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Objective:Continuous glucose monitoring (CGM) technology is used to compare the advantages of insulin degludec (IDeg) as a basal insulin regimen compared with insulin glargine (IGlar) in the treatment of adult type 1 diabetes mellitus.Methods:30 adult patients with T1DM admitted to Heji Hospital Affiliated to Changzhi Medical College from September 2019 to December 2020 were screened. According to the random number table method, the patients were randomly divided into two groups (insulin degludec group and insulin glargine group) at a ratio of 1∶1, respectively treated with IDeg, IGlar and aspartate insulin for 12 weeks. The main outcome measures were the coefficient of variation of blood glucose (CV), mean amplitude of glycemic excursions (MAGE), time in range (TIR), time above range (TAR) and time below range (TBR). The secondary outcome measures were mean blood glucose (MBG), standard deviation of blood glucose (SD), fasting blood glucose (FPG), 2 h postprandial blood glucose (2 h BG), hemoglobin A1c (HbA 1c), means of daily differences (MOOD), and the frequency of hypoglycemic events. Results:At 12 weeks of treatment, the HbA 1c, FPG, 2 h BG, MBG, SD, CV and MAGE of insulin degludec group were lower than those of insulin glargine group, with statistically significant difference (all P<0.05). The TIR in the insulin degludec group was significantly higher than that in the insulin glargine group [73(63, 75)% vs 43(28, 63)%, P<0.001], and the TAR was lower than that in the glycerine group [25(17, 23)% vs 35(33, 64)%, P=0.003]. From the curve spectrum of blood glucose level of the two groups, the stability of blood glucose in the insulin degludec group was better than that in the insulin glargine group. After 12 weeks of treatment, 8 cases (8/15) in insulin degludec group had HbA 1c<7.0%, and 4 cases (4/15) in insulin glargine group had HbA 1c<7.0%, without statistically significant difference ( P=0.264). There were 7 cases (7/15) in the insulin degludec group and 1 case (1/15) in the insulin glargine group who achieved high quality blood glucose control, with statistically significant difference ( P=0.035). At the 12th week of outpatient follow-up, the incidence of nocturnal hypoglycemic events in insulin degludec group was significantly lower than that in insulin glargine group (4/15 vs 11/15, P=0.027). Conclusions:Compared with insulin glargine, insulin degludec can achieve higher blood glucose compliance rate, lower blood glucose level and reduce blood glucose fluctuations in patients with type 1 diabetes.
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Objective To explore the therapeutic effect of alendronate combined with atorvastatin in the treatment of patients with type 2 diabetes mellitus complicated with osteoporosis. Methods 80 patients with diabetic osteoporosis( DOP) treated by endocrinology were selected. They were divided into observation group and control group by random number table method. The patients in the control group were given alendronate sodium, and the patients in the observation group were given alendronate and atorvastatin at the same time. The bone mineral density ( BMD) of the forearm,lumbar vertebra,femoral neck and femoral trochanter Numeric rating scales( NRS score) were measured before and after treatment. Results Before treatment,the BMD in forearm,lumbar vertebra,femoral neck and femoral trochanter, and NRS score between the two groups had no statistically significant differences ( all P >0.05).Aftertreatment,theBMDofforearm[(0.64±0.10)g/cm2vs.(0.68±0.11)g/cm2,t=2.563]andlumbar vertebrae[(0. 82 ± 0. 28) g/cm2 vs. (0. 70 ± 0. 11) g/cm2,t =2. 448],femoral neck[(0. 71 ± 0. 09) g/cm2 vs. (0.66±0.05)g/cm2,t=3.002],femoraltrochanter[(0.76±0.14)g/cm2vs.(0.70±0.08)g/cm2,t=2.302] of the observation group were higher than those of the control group,and the NRS score[(1. 32 ± 0. 10) points vs. (2. 47 ± 0. 67)points]was lower than the control group(t=23. 651,P<0. 05). There were 2 cases of nausea,1 case of abdominal pain and 1 case of muscle pain in the observation group,and 1 case of nausea occurred in the control group,the incidence rate of adverse reaction between the two groups had no statistically significant difference (χ2 =1. 478,P=0. 224). Conclusion Alendronate combined with atorvastatin can improve BMD,relieve pain in patients with DOP,and it is safe and worthy of clinical application.
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Objective To explore the therapeutic effect of alendronate combined with atorvastatin in the treatment of patients with type 2 diabetes mellitus complicated with osteoporosis. Methods 80 patients with diabetic osteoporosis( DOP) treated by endocrinology were selected. They were divided into observation group and control group by random number table method. The patients in the control group were given alendronate sodium, and the patients in the observation group were given alendronate and atorvastatin at the same time. The bone mineral density ( BMD) of the forearm,lumbar vertebra,femoral neck and femoral trochanter Numeric rating scales( NRS score) were measured before and after treatment. Results Before treatment,the BMD in forearm,lumbar vertebra,femoral neck and femoral trochanter, and NRS score between the two groups had no statistically significant differences ( all P >0.05).Aftertreatment,theBMDofforearm[(0.64±0.10)g/cm2vs.(0.68±0.11)g/cm2,t=2.563]andlumbar vertebrae[(0. 82 ± 0. 28) g/cm2 vs. (0. 70 ± 0. 11) g/cm2,t =2. 448],femoral neck[(0. 71 ± 0. 09) g/cm2 vs. (0.66±0.05)g/cm2,t=3.002],femoraltrochanter[(0.76±0.14)g/cm2vs.(0.70±0.08)g/cm2,t=2.302] of the observation group were higher than those of the control group,and the NRS score[(1. 32 ± 0. 10) points vs. (2. 47 ± 0. 67)points]was lower than the control group(t=23. 651,P<0. 05). There were 2 cases of nausea,1 case of abdominal pain and 1 case of muscle pain in the observation group,and 1 case of nausea occurred in the control group,the incidence rate of adverse reaction between the two groups had no statistically significant difference (χ2 =1. 478,P=0. 224). Conclusion Alendronate combined with atorvastatin can improve BMD,relieve pain in patients with DOP,and it is safe and worthy of clinical application.
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Objective To evaluate the clinical efficacy and effect of benazepril treat with diabetic nephropathy on Plasma NO and ET-1. Methods 100 cases of DN patients were divided into two groups by random number table (50cases), group A with basic treatment, group B increased benazepril. Selected another 50 cases of simple diabetic patients as control group, observed the plasma NO (nitric oxide) and ET-1 (ET-1) levels changes of three groups,and compared the clinical efficacy. Results The levels of NO, ET-1 and Ang II in A group and B group were significantly lower than those in control group (P<0.05); the level of NO in B group was higher than that in group A, and the level of ET-1 and Ang II was lower than that of group A(P<0.05). The total effective rate of B group was 86.00％, which was significantly higher than that of control group 58.00％(P<0.05). Conclusion The clinical application benazepril treat with DN can effectively regulated plasma NO and ET-1 levels, protect the kidneys, and improve the therapeutic effect.
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OBJECTIVE To investigate the effect of jujuboside A on glomerular cell apoptosis in diabetic rats, and to explore the possible mechanisms. METHODS SD rats were administered with streptozotocin 100 mg · kg-1 to estabilish the diabetic model. Diabetic SD rats received jujuboside A 10 and 20 mg · kg-1 daily for 4 weeks by lavage administration, respectively. The level of glycosylated hemoglobin (GHb) in the blood of each group was measured by fructosamine method. The morphological changes in glomerular cells were observed by PAS staining. Glomerular cell apoptosis was determined by TUNEL staining. The protein expression of Bcl-2 and Bax was detected by immunohistochemistry. The protein expression of cleaved caspase 9 and cleaved caspase 3 was detected by Western blotting. Trans?forming growth factor β1 (TGF-β1) mRNA expression was analyzed by qPCR. RESULTS Compared with model group, jujuboside A 10 and 20 mg·kg-1 treatment significantly reduced the level of GHb in blood (mmol · L- 1: 10.9 ± 0.8 vs 17.5 ± 1.5, P<0.05; 7.6 ± 0.5 vs 17.5 ± 1.5, P<0.05), PAS positive score of glomerular cells (26.8 ± 3.2 vs 36.4 ± 3.8, P<0.05; 18.4 ± 2.1 vs 36.4 ± 3.8, P<0.05) and the apoptosis of glomerular cells〔(8.2±0.8)%vs (17.6±1.8)%, P<0.05;(5.1±0.5)%vs (17.6±1.8)%, P<0.05〕. Moreover, Bcl-2 protein expression in kidney tissues was elevated (P<0.05), whereas Bax (P<0.05), cleaved caspase 9 (P<0.05) and cleaved caspase 3 (P<0.05) protein expression and TGF-β1 mRNA (P<0.05) expression were reduced after jujuboside A administration. CONCLUSION Jujuboside A can prevent glomerular cell apoptosis in diabetic rats, which may be associated with the regulation of mitochondrial apoptotic pathways and TGF-β1 expression.
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Objective To investigate the effects of pioglitazone on osteoblast proliferation and apoptosis.Methods MC3T3-E1 mouse osteoblastic cells were treated with 0, 5, 10, 20, 30, and 40 μmol/L pioglitazone for 24 h. Cell viability was measured by MTT, cell cycle and apoptosis were inspected with flow cytometry, the expressions of Bcl-2 and Bax proteins were examined via immuno-chemical staining. Results Survival of osteoblasts decreased in a dose-dependent manner. Compared with the control group, the cells in the G0/G1 and G2/M stages increased, while the cells in S stage decreased significantly. The percentage of apoptosis at 5 and 10 μmol/L were lower than that of the control group(P ＜ 0.05), While it was increased significantly at 30 and 40 μmol/L(P ＜0.01). Bax expression was attenuated at 10 μmol/L(P＜0. 01), returned to normal by 20 μmol/L, and was increased by 30 and 40 μmol/L(P ＜ 0. 01). Bcl-2 expression was enhanced at the dose ≤ 20 μmol/L(P ＜0.01). Positive correlation was found between the death rate and the expression intensity of Bax/Bcl-2(n = 15, r=0.796, P＜0.01). Conclusions Pioglitazone inhibits apoptosis of osteoblasts at low concentrations and protects the cells, but promotes their apoptosis at higher concentration, Bax/Bcl-2 may play an important role in mediating the piglitazone-induced apoptosis of osteoblasts. It inhibits DNA synthesis and cell proliferation.