To investigate the effect of atorvastatin on lipid metabolism in type 2 elder diabetes patients with hyperlipidemia, 26 patients with type 2 elder diabetes complicated with hyperlipidemia were treated with atorvastatin (10 mg/d) for 8 weeks. The serum triglyceride (TG), high density protein cholesterol (HDL-C) and low density protein cholesterol (LDL-C) were measured before and after the treatment. Meanwhile, the non-denaturing polyacrylamide gradient gel electrophoresis was used for detection of small-sized LDL(SLDL). Our results showed that TG dropped from 4.88 +/- 0.72 mmol/L to 2.65 +/- 0.32 mmol/L; HDL-C was increased from 0.85 +/- 0.31 mmol/L to 1.28 +/- 0.29 mmol/L; LDL-C was declined from 3.71 +/- 2.98 mmol/L to 2.10 +/- 1.22 mmol/L, sLDL-A was increased from (42.49 +/- 8.1)% to (53.27 +/- 7.5)%; LDL-B was decreased from (57.91 +/- 8.1)% to (46.73 +/- 7.5% ) (P<0.05). The level of blood glucose was not changed at the end of 8th week. It is concluded that atorvastatin has satisfactory lipid-regulating effects on type 2 elder diabetes patients with hyperlipidemia.
Anticholesteremic Agents/*therapeutic use ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Diabetes Mellitus, Type 2/*complications ; Diabetes Mellitus, Type 2/drug therapy ; Heptanoic Acids/*therapeutic use ; Hyperlipidemias/complications ; Hyperlipidemias/*drug therapy ; Pyrroles/*therapeutic use ; Triglycerides/blood

To investigate the effect of atorvastatin on lipid metabolism in type 2 elder diabetes patients with hyperlipidemia, 26 patients with type 2 elder diabetes complicated with hyperlipidemia were treated with atorvastatin (10 mg/d) for 8 weeks. The serum triglyceride (TG), high density protein cholesterol (HDL-C) and low density protein cholesterol (LDL-C) were measured before and after the treatment. Meanwhile, the non-denaturing polyacrylamide gradient gel electrophoresis was used for detection of small-sized LDL(SLDL). Our results showed that TG dropped from 4.88 +/- 0.72 mmol/L to 2.65 +/- 0.32 mmol/L; HDL-C was increased from 0.85 +/- 0.31 mmol/L to 1.28 +/- 0.29 mmol/L; LDL-C was declined from 3.71 +/- 2.98 mmol/L to 2.10 +/- 1.22 mmol/L, sLDL-A was increased from (42.49 +/- 8.1)% to (53.27 +/- 7.5)%; LDL-B was decreased from (57.91 +/- 8.1)% to (46.73 +/- 7.5% ) (P<0.05). The level of blood glucose was not changed at the end of 8th week. It is concluded that atorvastatin has satisfactory lipid-regulating effects on type 2 elder diabetes patients with hyperlipidemia.
Aged ; Anticholesteremic Agents ; therapeutic use ; Atorvastatin Calcium ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Diabetes Mellitus, Type 2 ; complications ; drug therapy ; Female ; Heptanoic Acids ; therapeutic use ; Humans ; Hyperlipidemias ; complications ; drug therapy ; Male ; Middle Aged ; Pyrroles ; therapeutic use ; Triglycerides ; blood

Summary: In order to confirm whether the mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were correlated with the serum parameters of glucose and lipid metabolism and to clarify the regulation of adiponectin receptor gene expression in diabetic states, serum adiponectin, mRNA levels of adiponectin in adipose tissue and mRNA levels of AdipoR1 in the skeletal muscles were examined in type 2 diabetic rats. The model of type 2 diabetes was prepared by feeding high fat diet and injecting low dosage of streptozotocin (STZ). The diabetic rats were screened out by oral glucose tolerance test. One group of type 2 diabetic rats received rosiglitazone. The serum adiponectin concentration was detected by using ELISA and mRNA levels were examined by RT-PCR. The serum adiponectin levels and mRNA levels of adiponectin in adipose tissue of type 2 diabetic rats were significantly decreased as compared with the normal control rats (P<0.05, P<0.01 respectively). No siglificant changes were observed in the expression of adiponectin receptor 1 in the skeletal muscle of type 2 diabetic rats. The mRNA levels of adiponectin in adipose tissue were reversely correlated with serum insulin (r=-0.66, P<0.05), triglyceride (r=-0.58, P<0.05), cholesterol (r=-0.49, P<0.05), interleukin-6 (r=-0.49, P<0.05) and tumor necrosis factor (r=-0.43, P<0.05). The expression of adiponectin receptors was not altered in the skeletal muscle of Type 2 diabetic rats. The decreased serum adiponectin was caused by the decreased expression of adiponectin mRNA in adipose tissue rather than the adiponectin receptors in the skeletal muscle, which could be improved by rosiglitazone.