The objective was to investigate the hypoglycemic action of catalpol in spontaneous diabetes db/db mice. 40 db/db mice were randomly divided into fi ve groups: model control gourp; db/db plus catalpol 40, 80, 120 mg/kg body wt. groups and db/db plus metformin 250 mg/kg group. Age-matched db/m mice were selected as normal control group. The mice were administered with corresponding drugs or solvent by gavage for 4 weeks. The oral glucose tolerance test was carried out at the end of 3rd week. After 4 weeks of treatment, the concentrations of fasting blood glucose (FBG), glycated serum protein (GSP), insulin (INS), triglyceride (TG), total cholesterol (TC) and adiponection (APN) in serum were detected. The protein expressions of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and glucose transporter-4 (GLUT-4) in skeletal muscle and adipose tissues were detected by western blot. Real time RT-PCR was used to detect the mRNA expressions of acetyl-CoA carboxylase (ACC) and Hydroxymethyl glutaric acid acyl CoA reductase (HMGCR) in liver. Our results showed that catalpol could significantly improve the insulin resistance, decrease the serum concentrations of INS, GSP, TG, and TC. The concentrations of APN in serum, the protein expression of phosphorylation-AMPKα1/2 in liver, phosphorylation-AMPKα1/2 and GLUT-4 in peripheral tissue were increased. Catalpol could also down regulate the mRNA expressions of ACC and HMGCR in liver. In conclusion, catalpol ameliorates diabetes in db/db mice. It has benefi t eff ects against lipid/glucose metabolism disorder and insulin resistance. The mechanism may be related to up-regulating the expression of phosphorylation-AMPKα1/2.

Introduction: Our study aimed to investigate the effect of atorvastatin on plaque calcification by matching the results obtained by 18 F-sodium fluoride ( 18 F-NaF) positron emission tomography (PET)/computed tomography (CT) with data from histologic sections. Methods and Results:The rabbits were divided into 2 groups as follows: an atherosclerosis group (n = 10) and an atorvastatin group (n = 10). All rabbits underwent an abdominal aortic operation and were fed a high-fat diet to induce atherosclerosis. Plasma samples were used to analyze serum inflammation markers and blood lipid levels. 18 F-NaF PET/CT scans were performed twice. The plaque area, macrophage number and calcification were measured, and the data from the pathological sections were matched with the 18 F-NaF PET/CT scan results. The mean standardized uptake value (0.725 6 0.126 vs. 0.603 6 0.071, P , 0.001) and maximum standardized uptake value (1.024 6 0.116 vs. 0.854 6 0.091, P , 0.001) significantly increased in the atherosclerosis group, but only slightly increased in the atorvastatin group (0.616 6 0.103 vs. 0.613 6 0.094, P = 0.384; 0.853 6 0.099 vs.0.837 6 0.089, P , 0.001, respectively). The total calcium density was significantly increased in rabbits treated with atorvastatin compared with rabbits not treated with atorvastatin (1.64 6 0.90 vs. 0.49 6 0.35, P , 0.001), but the microcalcification level was significantly lower. There were more microcalcification deposits in the areas with increased radioactive uptake of 18 F-NaF. Conclusions:Our study suggests that the anti-inflammatory activity of atorvastatin may promote macrocalcification but not microcalcification within atherosclerotic plaques. 18 F-NaF PET/CT can detect plaque microcalcifications.

Pioglitazone affects early vascular microcalcification, and pioglitazone-induced changes can be assessed using F-FDG-PET/CT.