Showing papers by "Nobuhiro Yamada published in 1993"
326 citations
TL;DR: Results demonstrate that the C-terminal region of human LPL is closely associated with the expression of enzyme mass and catalytic activity and shows that LPL-446 (Ser447-->stop), which is considered to be a common polymorphic form of LPL, exhibited higher activity than normal LPL (185% in medium).
87 citations
TL;DR: The expression of PDGF-beta receptor on human monocyte-derived macrophages suggests that PDGF influences the process of atherosclerosis by regulating the function of macrophage as well as smooth muscle cells in the vascular wall.
67 citations
TL;DR: It is suggested that subjects with apolipoprotein E4 should be controlled more strictly than other subjects from a viewpoint of reducing plasma cholesterol levels, as this study found total plasma cholesterol response to in-hospital diet therapy varies by apoliprotein E phenotypes.
Abstract: OBJECTIVE To investigate the effects of apolipoprotein E phenotype, which is an important genetic factor determining plasma cholesterol level, on plasma lipoprotein metabolism during a 7-day diet therapy of diabetes. RESEARCH DESIGN AND METHODS Diet therapy was performed in 242 subjects with NIDDM. Plasma lipid levels and apolipoprotein A-I, B, and E levels on hospital days 2 and 9 were compared in three phenotype groups, e2 (E2/2, and E2/3), e3 (E3/3), and e4 (E3/4 and E4/4). RESULTS No differences were observed in fasting blood glucose level, body mass index, age, duration of NIDDM, or medication among the three phenotype groups. Before starting the treatment, total plasma cholesterol did not vary by apolipoprotein E phenotype, although the mean plasma low-density lipoprotein cholesterol level in epsilon 4 patients was higher than in either e3 or e2 patients (e4, 145 ± 42; e3, 131 ± 34; e2, 128 ± 36 mg/dl; P P CONCLUSIONS Total plasma cholesterol response to in-hospital diet therapy varies by apolipoprotein E phenotypes, with subjects with apolipoprotein E2 showing the greatest response, whereas those with apolipoprotein E4 show the least. We suggest that subjects with apolipoprotein E4 should be controlled more strictly than other subjects from a viewpoint of reducing plasma cholesterol levels.
23 citations
TL;DR: It is concluded that the recruitment of monocyte/macrophages into injured nerves is enhanced in diabetes, thereby causing derangement of neural apo E metabolism, which might contribute to the development of diabetic neuropathy.
Abstract: Apolipoprotein (apo) E secreted by macrophages plays an important role in nerve injury and repair. We investigated the disturbance of neural apo E metabolism in diabetic rats and its relation to diabetic neuropathy. In BB/W rats, genetically diabetes prone rats, the secretion of apo E from sciatic nerves was 3-fold greater than that in control rats. Furthermore, a similar enhancement of apo E secretion was observed in injured nerves of STZ-induced diabetic rats (2-fold) as compared with those of nondiabetic rats, and this was reversible with insulin treatment. Histological examination of the nerves revealed more extensive infiltration of mononuclear cells in the injured nerves of STZ-induced diabetic rats than in those of non-diabetic rats. This is consistent with the findings that chemotactic activities for mononuclear cells, which were released from injured nerves, were greater in the STZ-induced diabetic rats than in the non-diabetic rats. From these results we conclude that the recruitment of monocyte/macrophages into injured nerves is enhanced in diabetes, thereby causing derangement of neural apo E metabolism. These abnormalities might contribute to the development of diabetic neuropathy.
10 citations
Journal Article•
TL;DR: The results indicate that the elevated plasma apo E in LCAT deficiency was related not only to the lack of LCAT in the plasma, but also to fat intake, and a low-fat diet may be effective in correcting lipid abnormalities.
Abstract: To study the metabolic abnormalities in familial lecithin-cholesterol acyltransferase (LCAT) deficiency, the effects of a long-term, low-fat diet and LCAT replacement therapy on plasma lipids and apolipoproteins were investigated in a patient with LCAT deficiency. The patient had elevated triglycerides (TG, 543.7 mg/dl) and phospholipids (PL, 350.3 mg/dl) and normal total cholesterol (TC, 206.9 mg/dl). Change to a low-fat diet reduced TC and TG by 20% and 75%, respectively. These reductions occurred mainly in the d < 1.006 fraction. At baseline, the patient had normal apolipoprotein B (apo B), low apolipoprotein A-I (apoA-I) and apolipoprotein A-II (apoA-II) and elevated apolipoprotein E (apo E). Long-term treatment with a low-fat diet increased plasma apoA-I and decreased apo E. However, urinary protein excretion did not change throughout the observed period. LCAT replacement with fresh frozen plasma (FFP) after the low-fat diet further reduced plasma apo E to the normal range. These results indicate that the elevated plasma apo E in LCAT deficiency was related not only to the lack of LCAT in the plasma, but also to fat intake. A low-fat diet may be effective in correcting lipid abnormalities. Moreover, plasma apo E may be a good indicator of the efficacy of diet therapy.
5 citations