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Review [Hyperlipidemia in endocrine disease] 2007
Hayashi N, Funahashi T. · Department of Metabolic Medicine, Osaka University. · Nippon Rinsho. · Pubmed #17824064 No free full text.
This publication has no abstract.
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| 27 |
Review [Familial type III hyperlipoproteinemia] 2007
Igarashi M. · Department of Laboratory Medicine, Yamagata University School of Medicine. · Nippon Rinsho. · Pubmed #17824053 No free full text.
This publication has no abstract.
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| 28 |
Review [Idiopathic hypertriglyceridemia] 2007
Hirata K. · Division of Cardiovascular Medicine, Kobe University Graduate School of Medicine. · Nippon Rinsho. · Pubmed #17824052 No free full text.
This publication has no abstract.
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| 29 |
Review [Familial hyperlipoproteinemia, type IV] 2007
Matsuura F. · Department of Cardiovascular Medicine, Osaka University. · Nippon Rinsho. · Pubmed #17824051 No free full text.
This publication has no abstract.
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| 30 |
Review [Primary hypercholesterolemia other than familial hypercholesterolemia and familial combined hyperlipidemia] 2007
Arai H. · Department of Geriatric Medicine, Kyoto University Graduate School of Medicine. · Nippon Rinsho. · Pubmed #17824050 No free full text.
This publication has no abstract.
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| 31 |
Review [Familial lipoprotein lipase deficiency] 2007
Tsukamoto K. · Department of Metabolic Diseases, Tokyo University. · Nippon Rinsho. · Pubmed #17824045 No free full text.
This publication has no abstract.
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| 32 |
Review [Intervention for hypertriglyceridemia] 2007
Nagao M, Oikawa S. · Division of Endocrinology and Metabolism, Department of Medicine, Nippon Medical School Hospital. · Nippon Rinsho. · Pubmed #17824043 No free full text.
This publication has no abstract.
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| 33 |
Review [Current trend of hyperlipidemia in Japan--comparison with the trend in United States and Europe] 2007
Arai H. · Department of Geriatric Medicine, Kyoto University Graduate School of Medicine. · Nippon Rinsho. · Pubmed #17824042 No free full text.
This publication has no abstract.
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| 34 |
Review [Classification of hyperlipidemias in Japan] 2007
Mori S, Ito H. · Tokyo Metropolitan Geriatric Hospital. · Nippon Rinsho. · Pubmed #17824041 No free full text.
This publication has no abstract.
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| 35 |
Review [Gene mutations responsible for hyperlipoproteinemia] 2007
Sato R, Okabayashi M, Kajinami K. · Department of Cardiology, Kanazawa Medical University. · Nippon Rinsho. · Pubmed #17824022 No free full text.
This publication has no abstract.
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| 36 |
Review [Molecular mechanism of atherogenesis in hyperlipidemia] 2007
Nishida M, Yamashita S. · Health Care Center, Osaka University. · Nippon Rinsho. · Pubmed #17824013 No free full text.
This publication has no abstract.
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| 37 |
Review [Evaluation of megatrials with antihyperlipidemic agents in Japan] 2007
Fukai S, Ouchi Y. · Department of Geriatric Medicine, Tokyo University Graduate School of Medicine. · Nippon Rinsho. · Pubmed #17821901 No free full text.
This publication has no abstract.
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| 38 |
Review Statin therapy for vascular failure. 2007
Inoue T, Node K. · Department of Cardiovascular and Renal Medicine, Saga University Faculty of Medicine, 5-1-1 Nabeshima, Saga 849-8501, Japan. · Cardiovasc Drugs Ther. · Pubmed #17682928 No free full text.
Abstract: There is increasing evidence that statins reduce cardiovascular events such as coronary artery disease or stroke in hypercholesterolemic patients in both primary and secondary prevention. The striking benefit achieved with statin treatments in patients with a wide range of cholesterol levels cannot be attributed to their cholesterol lowering effect alone. Substantial data has recently accumulated showing that statins exert various effects on multiple targets, namely pleiotropic effects, especially targeting the concept of 'vascular failure', including the improvement of vascular endothelial function, inhibition of vascular smooth muscle cell proliferation and migration, anti-inflammatory actions, anti-oxidative effects or stabilization of vulnerable plaques. These effects have potential in the treatments of coronary artery disease in various settings, such as prevention of its onset as well as its progression, or plaque rupture. Statin therapy should be more extensively applied even in normolipidemic patients if there are additional risk factors such as hypertension, diabetes mellitus, or others. Furthermore, statins may be used to intervene in earlier stage risk conditions such as postprandial hyperlipidemia or hyperglycemia, insulin resistant state, masked hypertension, or metabolic syndrome to further reduce mortality or morbidity of coronary artery disease and heart failure.
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| 39 |
Review [Metabolic syndrome and small dense LDL-cholesterol] 2007
Hirano T. · First Department of Internal Medicine, Showa University School of Medicine, Shinagawa-ku, Tokyo 142-8666. · Rinsho Byori. · Pubmed #17593688 No free full text.
Abstract: Recently, small dense low-density lipoprotein (sd-LDL) has been highlighted as a new risk factor for CHD. Sd-LDL is also closely associated with insulin resistance and hypertriglyceridemia, suggesting a high prevalence of these atherogenic particles in metabolic syndrome. It has been proposed that increased triglyceride (TG) production in the liver due to insulin resistance preferentially produces TG-rich very-low density lipoproteins (VLDL1), which finally generate sd-LDL particles. Sd-LDL is usually measured by electrophoresis or ultracentrifugation, but these methods are too laborious for general clinical use. Recently, we established a simple method for the quantification of sd-LDL-cholesterol (C) using heparin-magnesium precipitation with a filter, which selectively detects cholesterol in the denser LDL fraction with a density(d) =1.044-1.063g/ml. Patients with coronary heart disease (CHD) had substantially increased sd LDL-C levels, while their LDL-C levels were comparable to those of controls. Sd-LDL-C levels were positively correlated with TG, LDL C, and apolipoprotein B, and were inversely with HDL-C. Sd-LDL-C levels were also correlated positively with waist circumference, blood pressure, and insulin resistance index, and negatively with adiponectin level. Patients with type 2 diabetes and metabolic syndrome had substantially increased sd-LDL-C level. These results suggest that measurement of sdLDL-C is useful to evaluate overall atherogenic risks associated with metabolic syndrome and may be applicable to routine clinical examination.
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| 40 |
Review Lipoprotein glomerulopathy-like disease in a patient with type III hyperlipoproteinemia due to apolipoprotein E2 (Arg158 Cys)/3 heterozygosity. 2007
Karube M, Nakabayashi K, Fujioka Y, Yoshihara K, Yamada A, Matsunaga A, Saito T. · Division of Nephrology and Rheumatology, First Department of Internal Medicine, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-0061, Japan. · Clin Exp Nephrol. · Pubmed #17593519 No free full text.
Abstract: A 77-year-old woman developed nephrotic syndrome associated with type III hyperlipoproteinemia (III HLP) and increased apolipoprotein E (apo E). Apo E analysis disclosed E2/E3 heterozygosity in phenotypic and genotypic expressions, without any other mutations. A renal biopsy showed intraluminal and subendothelial thrombus-like deposits in the dilated capillary loops of the glomerulus that stained positive for lipids and apo E. Electron microscopy revealed tiny granular particles in the capillary lumina, as well as between the glomerular basement membrane and the endothelial cells. It was therefore concluded that III HLP associated with apo E2/E3 heterozygosity could induce lipoprotein glomerulopathy-like disease and nephrotic syndrome.
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| 41 |
Review [Hyperlipidemia] 2006
Iso H. · Public Health, Osaka University Graduate School of Medicine. · Nippon Rinsho. · Pubmed #17461223 No free full text.
This publication has no abstract.
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| 42 |
Review [Research and developmental strategy of anti-dyslipidemic agents] 2007
Tanimoto T. · · Nippon Yakurigaku Zasshi. · Pubmed #17435338 No free full text.
This publication has no abstract.
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| 43 |
Review [Molecular basis of metabolic syndrome] 2007
Tamori Y, Kasuga M. · Division of Diabetes, Digestive, and Kidney Diseases, Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine. · Nippon Shokakibyo Gakkai Zasshi. · Pubmed #17409656 No free full text.
This publication has no abstract.
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| 44 |
Review Metabolism of diacylglycerol in humans. 2007
Takase H. · Health Care Products Research Labs. No.1, Kao Corporation, 2-1-3 Bunka Sumida-ku, Tokyo 131-8501, Japan. · Asia Pac J Clin Nutr. · Pubmed #17392138 No free full text.
Abstract: Obesity resides upstream of the constituents of metabolic syndromes such as diabetes, hypertension, hyperlipidemia, and arteriosclerosis. Postprandial hyperlipidemia is also implicated in atherogenesis. Therefore, factors that influence the body adiposity and the magnitude of postprandial hyperlipidemia have been intensively investigated. Diacylglycerol (DAG) oil, which is defined to contain DAG 80% (w/w) or greater in the present presentation, is an edible oil with similar taste and usability compared with conventional edible oil rich in TAG. Safety of DAG has been widely evaluated and listed as a GRAS (Generally Recognized as Safe) substance by US FDA. The aim of this review was to summarize the metabolism and nutritional functions of DAG based on the data from scientific journals and conference publications. Effect of DAG ingestion on postprandial elevations of serum lipids was investigated in several dosages, food formula, and in subjects in various conditions. Postprandial triglyceride in serum and the chylomicron fraction are significantly smaller after DAG consumption compared with TAG with a similar fatty acid composition in healthy subjects, and was remarkably reduced in subjects with insulin resistance. Long-term DAG ingestion in controlled diet or free-living condition significantly decreased body adiposity and improved type II diabetic complications. A single dose DAG consumption significantly increased fat oxidation as compared to eucaloric TAG ingestion. DAG oil consumption might be beneficial in reducing the risk factors for lifestyle-related diseases such as obesity, visceral obesity, postprandial hyperlipidemia, insulin resistance, and atherosclerosis.
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| 45 |
Review [Role of RLP-induced inflammation in atherosclerosis] 2007
Yoshida M. · · Nippon Yakurigaku Zasshi. · Pubmed #17379966 No free full text.
This publication has no abstract.
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| 46 |
Review Circadian rhythms in the CNS and peripheral clock disorders: the circadian clock and hyperlipidemia. free! 2007
Kudo T, Horikawa K, Shibata S. · Department of Physiology and Pharmacology, School of Science and Engineering, Waseda University, 2-7-5 Higashi-fushimi, Nishitokyo-shi, Tokyo 202-0071, Japan. · J Pharmacol Sci. · Pubmed #17299248 links to free full text
Abstract: A circadian clock controls various physiological and behavioral rhythms. In mammals, a master circadian clock exists in the suprachiasmatic nucleus of the hypothalamus, and slave oscillators can be found in most tissues. These circadian oscillations are controlled by "clock genes". The negative feedback loop is thought to function as a molecular mechanism of the circadian clock. It is plausible that clock genes may control lipid metabolism through so-called clock-controlled genes and that lipid metabolism-related clock-controlled genes may play important roles in the circadian change of lipid metabolism. Recently research has focused on the relationships between the clock system and lipid metabolism. In this review, we discuss the following items: 1) circadian clock system, 2) effect of the diet on clock gene expression, 3) effect of clock mutation on lipid metabolism, and 4) effect of streptozotocin-induced diabetes and ob mutation on clock gene expression and lipid metabolism. In this review we have summarized how the circadian clock affects lipid metabolism through the expression of lipid metabolism-related clock-controlled genes and at the same time discussed how abnormal metabolism of lipid affects the expression of clock genes. Further experiments are needed to elucidate the detailed mechanism of interaction between clock genes and lipid metabolisms.
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| 47 |
Review Treatment of hyperlipidemia from Japanese evidence. free! 2006
Koba S, Sasaki J. · The Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan. · J Atheroscler Thromb. · Pubmed #17192691 links to free full text
Abstract: The treatment of hyperlipidemia is aimed at preventing cardiovascular disease (CVD) and coronary heart disease (CHD). As the incidence of CHD in Japan is about one-third lower and that of stroke is two-fold higher compared to Western countries, and the doses of lipid-lowering drugs used in foreign randomized controlled clinical trials (RCTs) are much higher than in general use in Japan, it remains unclear whether the results of RCTs conducted in Western countries could be extrapolated to Japanese patients. Recently, two major large-scale, prospective, RCTs in Japanese hypercholesterolmic patients, the Management of Elevated Cholesterol in the Primary Prevention of Adult Japanese (MEGA) study and the Japan EPA Lipid Intervention Study (JELIS), have been reported. Japanese epidemiological studies and Japanese clinical studies are reviewed. The evidence suggests that hypercholesterolemia, hypertriglyceridemia, and low HDL-cholesterol are strongly associated with increased CHD risk. Lipid-lowering medication shows beneficial effects even in low-risk populations; however, the data did not support that lower cholesterol is better. The safety and efficacy of hyperlipidemia treatment in Japanese patients are discussed.
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| 48 |
Review [Statins (HMG-CoA reductase inhibitors)] 2006
Gotoda T. · Department of Clinical and Molecular Epidemiology, Graduate School of Medicine, University of Tokyo. · Nippon Rinsho. · Pubmed #17087305 No free full text.
Abstract: Diabetic patients frequently show lipid abnormalities that include qualitative changes in lipid profile. Given the greatly increased risk of coronary heart disease (CHD) in diabetic patients with hyperlipidemia, most principal clinical guidelines recommend aggressively lowering lipid levels in such patients. In fact, several large-scale clinical intervention trials have successfully shown that lipid-lowering agents, particularly statins, could significantly reduce the CHD risk in diabetic patients with hyperlipidemia. According to our investigation on 9,000 Japanese diabetic patients, about a half had hyperlipidemia but only less than half of the hyperlipidemic patients received some lipid-lowering agents. Taken together, it should be concluded that more stringent and aggressive intervention should be recommended in the treatment of Japanese diabetic patients with hyperlipidemia.
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| 49 |
Review [Type 2 diabetes mellitus] 2006
Kashiwagi A. · Department of Medicine, Shiga University of Medical Science. · Nippon Rinsho. · Pubmed #17022497 No free full text.
This publication has no abstract.
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| 50 |
Review [Japan Arteriosclerosis Longitudinal Study] 2006
Ohashi Y, Ueshima H, Harada A. · Department of Biostatistics/Epidemiology and Preventive Health Sciences, Graduate School of Medicine, University of Tokyo. · Nippon Rinsho. · Pubmed #16983763 No free full text.
This publication has no abstract.
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