Over the last two decades, significant research attention has been given to the acute effect of a single bout of exercise on postprandial lipaemia. A large body of evidence supports the notion that an acute bout of aerobic exercise can reduce postprandial triacylglycerol (TAG) concentrations. However, this effect is short-lived emphasising the important role of regular physical activity for lowering TAG concentrations through an active lifestyle. In 1995, the concept of accumulating physical activity was introduced in expert recommendations with the advice that activity can be performed in several short bouts throughout the day with a minimum duration of 10 minutes per activity bout. Although the concept of accumulation has been widely publicised, there is still limited scientific evidence to support it but several studies have investigated the effects of accumulated activity on health-related outcomes to support the recommendations in physical activity guidelines. One area, which is the focus of this review, is the effect of accumulating exercise on postprandial lipaemia. We propose that accumulating exercise will provide additional physical activity options for lowering postprandial TAG concentrations relevant to individuals with limited time or exercise capacity to engage in more structured forms of exercise, or longer bouts of physical activity. The benefits of accumulated physical activity might translate to a reduced risk of cardiovascular disease in the long-term.
*Exercise ; Humans ; Hyperlipidemias/metabolism/pathology/*prevention & control ; Lipid Metabolism ; Postprandial Period ; Triglycerides/blood

OBJECTIVE: To construct a subtracted cDNA library of chronic intermittent hypoxia (CIH) rabbit liver by suppression subtractive hybridization (SSH). METHODS: Twenty-four rabbits were divided into 4 groups: ordinary feeding group, full-fat food group, ordinary feeding in chronic intermittent hypoxia group, and full-fat food in chronic intermittent hypoxia group. The mRNAs were extracted from different rabbit livers and converted into double-strand cDNA. After digestion with restriction enzyme, the cDNA of hyperlipidemia-sensitive rabbit group was subdivided into 2 portions and each one was lighted with different adaptors. Two rounds of both hybridization and suppression PCR obtained the differentially expressed cDNA. The PCR products were inserted into T/A vector to set up the subtractive cDNA library. The clones were selected and amplified by PCR and identified. RESULTS: Based on the pathology of the abdominal aorta and liver, and the amplified library contained 500 positive bacteria clones, including 462 clones, which had inserts from 250 to 700 bp by PCR analysis. A novel rabbit gene, Cthrc1, involved in CHI had been cloned. The GenBank Accession Number is XM_418373. CONCLUSION The molecular mechanism of CIH promoting atherogenesis formation is made clear.
Animals ; Gene Library ; Genetic Vectors ; Hyperlipidemias ; Hypoxia ; metabolism ; pathology ; Liver ; metabolism ; pathology ; Nucleic Acid Hybridization ; methods ; RNA, Messenger ; genetics ; Rabbits

OBJECTIVETo observe the effect of hyperlipidemia and atherosclerosis on rat myocardial expression of calcium-sensing receptor and apoptosis.

METHODSThe rat atherosclerosis model was induced by intraperitoneal injection of VD(3) (6 x 10(5) U/kg) and high cholesterol diet. Wistar rats were divided into two groups: (1) Control group; (2) AS group (n = 12 each). The expressions of CaSR, Bcl-2, Bax and caspase-3 were analyzed by Western blot and RT-PCR. Apoptotic cells were observed by TUNEL assay. The morphological changes of abdominal aorta and cardiac tissues were observed under optical and electro microscopes. The activity of LDH, CK, SOD and the content of MDA were assayed with ultraviolet spectrophotometer. The level of cTnT was detected by electrochemical immunofluorescence.

RESULTSCompared with control group, the activity of LDH and CK, the content of MDA and cTnT, the apoptosis index, the expression of CaSR, Bax and caspase-3 were significantly increased, but the SOD activity and Bcl-2 expression were significantly decreased, the myocardial ultrastructure injury was significantly aggravated in the AS group (all P < 0.05).

CONCLUSIONHyperlipidemia and atherosclerosis can up-regulate myocardial calcium-sensing receptor expression, promote myocardial apoptosis, aggravate oxidative stress and myocardial ischemia.

Animals ; Apoptosis ; Atherosclerosis ; metabolism ; pathology ; Disease Models, Animal ; Female ; Hyperlipidemias ; metabolism ; pathology ; Male ; Myocardium ; metabolism ; Oxidative Stress ; Rats ; Rats, Wistar ; Receptors, Calcium-Sensing ; metabolism

BACKGROUND: Hemolysis, icterus, and lipemia (HIL) cause preanalytical interference and vary unpredictably with different analytical equipments and measurement methods. We developed an integrated reporting system for verifying HIL status in order to identify the extent of interference by HIL on clinical chemistry results. METHODS: HIL interference data from 30 chemical analytes were provided by the manufacturers and were used to generate a table of clinically relevant interference values that indicated the extent of bias at specific index values (alert index values). The HIL results generated by the Vista 1500 system (Siemens Healthcare Diagnostics, USA), Advia 2400 system (Siemens Healthcare Diagnostics), and Modular DPE system (Roche Diagnostics, Switzerland) were analyzed and displayed on physicians' personal computers. RESULTS: Analytes 11 and 29 among the 30 chemical analytes were affected by interference due to hemolysis, when measured using the Vista and Modular systems, respectively. The hemolysis alert indices for the Vista and Modular systems were 0.1-25.8% and 0.1-64.7%, respectively. The alert indices for icterus and lipemia were <1.4% and 0.7% in the Vista system and 0.7% and 1.0% in the Modular system, respectively. CONCLUSIONS: The HIL alert index values for chemical analytes varied depending on the chemistry analyzer. This integrated HIL reporting system provides an effective screening tool for verifying specimen quality with regard to HIL and simplifies the laboratory workflow.
Blood Chemical Analysis/instrumentation/*methods/standards ; Female ; Hemoglobins/analysis ; *Hemolysis ; Humans ; Hyperlipidemias/metabolism/*pathology ; Jaundice/metabolism/*pathology ; Male ; Quality Control ; Reproducibility of Results

OBJECTIVETo explore the dynamic change of Phlegm-stasis in the rat atherosclerotic model as the time goes on.

METHODSAdopting high fat forage fed to develop the atherosclerotic model in rats, and the changes of blood lipid, hemorrheology, blood glucose, insulin and vascular smooth muscle cell (VSMC) actin expression were detected by biochemical and immunohistochemical assay at various time points after modeling.

RESULTSThe expression of VSMC actin gradually increased along with the change of model rats' Syndrome from Phlegm to stasis, i.e., the change of parameters, including blood lipid, hemorrheologic parameters, blood glucose, insulin and insulin sensitive indexes along with the aggravation of disease.

CONCLUSIONThe expression of VSMC actin could be the molecular mechanism for the Syndrome developing from Phlegm to stasis in atherosclerotic rats.

Actins ; biosynthesis ; Animals ; Arteriosclerosis ; complications ; metabolism ; pathology ; Diagnosis, Differential ; Female ; Hyperlipidemias ; blood ; complications ; pathology ; Male ; Medicine, Chinese Traditional ; Muscle, Smooth, Vascular ; metabolism ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo investigate the effect of heme oxygenase/carbon monoxide (HO-1/CO) system on lipid deposition at aortic intima and the mechanism involved in hyperlipidemic rabbits.

METHODSTotally 32 rabbits, were divided into four groups. One group as control. Three groups for the following treatments: 1.5% cholesterol ration (Ch group, n = 8); 1.5% cholesterol ration plus HO-1 inducer hemin (Hm group, n = 8); and instead of hemin, the HO-1 inhibitor, zinc protoporphyrin IX (Zn group, n = 8) was given by injection into the abdominal cavity. Experiments were lasted for 12 weeks. Rabbit aortas were then isolated as the samples for histopathologic and ultrastructural examination. The protein expressions of HO-1 and endothelin-1 (ET-1) were investigated by immunohistochemical staining and Western blot analysis.

RESULTSComparing with the Ch group, rabbits of the Hm group showed a remarkably less extent of lipid deposition at the aortic intima [(17.9 ± 3.0)% vs (54.0 ± 4.2)%], and rabbits of the Zn group had a marked extent of lesion development [(61.1 ± 3.5)%]. Lipid deposition, endothelial damage and neo-intimal formation were less severe in rabbits of the Hm group than those in the Zn or Ch group, respectively. Comparing with the control group, rabbits of the Ch group showed a significant decrease of aortic NO production and cNOS activity. However, there were an enhancement of CO production and HO-1 activity (P < 0.01). Compared with Ch group, rabbits of the Hm group showed a remarkable elevation of aortic HO activity and CO production, whereas rabbits of the Zn group showed a marked decrease of both parameters. Compared with the Ch group, rabbits of the Hm group demonstrated a marked reduction of aorta ET-1 expression, whereas Zn group had a significantly higher ET-1 expression.

CONCLUSIONSModulation of HO-1/CO system may improve vascular endothelial function and inhibit smooth muscle cell proliferation in hypercholesterolemic rabbits, likely through a compensatory mechanism and a reduction of ET-1 expression, eventually leading to an inhibition of atherosclerotic plaque development.

Animals ; Aorta ; metabolism ; pathology ; Carbon Monoxide ; metabolism ; Cholesterol ; pharmacology ; Endothelin-1 ; metabolism ; Enzyme Inhibitors ; pharmacology ; Heme Oxygenase-1 ; antagonists & inhibitors ; metabolism ; Hemin ; pharmacology ; Hyperlipidemias ; metabolism ; pathology ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Plaque, Atherosclerotic ; metabolism ; pathology ; prevention & control ; Protoporphyrins ; pharmacology ; Rabbits ; Tunica Intima ; metabolism ; pathology

OBJECTIVETo explore the effects of Guizhi Tang on the inflammatory cytokines in myocardial ischemia and hyperlipidemia rats.

METHODThe early changes of hyperlipid and atherosclerosis are caused by utilizing multiple factors including feeding hyperlipid and propylthiouracil and high doses of vitamin D3 for 12 weeks. Sixty male SD rats were randomly divided in to 5 groups: control group, model group, simvastatin group, low-dosage Guizhi Tang group, high-dosage Guizhi Tang group. At the end of six weeks treatment, pituitrin(pit) is abdominal cavity injected every 24 hours for a total of three times. Detecting the serum levels of SES, CRP, NO, SOD, MDA and the content of cardiac muscle tissue SOD, MDA, The expression of TNF-alpha in cardiac muscle tissue was detected by immunohistochemistry.

RESULTGuizhi Tang significantly decreased levels of SES, CRP and MAD, increased levels of NO and SOD, Guizhi Tang markedly decreased the level of protein expression of TNF-alpha in cardiac muscle tissue.

CONCLUSIONGuizhi Tang may inhibit the proinflammatory factors and oxidation in myocardial ischemia and hyperlipidemia rats.

Animals ; C-Reactive Protein ; metabolism ; Cytokines ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Hyperlipidemias ; blood ; metabolism ; pathology ; Inflammation ; metabolism ; Male ; Malondialdehyde ; blood ; metabolism ; Myocardial Ischemia ; blood ; metabolism ; pathology ; Myocardium ; metabolism ; pathology ; Nitric Oxide ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo investigate the effect of hyperlipidemia on vasa vasorum and vascular endothelial growth factor (VEGF) and study the role of vasa vasorum in arteriosclerosis.

METHODSThirty SD rats were randomized into normal control, hyperlipidemic and simvastatin treatment groups (n=10). In simvastatin group, hyperlipidemia was induced by a 4-week administration of atherogenic diet followed by a 16-week treatment with simvastatin at the daily dose of 10 mg/kg, and the rats in hyperlipidemic rats received no treatment. The changes in the aorta and vasa vasorum were examined, and serum lipid concentration and VEGF and NO levels were measured.

RESULTSCompared with the control group, the hyperlipidemic rats showed significantly thickened intima and media aorta and increased vasa vasorum density with lowered NO level, but VEGF underwent no significant changes. Simvastatin treatment significantly reduced the thickness of the intima and media aorta and increased vasa vasorum density in comparison with those in hyperlipidemic group. Simvastatin treatment also significantly increased VEGF and NO levels and a positive correlation was noted between their levels.

CONCLUSIONHyperlipidemia can impair the vasa vasorum and aortic endothelial function. Simvastatin increases VEGF and NO and promotes neogenesis of the vasa vasorum for the benefit of the aortic function.

Animals ; Aorta ; cytology ; Arteriosclerosis ; pathology ; physiopathology ; Endothelium, Vascular ; physiology ; Hyperlipidemias ; drug therapy ; pathology ; physiopathology ; Hypolipidemic Agents ; pharmacology ; Male ; Nitric Oxide ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Simvastatin ; pharmacology ; Vasa Vasorum ; cytology ; Vascular Endothelial Growth Factor A ; metabolism

OBJECTIVETo investigate the effect of tooth extraction with antibiotics on atherosclerosis, and to examine the expression of serum interleukin 6(IL-6) and the pathological changes of the carotid artery in chronic periodontitis(CP) rats with or without atherosclerosis(As).

METHODSA total of 44 SD rats were randomly divided into four groups, group A(normal control), group B(As), group C(CP), group D(CP+As). After model establishment, group C and group D were randomly divided into group C1/D1 (tooth extraction) and group C2/D2(tooth extraction with antibiotics) according to random number table and received the corresponding oral intervention treatment respectively. Serum IL-6 levels were determined by enzyme linked immunosorbent assay(ELISA) respectively one week before the intervention, one week after the first intervention, one, three, five weeks after the second intervention. The pathological changes of the carotid artery were accessed under light microscope.

RESULTSAt all sampling time points, the levels of serum IL-6 in group B, C, D were higher than that of group A, with group D1 being increased most obviously, significantly higher than that of group A(P< 0.001). One week after the second intervention, the content of IL-6 in group C and group D peaked[C1(127.0 ± 29.9) ng/L, C2: (120.6 ± 23.1) ng/L, D1: (175.1 ± 50.8) ng/L, D2: (160.5 ± 37.7) ng/L], and was significantly higher than that of group B[B: (43.4 ± 7.5) ng/L,P<0.001]. Then they all had varying degrees of decline, 5 weeks after the second intervention, group C1 and D1 were still higher than that of group B, but group C2 and D2 were lower than that of group B. At all sampling time points, the levels of serum IL- 6 in group C2/D2 were lower than those in group C1/D1, 5 weeks after the second intervention the difference was most obvious and statistically significant(P<0.001). Pathology showed that the carotid artery wall in group A was normal. The carotid artery wall was thickened in group B, inflammatory cells and foam cells could be seen, and elastic fibers disordered. The carotid artery wall in group C1 was uneven, foam cells and a small amount of inflammatory cells were visible, and elastic fiber disordered. Obvious thickening was not seen in the carotid artery wall of group C2, a small amount of foam cells and inflammatory cells were found, and elastic fiber mildly disordered. The carotid artery wall in group D1 was obviously uneven, calcium salt deposits were visible in the artery wall, a large amount of inflammatory cells and foam cells could be found, and elastic fiber disordered. Obvious thickening was not seen in the carotid artery wall of group D2, a small amount of inflammatory cells and a large amount of foam cells could be seen, and elastic fiber disordered.

CONCLUSIONSPeriodontitis and hyperlipidemia could increase the level of serum IL- 6 and the risk of the As. In chronic periodontitis rats with or without atherosclerosis, when periodontal inflammation was not controlled, tooth extraction may increase the risk of the As. At the time of tooth extraction, giving the anti-inflammatory treatment can reduce the risk to a certain extent.

Animals ; Anti-Bacterial Agents ; pharmacology ; Aorta ; chemistry ; pathology ; Atherosclerosis ; blood ; complications ; Carotid Arteries ; drug effects ; metabolism ; pathology ; Chronic Periodontitis ; blood ; complications ; Foam Cells ; pathology ; Humans ; Hyperlipidemias ; blood ; Interleukin-6 ; blood ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tooth Extraction ; adverse effects

OBJECTIVE: To establish the hyperlipoidemia model and observe its effect on the expression of plasma vWF, PAl-1 and t-PA after endothelial cell injury caused by the model at different time in rats. METHODS: Sixty male Sprague-Dawley rats weighing (200+/-20)g were randomly divided into 6 groups (n=10 in each): high flat composition for 7 weeks (Group A7), 8 weeks (Group A8)and 9 weeks(Group A9), common bait vessel feeding for 7 weeks(Group C7), 8 weeks(Group C8) and 9 weeks (Group C9). When it reached the setting time, the rats were put to death and the serum was separated to detect the blood-fat immediately. Meanwhile, the pathological sections of the rat aorta were made to observe the endothelial injury. The blood plasma was separated and the content of the blood plasma PAl-1, t-PA and vWF was detected by ELISA assay. RESULTS: (1)TG, TC and LDL of the rats intragastrically administrated high flat composition were higher than those of the control group,and HDL increased with time at first, but lowered when longer than 9 weeks. (2) There were no lesions in the aortic endothelium in all rats of Group C through optical microscope,while different lesions in the aortic endothelium in all rats of Group A were observed. (3)In the 3 groups A, the plasma vWF and PAI-1 were gradually increasing with time while t-PA gradually decreased. (4) There was no significant difference of vWF between Group A7 and Group A8. PAI-I increased gradually with the aggravation of endotheliocytes in Group A; and t-PA decreased gradually with the aggravation of endothelium in Group A. CONCLUSION (1) As intragastric administration prolongs, the plasma lipid of rats keeps increasing with the aggravation of the endodermis injury. (2) PAI-1, t-PA and vWF are the molecular markers of vascular endothelial cell injury in rats. (3) PAI-l and t-PA are more sensitive than vWF in reflecting the endothelial cell injury in hyperlipemia early metaphase.
Animals ; Aorta ; pathology ; Endothelial Cells ; pathology ; Hyperlipidemias ; blood ; pathology ; Male ; Plasminogen Activator Inhibitor 1 ; blood ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tissue Plasminogen Activator ; blood ; von Willebrand Factor ; metabolism