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福島四郎教授還暦記念特

"Appellation contrôlée" in French Law

伊沢孝平教授還暦記念特

Low body mass index is a risk factor forimpaired endothelium-dependent vasodilation in humans: role of nitric oxide and oxidative stress

AbstractObjectivesThe purpose of this study was to evaluate the relationship between body mass index (BMI), including low BMIs, and endothelial function.BackgroundEpidemiologic study has demonstrated that not only obesity but also a low BMI may be a risk factor for cardiovascular disease.MethodsThe forearm blood flow (FBF) response to acetylcholine (ACh) and isosorbide dinitrate (ISDN) was measured in 87 healthy young men (15 low BMI, 51 normal, 14 obese, and 7 extremely obese).ResultsPlasma concentrations of 8-hydroxy-2′-deoxyguanosine and serum concentrations of malondialdehyde-modified low-density lipoprotein were higher in low BMI, obese, and extremely obese subjects than in normal subjects and were similar among the low BMI, obese, and extremely obese groups. The FBF response to ACh was greater in the normal group than in the other groups (p < 0.001), and was lower in the extremely obese group as compared with the other groups (p < 0.001). The ACh-stimulated vasodilation was similar between the low BMI group and the obese group. The ISDN-stimulated vasodilation was similar in all four groups. There were no significant differences in ACh-stimulated vasodilation between the four groups after the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine infusion. Co-infusion of vitamin C augmented the FBF response to ACh in low BMI, obese, and extremely obese groups—but not in normal BMI group.ConclusionsThese findings suggest that not only obesity but also a low BMI may be a risk factor for impaired endothelium-dependent vasodilation through the increased oxidative stress, leading to the reduced bioavailability of NO

Serum Apolipoprotein M Levels are Correlated with Biomarkers of Coagulation

Background:Apolipoprotein M (ApoM) is bound to high-density lipoprotein (HDL) in plasma, and HDL has anticoagulation effects. However, the association between ApoM and biomarkers of coagulation was unclear. Therefore, we investigated relationships between ApoM and biomarkers of coagulation. Methods: Serum samples from 233 Japanese participants including with diabetes mellitus, hypertension, dyslipidemia, or healthy controls were analyzed. Serum ApoM levels were measured using Enzyme-Linked Immuno-Sorbent Assay(ELISA). Results:Analysis of all 233 participants showed that ApoM levels were positively correlated with age (r＝0.284, p＜0.001), total cholesterol (TC;r＝0.477, p＜0.001), HDL-cholesterol (HDL-C;r＝0.234, p＜0.001) and lowdensity lipoprotein cholesterol (LDL-C;r＝0.331, p＜0.001). Higher ApoM levels were correlated with shorter activated partial thromboplastin time(APTT;r＝－0.226,p＝0.001) and prothrombin time(PT,％;r＝0.326,p＜ 0.001). Separate analysis of the 115 healthy controls showed that ApoM levels were positively correlated with age, TC, HDL-C and LDL-C, and higher ApoM levels were correlated with shorter PT. Conclusion:Serum levels of ApoM may influence biomarkers of coagulation

Dietary oleic acid contributes to the regulation of food intake through the synthesis of intestinal oleoylethanolamide

IntroductionAmong the fatty acid ethanolamides (FAEs), oleoylethanolamide (OEA), linoleoylethanolamide (LEA), and palmitoylethanolamide (PEA) are reported to be involved in feeding regulation. In particular, OEA is well characterized as a satiety signal. Following food consumption, OEA is synthesized from oleic acid (OA) via an N-acyl phosphatidylethanolamine-specific phospholipase D-dependent pathway in the gastroenterocytes, and OEA induces satiety by recruiting sensory fibers. Thus, we hypothesized that dietary OA is an important satiety-inducing molecule. However, there has been no direct demonstration of the effect of dietary OA on satiety induction without the influence of the endogenous biosynthesis of OA from stearic acid (SA) or other FAEs.MethodsIn this study, we used two experimental diets to test our hypothesis: (i) an OA diet (OAD; 38.4 mg of OA/g and 7.2 mg of SA/g) and (ii) a low OA diet (LOAD; 3.1 mg of OA/g and 42.4 mg of SA/g).ResultsRelative to mice fed the OAD, mice fed the LOAD for two weeks exhibited reduced levels of jejunal OEA but not jejunal LEA and PEA. The LOAD-fed mice showed an increase in food intake and body weight gain. Moreover, LOAD-induced increase in food intake was immediately observed after the switch from the OAD, whereas these effects were diminished by the switch back to the OAD. Furthermore, treatment with OA and OEA diminished the effects of LOAD on food intake.ConclusionCollectively, these results show that dietary OA is a key factor in the reduction of food intake and increase in satiety mediated by OEA signaling