ABCA1 p.Leu162Val
| Predicted by SNAP2: | A: N (72%), C: N (66%), D: D (66%), E: D (59%), F: N (87%), G: D (53%), H: N (66%), I: N (87%), K: N (57%), M: N (93%), N: N (61%), P: N (57%), Q: N (72%), R: N (61%), S: N (66%), T: N (82%), V: N (87%), W: N (53%), Y: N (82%), |
| Predicted by PROVEAN: | A: N, C: N, D: D, E: N, F: N, G: D, H: D, I: N, K: N, M: N, N: D, P: N, Q: N, R: N, S: N, T: N, V: N, W: D, Y: N, |
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[hide] PPARS, metabolic disease and atherosclerosis. Pharmacol Res. 2001 Nov;44(5):345-52. Fruchart JC, Staels B, Duriez P
PPARS, metabolic disease and atherosclerosis.
Pharmacol Res. 2001 Nov;44(5):345-52., [PMID:11712864]
Abstract [show]
PPAR-alpha belongs to the family of nuclear receptors. Activated PPAR-alpha stimulates the expression of genes involved in fatty acid and lipoprotein metabolism. PPAR-alpha activators, such as the normolipidaemic fibric acids, decrease triglyceride concentrations by increasing the expression of lipoprotein lipase and decreasing apo C-III concentration. Furthermore, they increase HDL-cholesterol by increasing the expression of apo A-I and apo A-II. PPAR-alpha activation by fibric acids improves insulin sensibility, and decreases thrombosis and vascular inflammation. PPAR-alpha activators (gemfibrozil) decrease the risk of coronary heart disease in patients with normal LDL-cholesterol and low HDL-cholesterol (VA-HIT) and they slow the progression of premature coronary atherosclerosis (BECAIT) (bezafibrate), particularly in patients with type 2 diabetes (DAIS) (fenofibrate).
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No. Sentence Comment
88 Two polymorphisms were detected in PPAR-alpha gene, one in intron 3 and a missense mutation, leucine 162 to valine, in the DNA binding domain [41].
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ABCA1 p.Leu162Val 11712864:88:93
status: NEW94 In another recent report [42] association studies were undertaken in two populations of type 2 diabetic patients from Pondichery and from France [L162V (exon 5) and A268V (exon 7) polymorphisms].
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ABCA1 p.Leu162Val 11712864:94:146
status: NEW[hide] Pharmacogenetics in diabetes. Curr Diab Rep. 2009 Apr;9(2):172-81. Pearson ER
Pharmacogenetics in diabetes.
Curr Diab Rep. 2009 Apr;9(2):172-81., [PMID:19323963]
Abstract [show]
Genetic variation can impact on efficacy and risk of adverse events to commonly used oral agents in -diabetes. Metformin is not metabolized and its mechanism of action remains debated; however, several cation transporters have been identified. Variation in these pharmacokinetic genes might influence metformin response. Conversely, although the cytochrome P450 system has been implicated in sulfonylurea response in some small studies, to date variants affecting pharmacodynamics, including those in ABCC8 (SUR1) and TCF7L2, are the most promising. For thiazolidinedione response, variants in PPARG or ADIPOQ (adiponectin) have been variably associated with response. With increasing well-phenotyped cohorts and new methods, including genome-wide association studies, the next few years offer great hope to use pharmacogenetics to unravel drug and disease mechanisms, as well as the possibility to individualize therapy by genotype.
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140 In a study of another glitazar (dual-acting PPAR-γ/-α agonists), ragaglitazar, edema was less in those carrying the protective Ala allele at Pro12Ala PPAR-γ than the wild-type patients, and was not influenced by the Leu162Val SNP in PPAR-α [53].
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ABCA1 p.Leu162Val 19323963:140:234
status: NEW