Hyperlipidemias: Yokote K

Teramoto T, Sasaki J, Ueshima H, Egusa G, Kinoshita M, Shimamoto K, Daida H, Biro S, Hirobe K, Funahashi T, Yokote K, Yokode M, Anonymous00494. · Committee for Epidemiology and Clinical Management of Atherosclerosis. · J Atheroscler Thromb. · Pubmed #18480589 links to  free full text

This publication has no abstract.

Hayashi T, Yokote K, Saito Y, Iguchi A. · Nagoya University Graduate School of Medicine, Department of Geriatrics, 65 Tsuruma-cho, Showa-ku, Nagoya City, 466-8550, Japan. · Expert Opin Pharmacother. · Pubmed #17927486 No free full text.

Abstract: Pitavastatin, (+)-monocalcium bis(3R,5S,6E)-7-(2-cyclopropyl-4-[4-fluorophenyl]-3-quinolyl-3,5-dihydroxy-6-heptenoate), is a totally synthetic statin developed in Japan with a molecular weight of 880.98. Pitavastatin achieves its potent pharmacologic action by strongly binding and inhibiting the active site of 3-hydroxy-3-methyl-glutaryl-CoA reductase, and has potent low-density lipoprotein-cholesterol-lowering effects similar to atorvastatin and rosuvastatin. One other characteristic of the agent is that pitavastatin is minimally metabolized by the cytochrome P450 isozymes; it undergoes glucuronidation and is converted to the inactive lactone form, and, therefore, the incidence of any drug interactions is reduced. Due to the promising results observed in clinical trials, it has the potential to be an excellent addition to the worldwide lipid management market.

Yokote K, Honjo S, Kobayashi K, Fujimoto M, Kawamura H, Mori S, Saito Y. · No affiliation provided · J Am Geriatr Soc. · Pubmed #15341572 No free full text.

This publication has no abstract.

Mori S, Murano S, Yokote K, Takemoto M, Asaumi S, Take A, Saito Y. · Second Department of Internal Medicine, School of Medicine, Chiba University, Inohana, Chiba, Japan. · Int J Obes Relat Metab Disord. · Pubmed #11410834 links to  free full text

Abstract: OBJECTIVE: Studies were made on the abnormality of glucose and lipid metabolism and its cause in four patients with Werner's syndrome to infer the reason for accelerated atherogenesis in this syndrome. RESULTS: Of these four patients, hypercholesterolemia was found in three, hypertriglyceridemia in four, hypoalphalipoproteinemia in two and hypertension in two. All the patients had insulin-resistant diabetes mellitus and three of them had apparent hyperinsulinemia. Abdominal computed tomography revealed that all of them had visceral fat obesity, namely augumented intra-abdominal adipose tissue. CONCLUSION: The clinical features of these patients resemble those recently designated as insulin resistant syndrome (syndrome X) or visceral fat syndrome. The metabolic abnormality may be one of important factors in the accelerated atherogenesis in this syndrome.

Takemoto M, Tada K, Nakatsuka K, Moriyama Y, Kazui H, Yokote K, Matsumoto T, Saito Y, Mori S. · Second Department of Internal Medicine, Chiba University School of Medicine. · Nippon Ronen Igakkai Zasshi. · Pubmed #10655737 No free full text.

Abstract: In order to elucidate a possible mechanism for accelerated atherogenesis as well as enhanced vascular calcification observed during the normal aging process, we measured plasma osteopontin (OPN) levels and examined their relation to aging and certain disease parameters. In all cases examined, no significant relation was found between the plasma OPN level and age, body mass index, blood pressure, plasma levels of glucose and insulin, serum levels of creatinine, triglyceride, and high density lipoprotein cholesterol. On the other hand, a significant negative correlation was found between the plasma OPN level and serum total cholesterol concentration (n = 78, r = -0.355, p = 0.0014). The serum level of low density lipoprotein (LDL) cholesterol, calculated by the formula of Friedewald, also showed a significant negative correlation to the plasma OPN level (n = 78, r = -0.301, p = 0.0075). In cases without diabetes mellitus and hypertension, a significant positive correlation was found between the plasma OPN level and age (n = 22, r = 0.445, p = 0.0378). It is postulated that OPN plays a negative regulatory role in the development of vascular calcification. Therefore, the observed negative relationship between the plasma OPN level and the serum levels of total cholesterol and LDL cholesterol, suggests a possibility that hypercholesterolemia facilitates vascular calcification by suppressing OPN synthesis. On the other hand, in non-diabetic and normotensive cases, the positive relationship between the plasma OPN level and age may reflect a defense mechanism against age-related increase of vascular calcification.