ABSTRACT
Objective:To investigate the hypoglycemic effect of curcumin on type 2 diabetic rats and its effect on the signaling pathway of endoplasmic reticulum stress RNA-dependent protein kinase like-CCAAT/enhancer binding protein homologous protein (PERK-CHOP).Methods:A total of 45 male SD rats were randomly divided into normal control group, model group and curcumin treatment group, with 15 rats in each group. The rats were given high-fat as well as high-sugar diet and intraperitoneally injected with streptozotocin (35 mg/kg, twice, once/day) to establish type 2 diabetes rat model. After the successful establishment of the model, the rats in the curcumin treatment group were given intragastrically with 200 mg/kg curcumin for 30 days. Serum adiponectin level was detected by ELISA, glucose was detected by glucose oxidase, Western blot was used to detect the expressions of PERK, p-PERK, CHOP and ATF4 protein levels in the pancreatic tissues of rats in each group, and mRNA expressions of PERK and CHOP in the pancreatic tissues of rat in each group were detected by real-time PCR.Results:Compared to the model group, the level of blood glucose (14.86 ± 2.77 mmol/L vs. 30.04 ± 3.25 mmol/L) in the curcumin treatment group significantly decreased, and the serum adiponectin level (94.12 ± 16.34 mg/L vs. 53.91 ± 9.08 mg/L) significantly increased ( P<0.05). The expressions of PERK mRNA (0.85 ± 0.07 vs. 1.64 ± 0.28), CHOP mRNA (0.53 ± 0.04 vs. 1.18 ± 0.33), PERK (1.12 ± 0.31 vs. 2.24 ± 0.43), P-PERK (1.23 ± 0.19 vs. 3.89 ± 0.32), CHOP (0.65 ± 0.07 vs. 0.92 ± 0.11) and ATF4 (0.73 ± 0.26 vs. 1.15 ± 0.31) in the curcumin treatment group significantly decreased ( P<0.05). Conclusions:Curcumin has hypoglycemic effect on type 2 diabetes rats, which can enhance the sensitivity of target tissues to insulin by increasing adiponectin levels. Curcumin can down-regulate the expression of PERK/P-PERK/CHOP/ATF4 protein levels in endoplasmic reticulum stress signal pathway, and reduce stress degree.
ABSTRACT
We aimed to evaluate the influence of exogenetic insulin on bone mineral density [BMD] in Type 2 Diabetes Mellitus [T[2]DM]. Group A included 120 cases of middle-aged male patients with type 2 diabetes mellitus were administrated exogenetic insulin [40 cases in Group A[1]: for less than 1 year; 40 cases in Group A[2]:for 1 to 3 years; 40cases in Group A[3]: for 3 to 5 years], and another 120 cases [Group B] of middle-aged male patients with type 2 diabetes mellitus were administrated insulin secretagogues. The measurements of BMD of lumbar vertebra [L2-4], collum femoris and total body were conducted with dual-energy X-raya bsorptiometry, followed by the determination of glycosylated hemoglobin, plasma insulin concentration [fasting and postprandial], and fasting C-peptide. Our results revealed that there was no statistical difference of BMD [P>0.05] between patients in Group A[1]or A[3]andpatients in Group B [B[1], B[2] or B[3]], while the BMD in Group A[2] increased significantly [P<0.05]. And the fracture risk in Group A[3] increased significantly [P<0.05] compared with Group B [B[1], B[2] or B[3]], Taken together, exogenetic insulin significantly increased BMD and fracture risk of middle-aged male patients with type 2 diabetes mellitus