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To investigate the role and mechanism of calcium-sensing receptor (CaSR) in the proliferation and migration of renal artery smooth muscle cells (RASMCs) under insulin resistance. Methods RAMSCs in the logarithmic growth stage were randomly divided into control, pure model, model + GdCl
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Aim To investigate the protective role of salvianolic acid B ( Sal B ) on cardiac hypertrophy in type 2 diabetes mice , and to explore its influence on peroxisome proliferator activated receptors-α( PPARα) .Methods The type 2 diabetes melitus ( T2DM) mouse model was established by 4 weeks ' high fat diets feeding and one time STZ intraperitoneal injection .The animals were randomly divided into:control, T2DM, T2DM+SalB(100 mg· kg -1 · d-1 ) and Sal B(100 mg· kg -1 · d-1 ) groups.Eight weeks later, heart weight, tibial length, cross section area of cardiomyocytes , protein expression of PPARαin heart tissue were recorded .In vitro, high glucose and high insulin ( HGI ) were used to induce hypertrophic growth in cultured neonatal rat cardiomyocytes ( NRC-Ms) .And cell surface area , 3 H-leucine incorporation , 3 H-D-glucose uptake and PPARαprotein level were measured to observe the effect of Sal B and MK 886, a PPARαinhibitor.Results In T2DM model mice, Sal B could lower heart weight/tibial length and cross sec-tion area of cardiomyocytes , while PPARαprotein level in hearts were improved .In cultured cardiomyocytes , Sal B ( 10 ～100 μmol · L-1 ) ameliorated the in-creased levels of cell surface area ,3 H-leucine incorpo-ration and improved the decreased 3 H-D-glucose up-take and PPARαexpression induced by HGI . But those function could be abolished by MK 886.Conclu-sion Sal B ameliorates cardiac hypertrophy in T 2DM mice, which may be related to its function on PPARαactivation .
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Objective To study serum insulin level change and its clinical significance in the patients with chronic kidney dis-ease (CKD).Methods 800 cases of patients with chronic kidney disease were observed with 400 cases of healthy people as control group at the same time.According to whether there was a complication of diabetic,chronic nephropathy was divided into two groups:diabetic nephropathy chronic renal failure group (425 cases)and non-diabetic nephropathy chronic renal failure (375 cases).According to the classification standard,chronic renal failure and the diabetic nephropathy group was di-vided into four groups:type 1 diabetes (105 cases),type 2 diabetes (135 cases),gestational diabetes (95 cases),diabetes with other reasons(90 cases).Relevant clinical information was collected,including age,gender,height,weight,and the cor-responding body mass index (BMI)was calculated based on height and weight.After some laboratory examinations,related parameters of the research were collected,including object of urea(Urea),serum creatinine (SCr),fasting plasma glucose (FPG),fasting insulin (FIns).According to the corresponding formula,insulin sensitive index (ISI)and glomerular filtration rate (GFR)were calculated based on the above parameters.Statistical comparison was made after collection.Results Urea, Scr,FPG and FIns of the patients with chronic kidney disease were significantly higher than those of normal control group (t=36.788,35.612,137.216,9.294;all P=0.000 respectively).Age,gender and BMI calculatedfrom height and weight in three groups had differences,but they were not statistically significant (F=1,363,P=0.256;F=1.577,P=0.454;F=1.641,P=0.194),and had no effect on the occurrence of chronic kidney disease development.Comparison of patients with different types of diabetes and chronic kidney disease,when a group had higher FIns and lower ISI,it also had a smaller GFR,and the differences between groups were statistically significant (F=12.01,P=0.000;F=3.891,P=0.009;F=3.774,P=0.011).Conclusion The serum insulin were closely related to CKD.Observing the serum insulin can have a dee-per understanding of the disease development,make a more effective treatment and predict the probability to be recover.
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Aim To study the protective effects of SEP on the hypertrophic myocardial cells induced with high glucose and high insulin and the mechanism. Methods The protein content was assayed with Lowrys meth-od;the cardiomyocytes area was measured by computer photograph analysis system;the expression of ANF and PPAR-α was determined by RT-PCR;APS was select-ed as control drug. Results Compared with conctrol group,the protein content,cardiomyocytes area and the expression of ANF and PPAR-α of high glucose and high insulin group were significantly increased. Com-pared with conctrol group,the SEP of different dosages were able to decrease the protein content, area, the expression of ANF mRNA and PPAR-α mRNA of cul-tured hypertrophic myocadial cells induced with high glucose and high insulin. Conclusion SEP can pre-vent cardiomyocyte hypertrophy induced by high glu-cose and high insulin, which is related to its inhibition on PPAR-α signaling path.
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Objective To explore the influence of melatonin receptor agonist Neu-P11 on the expression of IRS-1 and GLUT-4 in insulin-resistant 3T3-L1 adipocytes. Methods Insulin resistant 3T3-L1 adipocytes were induced with high glucose/ high insulin for 24 hours, and then they were divided into 4 treatment groups; melatonin, Neu-P11, melatonin+luzindole and Neu-P11 + luzindole. And non-treated insulin-resistant 3T3-L1 adipocytes were taken as control. Glucose consumption was detected by enzymatic method. IRS-1 and GLUT-4 protein expressions were detected by Western blotting analysis. Results After the insulin-resistant adipocytes were treated with melatonin and Neu-P11, the glucose consumption andthe expressions of IRS-1, GLUT-4 proteinswere significantly increased compared with the non-treated control group (P<0. 05). The expressions of IRS-1, GLUT-4 proteins in melatonin + luzindole (melatonin receptor antagonist) and Neu-P11 + luzindole groups were significantly decreased compared with melatonin alone or Neu-P11 alone groups (P<0. 05), and were similar to those in thenon-treated control group. Conclusion Melatonin receptor agonist Neu-P11 can increase glucose consumption, insulin sensitivity in insulin resistant-adipocytes, which might be associated with the up-regulation of IRS-1 and GLUT-4 protein expression.
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AIM: To study the role of peroxisome proliferator-activated receptor-α (PPAR-α) signal transduction pathway in cardiac hypertrophy induced by high glucose and insulin (HGI). METHODS: The cultured neonatal rat cardiomyocytes were used to observe the effect of fenofibrate (FF), a selective PPAR-α agonist, on cardiomyocyte hypertrophy induced by HGI (glucose at concentration of 25.5 mmol/L and insulin at 0.1 μmol/L). The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area, protein content, and mRNA expression of atrial natriuretic factor (ANF). The expressions of mRNA and protein were assayed by real -time PCR and Western blotting. RESULTS: In cultured cardiomyocytes, HGI induced profound change of hypertrophic morphology, the significant increase in cell surface area, protein content and ANF mRNA expression compared to those in vehicle control (P<0.01), but the expressions of PPAR-α mRNA and protein decreased significantly (P<0.05). At the same time, the expression of cyclooxygenase 2 (COX-2), one of the PPAR-α downstream effectors was obviously elevated (P<0.05). However, FF (0.1, 0.3 and 1 μmol/L) inhibited the cardiomyocyte hypertrophy induced by HGI in a concentration-dependent manner (P<0.01). FF at concentration of 0.3 μmol/L increased the expressions of PPAR-α in both mRNA and protein levels (P<0.05) and inhibited the expressions of COX-2 (P<0.05), which were abolished by MK 886 (0.3 μmol/L), a selective PPAR-α antagonist (P<0.05). CONCLUSION: PPAR-α signal transduction pathway and its downstream effector COX-2 might involve in the cardiomyocyte hypertrophy induced by HGI.
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Aim To study effects of pioglitazone on cardiac fibroblast proliferation induced with high glucose and high insulin.Methods The neonatal rat cardiac fibroblasts were cultured and treated with different factors.The cellular number was determined by crystal violet uptake;the DNA synthesis was assayed with thymidine intake method;the percentage of S+G_2+M in the cell cycle was determined by flow cytometry.Results Pioglitazone inhibited the cell number、DNA synthesis and the percentage of S+G_2+M in the cell cycle of cultured cardiac fibroblasts induced with high glucose and high insulin.Conclusion Pioglitazone inhibits cardiac fibroblast proliferation induced with high glucose and high insulin and the effective mechanism of pioglitazone on cardiac fibroblast proliferation needs further study.
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Aim To study the effects of pioglitazone on the hypertrophic myocardial cells induced with high glucose and high insulin. Methods Using cultured myocardial cells as a model, The protein content was assayed with Lowrys method; The contracting frequency was counted by the inverted microscope;The protein synthesis was assayed with leucine intake method;The cardiomyocytes volumes was measured by computer photograph analysis system; the cellular hypertrophy was observed. Results Compared with verapamil, Pioglitazone significantly inhibited the protein content, cellular protein synthesis and volumes of cultured hypertrophic myocardial cells induced with high glucose and high insulin. Meanwhile pioglitazone and verapamil inhibited myocardial cells contracting frequency too. Conclusions Pioglitazone inhibited cardiac hypertrophy of cultured myocardial cells induced with high glucose and high glucose. The mechanism of the effect of pioglitazone on cardiac hypertrophy needs further study.
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AIM:To study the role of peroxisome proliferator-activated receptor-? (PPAR-?) signal transduction pathway in cardiac hypertrophy induced by high glucose and insulin (HGI). METHODS:The cultured neonatal rat cardiomyocytes were used to observe the effect of fenofibrate (FF),a selective PPAR-? agonist,on cardiomyocyte hypertrophy induced by HGI (glucose at concentration of 25.5 mmol/L and insulin at 0.1 ?mol/L). The cardiomyocyte hypertrophic responses were assayed by measuring the cell surface area,protein content,and mRNA expression of atrial natriuretic factor (ANF). The expressions of mRNA and protein were assayed by real -time PCR and Western blotting. RESULTS:In cultured cardiomyocytes,HGI induced profound change of hypertrophic morphology,the significant increase in cell surface area,protein content and ANF mRNA expression compared to those in vehicle control (P