarin treatment group and were given abdominal injection (100 mg?kg -1 ?d -1 ) for 4 weeks. By the end of the experiment, Western blot and computer i mage pattern analyze system were used to analysis expression of PKB in skeletal muscles. RESULTS(1) The model group showed a hyperglycemia, hype rinsulinism and obviously visceral obesity by high fat-feeding, the insulin res istance index (ISI) decreased while the HOMA insulin resistance index (HOMA-IR) increased compared to the normal group, insulin resistance was induced in this way; (2) Compared with the pathology control group:fasting blood glucose (FBG), fasting insulin (FINS), visceral fat mass and the HOMA insulin resistance index (HOMA-IR) of the treating group were significantly decreased whereas the insuli n index (ISI) enhanced. Expression of PKB was markedly increased by puerarin tre atment. CONCLUSIONPuerarin injection can significantly elevate e xepression of PKB and ameliorate the state of insulin resistance. Improved biolo gic effect of insulin and prevention of the deleterious effect of fat may be in volved in the mechanism concerned.
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Objective To determine whether treatment with Gliclazide (Diamicron) is able to prevent development of microvascular complications in type 2 diabetes mellitus. Methods This trial was carried out in seven centers of the National Diabetes Mellitus Collaborative Study Group. Two hundred and eighty five patients with type 2 diabetes mellitus were recruited from six areas of China and divided into Gliclazide group (n=155) and Glibenclamide group (n=130). Age, sex, duration of diabetes and body mass index were recorded at entry. Fasting and 2h postprandial blood glucose were measured monthly while HbA 1c was determined at 3 month interval. Retinal photography and fluorescein angiography were performed in the 1st and 3rd year.Results There were no significant differences in age, sex, blood pressure, duration of diabetes, mean blood glucose and HbA 1c between the Gliclazide and Glibenclamide groups at baseline, in the 2nd and 3rd follow up year. There were no significant differences in retinopathy between the two groups at baseline, but at the end of the 3rd year, the subjects in Gliclazide group with retinopathy progression over one grade were significantly less than those in Glibenclamide group (2.58% vs 18.46%, P