1.The Effect of Laboratory Mental Stress on Serum Levels of Glucose and Insulin
Xin CHEN ; Ying ZHAO ; Baotang YANG
Chinese Mental Health Journal 1991;0(05):-
Objective: To study the effect of laboratory menta l stress on serum levels of glucose and insulin Methods: 48 heal thy male college students were recruited Fasting serum glucose test and insuli n measurement were done before and after mental arithmetic test Result s: Glucose level increased after arithmetic test (434?079/477?0 70, t=381, p
2.ADRP antisense oligodeoxynucleotides reduce cellular cholesterol and the expression of ADRP in atherosclerotic lesions
Zhonghua YUAN ; Yongzong YANG ; Weidong YIN ; Xianqing TANG ; Guanghui YI ; Baotang YANG ; Zaiyang WAN
Chinese Journal of Pathophysiology 1986;0(04):-
AIM: To investigate the relationship betw een ADRP and the development of atherosclerosis. METHODS: Antisense oligodeoxynucleotide of mouse ADRP was constr ucted. The mouse peritoneum macrophages were cultured with Ox-LDL or Ox-LDL plus the antisense fragment. The cellular cholesterol was measured and the expressio n of ADRP was observed with RT-PCR and western blotting. New Zealand white rabbi ts were fed with high cholesterol chow for 12 weeks. The levels of serum lipid a nd cholesterol content of aortic wall were investigated. The areas of fatty stre ak of the aortas was measured after staining with Sudan Ⅳ. The aortic, and live r specimens with HE and immunohistochemistry staining were observed under light microscopes. RESULTS: Antisense oligodeoxynucleotides of mouse ADRP decreased cellular cholesterol ester, induced cellular lipid droplets and the expression of ADRP. The expression of ADRP was induced by high-cholesterol-diet feeding in rabbit atherosclerotic lesions. The fatty streak of the aorta with immunohistoch emistry staining was strongly positive for ADRP in animals fed with high cholest erol chow, and the liver was negative with or without high cholesterol chow. CONCLUSIONS: The expression of ADRP in vessel walls is related t o the atherosclerosis, and has a potential role in lipid accumulation in macroph ages and pathogenesis of atherosclerosis.
3.Atherosclerosis induced by diabetogenic diet in New Zealand white rabbits
Weidong YIN ; Baotang YANG ; Shanchun ZHANG ; Zhonghua YUAN ; Guanghui YI ; Yongzong YANG
Chinese Journal of Pathophysiology 2001;17(8):768-
To observe the effects of diabetogenic (high fat high sucrose, lacking choleserol) diet on atherogenesis in New Zealand white rabbits. Two groups of New Zealand white rabbits received regular rabbit chow (the normal control), or high fat high sucrose diet for 4 months. The levels of plasma total cholesterol, HDL cholesterol, triglycerides, insulin, and glucose were investigated, the areas of fatty streak of the aortae were measured after staining with Sodan IV, and the aortic, coronary specimens were observed with light and electron microscopies. The plasma glucose, triglycerides, and total cholesterol were increased significantly by high fat high sucrose feeding. At the end of 4 months, the early charateristics of atherosclerosis were present in the animals' vascular specimens. Our findings suggest that high fat high sucrose feeding can induce hyperglycemia, hypertriglyceridemia and atherosclerosis in New Zealand white rabbits, and this could be a potential animal model for studying the mechanisms of diabetes-accelerated atherosclerosis. This study raised a question: What is the mechanism by which high fat high sucrose feeding induces atherosclerosis?. The related hypothesis was given in this article.
4.Change of CD36 expression in minipigs fed high fat/high cholesterol diet
Xin CHEN ; Yulin TU ; Guanghui YI ; Beibing WANG ; Daming FENG ; Wenqing SUN ; Baotang YANG ; Zaiyang WAN ; Zhong REN ; Yongzong YANG
Chinese Journal of Pathophysiology 2000;0(07):-
AIM: In order to investigate the change of CD36 expression in atherosclerosis. METHODS: Chinese minipigs were fed a normal control diet (CD) or a high fat/high cholesterol diet (HFHC) for 12 months after common carotid artery injury induced by balloon denudation. Plasma total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) were determined by commercially enzymatic methods. CD36 mRNA and protein levels were determined by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting and immunohistochemistry, respectively. RESULTS: After HFHC for 12 months, plasma total cholesterol, HDL cholesterol and triglyceride in HFHC minipigs were increased compared with the control. CD36 expression and aorta PPAR? in HFHC minipigs were upregulated. CONCLUSION: HFHC may induce hyper cholesterolemia, hypertriglyceridemia and upregulation of CD36 and aortic PPAR? expression.