Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to verify the effect of a Chinese herbal medicine Jiang-Zhi Zhong-Yao-Pian to reduce serum lipoid. Efficacy was observed in 30 cases of hyperlipemia; 20 cases administered with evening primose oil capsules were taken as controls. Each group took drugs for two or three months. The results were as follows: After treatment as compared with before treatment, the serum levels of TC, TG and TXB2 dropped from 264.28 +/- 70.52 mg%, 393.52 +/- 250.42 mg% and 110.75 +/- 43.52 pg/ml to 225.60 +/- 50.93 mg%, 264.97 +/- 252.81 mg% and 88.82 +/- 46.50 pg/ml respectively (P less than 0.001, less than 0.01, less than 0.05). However, in the group taking evening primrose oil capsules, TC, TG and TXB2 in comparing with the pre-treatment levels were changed from 251.33 +/- 58.24 mg%, 316.35 +/- 104.93 mg% and 131.53 +/- 49.77 pg/ml to 244.30 +/- 43.28 mg%, 272.10 +/- 92.52 mg% and 115.33 +/- 47.49 pg/ml respectively (P greater than 0.05, less than 0.05, greater than 0.05). This medicine had no side-effect. The results showed that the herbal formula might be useful to reduce serum TC, TG and TXB2.
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PMID:[Effect of jiang-zhi zhong-yao-pian on total cholesterol, triglyceride, TXB2, 6-keto-PGF1 alpha in hyperlipemic patients]. 205 86

A total of 51 cases with hyperlipidemia, who were defined deficiency symptom-complex complicated by symptoms of excessiveness in TCM were studied clinically. The patients were divided into two groups at random. One group was treated with Xiaobu Jianfei Pian (XJP) as treated group, another with Fangfeng Tongsheng San as a control. It was found that XJP was able to lower total serum cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein (apo) B significantly (P less than 0.001, 0.001, 0.001) while it had markedly improved clinical symptoms. It was also observed that XJP had good effects on the ratios of apoA1/B and TC/HDL-C, and was able to reduce body weight index. All of these were better than those of the control group statistically. These evidences indicate that XJP possesses clinical therapeutic effects on both lipid-lowering and lipid-adjusting, which suggest that XJP may be an effective anti-hyperlipidemia medicine.
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PMID:[Hyperlipidemia treated with xiaobu jianfei pian]. 226 40

More than half of the patients with angiographically confirmed premature coronary heart disease (CHD) have a familial lipoprotein disorder. Familial combined hyperlipidaemia (FCHL) represents the most common genetic dyslipidemia with a prevalence of 1.0-2.0%. FCHL is estimated to cause 10-20% of premature CHD and is characterized by elevated levels of cholesterol, triglycerides, or both. Attempts to characterize genes predisposing to FCHL have been hampered by its equivocal phenotype definition, unknown mode of inheritance and genetic heterogeneity. In order to minimize genetic heterogeneity, we chose 31 extended FCHL families from the isolated Finnish population that fulfilled strictly defined criteria for the phenotype status. We performed linkage analyses with markers from ten chromosomal regions that contain lipid-metabolism candidate genes. One marker, D1S104, adjacent to the apolipoprotein A-II (APOA2) gene on chromosome 1, revealed a lod score of Z = 3.50 assuming a dominant mode of inheritance. Multipoint analysis combining information from D1S104 and the neighbouring marker D1S1677 resulted in a lod score of 5.93. Physical positioning of known genes in the area (APOA2 and three selectin genes) outside the linked region suggests a novel locus for FCHL on 1q21-q23. A second paper in this issue (Castellani et al.) reports the identification of a mouse combined hyperlipidaemia locus in the syntenic region of the mouse genome, thus further implicating a gene in this region in the aetiology of FCHL.
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PMID:Linkage of familial combined hyperlipidaemia to chromosome 1q21-q23. 953 21

Through a positional cloning approach, the thioredoxin-interacting protein gene (Txnip) was recently identified as causal for a form of combined hyperlipidemia in mice (Bodnar, J. S., A. Chatterjee, L. W. Castellani, D. A. Ross, J. Ohmen, J. Cavalcoli, C. Wu, K. M. Dains, J. Catanese, M. Chu, S. S. Sheth, K. Charugundla, P. Demant, D. B. West, P. de Jong, and A. J. Lusis. 2002. Positional cloning of the combined hyperlipidemia gene Hyplip1. Nat. Genet. 30: 110-116). We now show that Txnip-deficient mice in the fed state exhibit a metabolic profile similar to fasted mice, including increased levels of plasma ketone bodies and free fatty acids, decreased glucose, and increased hepatic expression of peroxisome proliferator-activated receptor-gamma coactivator-1alpha, phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, and acyl-CoA oxidase. Dramatic differences in the expression of key metabolic enzymes were also observed in other tissues, and the fat-to-muscle ratio of Txnip-deficient mice was increased by approximately 40%. We demonstrate an effect of Txnip on the redox status, as the Txnip-deficient mice in the fed state had a significant increase in the ratio of NADH to NAD(+). Surprisingly, we observed that Txnip-deficient mice and wild-type mice had similar levels of thioredoxin activity, suggesting that the effects of Txnip deficiency may be mediated in part by other interactions. These results indicate a role for Txnip in the metabolic response to feeding and the maintenance of the redox status.
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PMID:Thioredoxin-interacting protein deficiency disrupts the fasting-feeding metabolic transition. 1552 Apr 47