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1.
Chinese Journal of Applied Physiology ; (6): 345-349, 2018.
Article in Chinese | WPRIM | ID: wpr-773747

ABSTRACT

OBJECTIVE@#To explore effects of exercise on the expression of adiponectin mRNA and protein in visceral adipose tissue, plasma adiponectin concentration, and insulin resistance of aged obese rats.@*METHODS@#Male SD rats age to 21 days old were fed with high-fat diet (fat percentage was 36.3% to 40.0%) for three stages of adolescence, maturity and old age to establish elderly obesity rats model. When the rats aged to 60 weeks old, natural growing elderly rats were randomly divided into control group (C) and aged exercise group (AE), =6; elderly obesity rats were randomly divided into obesity control group (OC) and obesity exercise group (OE), =6. The treadmill grade was 0°, the exercise speed and time were 15 m/min×15 min, 4 groups each time, between consecutive groups the rats had 5 minutes rest, the rats were exercised for 60 minutes every day, five days a week, continuous exercise for 8 weeks. Then, the expressions of adiponectin mRNA and protein in visceral adipose tissue were determined. The concentrations of blood glucose, plasma adiponectin and insulin were measured. Insulin resistance was calculated.@*RESULTS@#Comparison with control group, the expressions of adiponectin mRNA and protein were obviously decreased, the concentration of blood glucose and insulin resistance were significantly increased in obesity control group, while the expressions of adiponectin mRNA and protein were obviously increased. Comparison with obesity control group, the expressions of adiponectin mRNA and protein, the concentration of plasma adiponectin were obviously increased, the concentration of blood glucose and insulin resistance were significantly decreased in obesity exercise group.@*CONCLUSIONS@#Adiponectin mRNA and protein expression in visceral adipose tissue is decreased and accompanied by high blood glucose and insulin resistance in elderly obesity rats. Exercise can increase the adiponectin mRNA and protein expression in visceral adipose tissue, elevate levels of plasma adiponectin, and decrease the level of blood glucose and insulin resistance in elderly obesity rats.


Subject(s)
Animals , Male , Rats , Adiponectin , Adipose Tissue , Blood Glucose , Insulin Resistance , Obesity , Rats, Sprague-Dawley
2.
Journal of Experimental Hematology ; (6): 986-990, 2010.
Article in Chinese | WPRIM | ID: wpr-237610

ABSTRACT

This study was aimed to explore the effects of peptidoglycan (PGN) on proliferation and cell cycle of human bone marrow mesenchymal stem cells (MSCs). MSCs were isolated from human bone marrow by density gradient centrifugation. The purity of MSCs with the spindle fibroblastic morphology was identified by microphotography and the phenotypes were detected by flow cytometry (FCM). MSCs incubated with different doses of PGN (1, 10, 20 μg/ml) were used as test groups, and those incubated without PGN were regarded as control group. The isolated and cultured MSCs were inoculated into 96-well plates according to a certain concentration. Cell cycle was measured by flow cytometry after incubated with PGN for 72 hours. The results showed that the cell proliferation index was significantly increased in dose and time dependent manners after MSCs was incubated with PGN. Its effects on the proliferation of MSCs were highest in 10 μg/ml group. Compared with the control group, PGN could significantly decrease proportion of MSCs in G₀/G₁ phase and increase them in S and G₂/M phases (p < 0.05). It is concluded that PGN can promote more MSCs to enter the DNA synthesis phase and proliferate many much MSCs in dose and time dependent manners.


Subject(s)
Humans , Bone Marrow Cells , Cell Biology , Cell Cycle , Cell Proliferation , Cells, Cultured , Flow Cytometry , Mesenchymal Stem Cells , Cell Biology , Peptidoglycan , Pharmacology , Toll-Like Receptor 2
3.
Chinese Medical Sciences Journal ; (4): 208-212, 2009.
Article in English | WPRIM | ID: wpr-302619

ABSTRACT

<p><b>OBJECTIVE</b>To explore the molecular mechanism of type 2 diabetes in intrauterine growth restricted adult rats through determination of blood glucose and expression of gluconeogenic enzymes in liver.</p><p><b>METHODS</b>Male intrauterine growth restriction (IUGR) offspring induced by maternal protein-malnutrition and normal controls were studied. The body weights of offspring rats were weighted from birth to 12 weeks of age. Fasting plasma glucose and insulin levels were determined by glucose oxidase method and enzyme-linked immunosorbent assay (ELISA) respectively at 1 week, 8 weeks, and 12 weeks. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha), phosphoenolpyruvate carboxykinase (PEPCK), and glucose-6-phosphatase (G6Pase) mRNA and protein levels in liver were measured by real time RT-PCR and Western blot in newborn rats (Week 1) and adult rats (Week 12).</p><p><b>RESULTS</b>Birth weights of IUGR rats were significantly lower than those of controls until 4 weeks later, when IUGR rats caught up to controls. Between 8 and 12 weeks, the growth of IUGR rats surpassed that of controls. No significant differences were observed in blood glucose and insulin levels at newborn rats between the two groups. However, by the end of 8 weeks IUGR rats developed hyperinsulinemia and high insulin resistance index. At the age of 12 weeks, IUGR rats had mild fasting hyperglycemia. In addition, hepatic PGC-1 alpha mRNA and protein levels as well as hepatic mRNA levels of PEPCK and G6Pase at Week 1 and Week 12 in IUGR rats were all significantly higher than those of controls (P<0.05).</p><p><b>CONCLUSIONS</b>As a result of intrauterine malnutrition, the expression of gluconeogenic genes is exaggerated in offspring. This change stays through adulthood and may contribute to the pathogenesis of type 2 diabetes.</p>


Subject(s)
Animals , Female , Male , Rats , Fetal Growth Retardation , Metabolism , Gluconeogenesis , Glucose , Metabolism , Glucose-6-Phosphatase , Genetics , Liver , Metabolism , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha , RNA, Messenger , RNA-Binding Proteins , Genetics , Rats, Wistar , Transcription Factors , Genetics
4.
Chinese Journal of Contemporary Pediatrics ; (12): 753-756, 2009.
Article in Chinese | WPRIM | ID: wpr-304596

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of intrauterine growth retardation (IUGR) caused by malnutrition during pregnancy on the acetylation of histone H3 and expression of histonedeacetylase1(HDAC1) in the hepar of the adult offspring and to explore the relationship between them.</p><p><b>METHODS</b>Male 8-week-old offspring from maternal protein-malnutrition dams were studied. The expression of HDAC1 mRNA in the hepar was measured by fluorescent quantization RT-PCR. The levels of hepatic nuclear HDAC1 protein and acetylation of histone H3/K9 were assessed by Western blot.</p><p><b>RESULTS</b>The hepatic HDAC1 mRNA expression in IUGR rats was reduced to 54% of that of normal control rats (t=2.042, p<0.05). A decline in nuclear expression of HDAC1 protein (438 +/- 47) was also noted when compared with normal controls (1,128 +/- 110) (t=2.179, p<0.05). In contrast, the percentage of acetylated histone H3/K9 in IUGR rats (17.3 +/- 1.6%) increased significantly compared with that of normal control rats (10.5 +/- 1.2%) (t=3.597, p<0.01). The level of acetylated histone H3/K9 was negatively correlated with the HDAC1 protein concentration (r=-0.781, p<0.01).</p><p><b>CONCLUSIONS</b>Increased hepatic acetylation of histone H3 in the IUGR offspring might be caused by decreased HDAC1 expression in nuclear protein. This may contribute to the transcription change of some genes in the hepar.</p>


Subject(s)
Animals , Female , Male , Pregnancy , Rats , Acetylation , Fetal Growth Retardation , Metabolism , Histone Deacetylase 1 , Genetics , Histones , Metabolism , Liver , Metabolism , RNA, Messenger , Rats, Wistar
5.
Chinese Journal of Endemiology ; (6): 484-487, 2008.
Article in Chinese | WPRIM | ID: wpr-642659

ABSTRACT

Objective To investigate the effects of different concentrations of sodium fluoride on the morphologic characteristics of primarily cultured thyroid cells of SD rats and in order to obtain important proof for approaehing the mechani8m of thyroid gland damage caused by fluoride.Methods Thyroid cells of SD rat were primarily culture for 96 hours,and cell density was adjusted to 5.0×108/L Cell suspension with 5 ml Wills seeded into 6 weII plates,after 12 hours,0(contr01),10.100,1000 μmol/L of sodium fluoride was added into the well, witll each well representing different level of treatment group.Finally the cultured thyroid cells were collected for morph010gic study.Results Under microscope,the transparency of the control thyroid cells Was good,and cells gathered in cluster and adhered to wall.But a lot of cells treated with fluoride suspended,and lost their transparency-under scaning delectron microscope,the control calls showed integrated membrane and tightness to each other,as well as clear boundary between cells normal proliferation.While the thyroid cells treated with 10,100 μmol/L sodium fluoride 0bviouslv shrinked and deformed,and the cells treated with 1000 μmol/L of sodium fluoride were broken-Conclusions nuoride can affect the growth and development of thyroid cell and damage the structure and morphology.Sodium fluoride affects the morphologie characteristics of thyroid cells in a dose-response manner.

6.
Chinese Journal of Medical Genetics ; (6): 537-541, 2004.
Article in Chinese | WPRIM | ID: wpr-328831

ABSTRACT

<p><b>OBJECTIVE</b>To establish the mouse model of Gly374Arg mutation in fibroblast growth factor receptor 3(Fgfr3) and to analyze the phenotype of the mutant mice.</p><p><b>METHODS</b>The double PCR was used to introduce Gly374Arg point mutation into mouse Fgfr3. The electroporation of embryonic stem(ES) cells was carried out with targeting vector. The targeted ES cells were screened by Positive-Negative Selection of G418 and Ganciclovir, and Southern blot. The correct targeted ES cells were microinjected into blastula. Finally, mutant mice were obtained by crossing between EIIa-Cre transgenic mice and mice carrying recombined mutant Fgfr3 allele. The mice were genotyped by PCR, and phenotype was observed by skeleton staining, histology, etc.</p><p><b>RESULTS</b>Fgfr3-Gly374Arg mutant mice exhibited small size, short tail, macrocephaly and had dome-shaped heads, the epiphyseal growth plates of mutant mice were narrower, and the hypertrophic chondrocyte zone was also obviously decreased. Meanwhile, the majority of female mice were infertile, and the uterus, ovary and mammal gland in mutant female mice were also smaller and underdeveloped.</p><p><b>CONCLUSION</b>The model of Fgfr3-Gly374Arg mutation causing achondroplasia in mice has been established successfully.</p>


Subject(s)
Animals , Female , Humans , Male , Mice , Achondroplasia , Genetics , Pathology , Amino Acid Substitution , Disease Models, Animal , Ovary , Pathology , Point Mutation , Protein-Tyrosine Kinases , Genetics , Receptor, Fibroblast Growth Factor, Type 3 , Receptors, Fibroblast Growth Factor , Genetics , Uterus , Pathology
7.
Chinese Journal of Obstetrics and Gynecology ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-682963

ABSTRACT

Objective To discuss the effects of abnormal nutritional supply during pregnancy on the adult insulin and leptin resistance in rats.Methods We established the pregnant rat models given either low protein or high nutrition diet,and normal diet group served as control.There were 12 pregnant rats in each group.After vaginal delivery,the pups birth weight were measured.The randomly selected small for gestational age(SGA)from low protein diet group,large for gestational age(LGA)pups from high nutrition diet group and normal birth weight pups from control group were studied at both 4 weeks and 12 weeks after being born.Each group contained 36 rats.The insulin and leptin level were measured by the method of ELISA,and insulin sensitive index were calculated respectively.Results The pups of mothers served with low protein showed obviously lower birth weight than those mothers with normal diet(P0.05),while the weight of fat around kidney,the ratio of fat and body weight(FW/BW)were(0.36?0.14)g,6.5?0.3,which were higher than those of control (0.19?0.13)g,3.4+O.3(P

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