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

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 observe the protection of Huanglian Jiedu Decoction (HJD) on high fat diet induced liver damage mice [hyperlipidemic mice lacking apolipoprotein E (ApoE(-/-))].

METHODSWild type mice were divided into the wild common food group and the wild hyperlipidemia group. ApoE(-/-) mice were divided into the ApoE(-/-) common food group, the ApoE(-/-) hyperlipidemia group, and the ApoE(-/-) hyperlipidemia plus HJD group, 5 in each group. In the present study, wild type mice and homozygous apoE(-/-) mice were fed with a chow diet or a high cholesterol Western diet for 4 weeks. HJD at the daily dose of 5 g/kg was given to mice in the ApoE(-/-) hyperlipidemia plus HJD group by gastrogavage. The plasma levels of total cholesterol (TC), triglyceride (TG), low density cholesterol protein (LDL-C) were detected. The pathohistological changes of the liver were observed by Eosin and Hematoxylin (HE) staining. The liver macrophages and their subtype ratios, as well as macrophage surface receptor CD206 and CD36 were detected by flow cytometry.

RESULTSTypical pathological changes of simple fatty liver were manifested in the ApoE(-/-) hyperlipidemia group, TC, TG, and LDL-C increased, the macrophage ratio increased, the expression level of macrophage surface receptor CD206 decreased, showing statistical difference when compared with the ApoE(-/-) common food group (P < 0.01, P < 0.05). The ratio of alternatively activated macrophages (M2) subpopulations was lower in the ApoE(-/-) hyperlipidemia group than in the wild common food group (P < 0.05). There was no obvious change in the expression level of CD36. After intervened by HJD for 4 weeks, there was no obvious improvement in blood lipids. But the ratio of CD206+ M2 macrophages was significantly improved, when compared with the ApoE(-/-) hyperlipidemia group (P < 0.05). The pathological changes of fatty liver were significantly attenuated.

CONCLUSIONSThe liver protection effect of HJD might be associated with immunoregulation of M2 macrophage subpopulations and injured tissue repairmen. Its immunoregulation and liver protection were independent from lipids lowering.

Animals ; Apolipoproteins E ; genetics ; Cholesterol, LDL ; blood ; Diet, High-Fat ; adverse effects ; Drugs, Chinese Herbal ; pharmacology ; Fatty Liver ; metabolism ; pathology ; prevention & control ; Hyperlipidemias ; metabolism ; pathology ; prevention & control ; Liver ; cytology ; metabolism ; pathology ; Macrophages ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Triglycerides ; blood

OBJECTIVETo study on the regulatory mechanism of lipid metabolism disorders in the blood fat of hyperlipemia rat model with Olive Antihyperlipidemia capsule, and do systematic observation on the functions of this medicine on low And high density lipoprotein receptor in rat liver gene expression, and then to clarify the mechanism of action of this medicine on treating hyperlipemia.

METHODTo select SD rat as investigated subject. The hyperlipemia rat models were made with feeding high-fat forage and were randomly divided into six groups based on the total cholesterol level at the ratsfasting for 12 hours: group A, B, C, D, E and group F. The samples in the research were collected and analyzed the changes of LDLR/SR-B1 gene expression in rat's liver by RT-PCR.

RESULTOlive Antihyperlipidemia capsule can markedly enhance LDLR/SR-B1 gene expression in rat's liver and finally accomplish the purpose of reducing blood fat. The experiment shows this medicine has the remarkable effect on hyperlipidemia and proved the theoretical system of treating hyperlipemia for curing the liver is correct.

CONCLUSIONOlive Antihyperlipidemia capsule has an applicable value on preventing the cause, enhance LDLR/SR-B1 gene expression in rat's liver and finally accomplish the purpose of reducing blood fat and development of hyperlipemia and its complications.

Animals ; Capsules ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Gene Expression Regulation ; drug effects ; Hyperlipidemias ; genetics ; pathology ; prevention & control ; Hypolipidemic Agents ; isolation & purification ; pharmacology ; Lipoproteins, HDL ; genetics ; Liver ; metabolism ; Male ; Olea ; chemistry ; Plants, Medicinal ; chemistry ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, LDL ; genetics ; Receptors, Lipoprotein ; genetics ; Scavenger Receptors, Class B ; genetics

OBJECTIVETo investigate the effect of Antrodia cinnamomea on gene expression related to aortal endothelial injury of rats with hyperlipidemia.

METHODFifty SD rats were randomly divided into five groups: the normal control group (NG), the model group (MG), the antrodia cinnamomea groups of low, middle and high doses (AC-LG, AC-MG, AC-HG, 250, 500, 1 000 mg x kg(-1)). The rats were fed with high-fat diets to establish the hyperlipidemia model. After the drug administration for 10 weeks, their serum lipid, SOD, MDA and ox-LDL, LOX-1, P38 MAPK and NF-kappaB mRNA and protein expression were respectively determined, and the aortal endothelial injury was observed under electron microscope.

RESULTIn the model group, the contents of TC, TG and LDL-C significant increased (P < 0.01), whereas the content of HDL-C significant decreased (P < 0.01). Compared with the model group, both the AC-M group and the AC-H group showed reduction in endothelial injury and significant decrease in the content of TC, TG and LDL-C (P < 0.05 or P < 0.01). The content of HDL-C increased, but with no significant difference. SOD activity in serum remarkably increased (P < 0.05 or P < 0.01), MDA and ox-LDL levels dramatically decreased (P < 0.05 or P < 0.01).

CONCLUSIONA. cinnamomea can alleviate endothelial lipid injury by inhibiting the expressions of LOX-1, P38MAPK and NF-kappaB in aorta and better protect aortal endothelial cells from oxidative lipid injury.

Animals ; Antrodia ; chemistry ; Aorta ; drug effects ; metabolism ; ultrastructure ; Atherosclerosis ; blood ; genetics ; prevention & control ; Biological Products ; pharmacology ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Endothelium, Vascular ; drug effects ; metabolism ; pathology ; Enzyme-Linked Immunosorbent Assay ; Gene Expression ; drug effects ; Hyperlipidemias ; blood ; genetics ; prevention & control ; Lipoproteins, LDL ; blood ; Male ; Malondialdehyde ; blood ; Microscopy, Electron ; NF-kappa B ; blood ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Scavenger Receptors, Class E ; blood ; genetics ; metabolism ; Superoxide Dismutase ; blood ; Triglycerides ; blood ; p38 Mitogen-Activated Protein Kinases ; blood ; genetics ; metabolism