Table 1.
Demographic information of participants in this study.
Figure 1.
Effects of CYSKT on the levels of HbA1c and blood glucose in type 2 diabetic mice.
Type 2 diabetic mice were administered orally 200 mg/kg CYSKT for 30 consecutive days. Blood samples were collected every 10 days and measured for HbA1c levels (A) and fasting blood glucose levels (B). Glucose tolerance test was performed on 30th day after CYSKT administration. Mice were fasted for 4 h, glucose (1 g/kg) was injected intraperitoneally, and the blood glucose levels at intervals were measured (C). Values are mean ± SD (n = 5). *p<0.05, **p<0.01, ***p<0.001, compared with mock.
Figure 2.
Effect of CYSKT on blood glucose levels in normal mice.
Normal mice were administered orally various amounts of CYSKT. Glucose (4 g/kg) was injected intraperitoneally 15 min later, blood samples were collected at intervals, and blood glucose levels were measured by a glucometer (A). (B) AUC of glucose tolerance assay. Values are mean ± SD (n = 5). *p<0.05, **p<0.01, compared with mock.
Table 2.
Pathways significantly regulated by CYSKT in type 2 diabetic mice*.
Figure 3.
Effects of CYSKT on IR phosphorylation and GLUT-4 translocation.
(A) Phospho-IR ELISA. Left panel: HepG2 cells were treated with 0.5 µM insulin or various amounts of CYSKT. Ten minutes later, cellular proteins were collected and the levels of phosphorylated IR were measured by ELISA. Values are mean ± SD (n = 6). Right panel: BALC/c mice were given orally with various amounts of CYSKT. One hour later, mice were sacrificed, and livers were collected for analysis. Values are mean ± SD (n = 6). *p<0.05, ***p<0.001, compared with mock. (B) Phospho-IR ELISA. Type 2 diabetic mice were administered orally 200 mg/kg CYSKT for 30 days. Proteins were extracted from intestines and muscles, and the levels of phosphorylated IR were measured by ELISA. Values are mean ± SD (n = 5). *p<0.05, **p<0.01, ***p<0.001, compared with mock. (C) IHC. Type 2 diabetic mice were administered orally 200 mg/kg CYSKT for 30 consecutive days. Muscle tissues were collected and the sections were stained by IHC using antibody against GLUT-4 (100× and 400× magnification). Photos are representative images (n = 5).
Figure 4.
Effects of CYSKT on renal function indexes and survival rate in type 2 diabetic mice.
(A) CYSKT (200 mg/kg) was orally given to type 2 diabetic mice for 30 consecutive days. The levels of BUN and creatinine in sera were measured by an autoanalyzer. Values are mean ± SD (n = 5). **p<0.01, compared with mock. (B) Long-term survival rate. Type 2 diabetic mice were administered orally with 200 mg/kg CYSKT and/or 20 mg/kg TZD for 120 consecutive days. The number of death was observed daily.
Table 3.
Gene-expression connection of CYSKT treatments with disease states*.