|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Common genetic variations in CLOCK transcription factor are associated with nonalcoholic fatty liver disease显示文摘AIM: To investigate the role of gene variants and derived haplotypes of the CLOCK transcription factor in nonalcoholic fatty liver disease (NAFLD) and their relation with the disease severity. METHODS: A total of 136 patients with NAFLD and 64 healthy individuals were studied. Liver biopsy was performed in 91 patients. Six tag SNPs showing a minor allele frequency > 10% (rs1554483 C/G; rs11932595 A/G; rs4580704 C/G; rs6843722 A/C; rs6850524 C/G and rs4864548 A/G) encompassing 117 kb of chromosome 4 and representing 115 polymorphic sites (r2 > 0.8) were genotyped. RESULTS: rs11932595 and rs6843722 showed signifi cant associations with NAFLD (empiric P = 0.0449 and 0.023, respectively). A significant association was also observed between clinical or histologic spectrum of NAFLD and rs1554483 (empiric P = 0.0399), rs6843722 (empiric P = 0.0229) and rs6850524 (empiric P = 0.00899) and between fibrosis score and rs1554483 (empiric P = 0.02697), rs6843722 (empiric P = 0.01898) and rs4864548 (empiric P = 0.02697). Test of haplotypic association showed that CLOCK gene variant haplotypes frequencies in NAFLD individuals significantly differed from those in controls (empiric P = 0.0097). CONCLUSION: Our study suggests a potential role of the CLOCK polymorphisms and their haplotypes insusceptibility to NAFLD and disease severity. | Silvia Sookoian Gustavo Castao Carolina Gemma Tomas Fernández Gianotti Carlos Jose Pirola | 2007 | World Journal of Gastroenterology2007,13,31: | 5 |
| 2 | Role of ABCC2 common variants in intrahepatic cholestasis of pregnancy显示文摘The pathogenesis of intrahepatic cholestasis of pregnancy (ICP), a disorder that adversely affects maternal wellbeing and fetal outcome, is unclear. However, multiple factors probably interact along with a genetic predisposition. We would like to add some comments on a paper recently published concerning the role of ABCB11 and ABCC2 polymorphisms in both ICP and contraceptive-induced cholestasis, especially in the light of our recently published findings about a positive association between ICP and ABCC2 common variants. | Silvia Sookoian Gustavo Castao Carlos J Pirola | 2008 | World Journal of Gastroenterology2008,14,13: | 4 |
| 3 | Epigenetic modification of liver mitochondrial DNA is associated with histological severity of nonalcoholic fatty liver disease显示文摘 | Carlos Jose Pirola Tomas Fernández Gianotti Adriana Laura Burgue?o Manuel Rey-Funes Cesar Fabian Loidl Pablo Mallardi Julio San Martino Gustavo Osvaldo Casta?o S Sookoian | 2013 | Gut2013,,9: | 2 |
| 4 | Protein acetylation mechanisms in the regulation of insulin and insulin-like growth factor 1signalling显示文摘 | Pirola L Zerzaihi O Vidal H | 2012 | Mol Cell Endocrinol2012,362,12: | 1 |
| 5 | Protein acetylation mechanisms in the regulation of insulin and insulin-like growth factor 1 signalling显示文摘 | Pirola L Zerzaihi O Vidal H | 2012 | Mol Cell Endocrinol2012,362,12: | 1 |
| 6 | Genetic variation in transmembrane 6 superfamily member 2 and the risk of nonalcoholic fatty liver disease and histological disease severity显示文摘 | Silvia Sookoian Gustavo O. Casta?o Romina Scian Pablo Mallardi Tomas Fernández Gianotti Adriana L. Burgue?o Julio San Martino Carlos J. Pirola | 2015 | Hepatology2015,,2: | 1 |
| 7 | Circulating levels and hepatic expression of molecular mediators of atherosclerosis in nonalcoholic fatty liver disease显示文摘 | Silvia Sookoian Gustavo O. Casta?o Adriana L. Burgue?o María Soledad Rosselli Tomas Fernández Gianotti Pablo Mallardi Julio San Martino Carlos Jose Pirola | 2009 | Atherosclerosis2009,,2: | 1 |
| 8 | Effect of the flavanolignans of Silybum marianum L, on lipid peroxidation in rat liver microsomes and freshly isolated hepatocytes 显示文摘 | Bosisio E Benelli C Pirola O | 1992 | Pharmacol Res1992,25,2: | 1 |
| 9 | Protein acetylation mechanisms in the regulation of insulin and insulin-like growth factor 1 signalling显示文摘 | Pirola L Zerzaihi O Vidal H | | 0,,1: | 1 |
| 10 | Maternal low protein diet induces persistent expression changes in metabolic genes in male rats显示文摘BACKGROUND Perinatal exposure to a poor nutritional environment predisposes the progeny to the development of metabolic disease at the adult age,both in experimental models and humans.Numerous adaptive responses to maternal protein restriction have been reported in metabolic tissues.However,the expression of glucose/fatty acid metabolism-related genes in adipose tissue and liver needs to be described.AIM To evaluate the metabolic impact of perinatal malnutrition,we determined malnutrition-associated gene expression alterations in liver and adipose tissue.METHODS In the present study,we evaluated the alterations in gene expression of glycolytic/Krebs cycle genes(Pyruvate dehydrogenase kinase 4 and citrate synthase),adipogenic and lipolytic genes and leptin in the adipose tissue of offspring rats at 30 d and 90 d of age exposed to maternal isocaloric low protein(LP)diet throughout gestation and lactation.We also evaluated,in the livers of the same animals,the same set of genes as well as the gene expression of the transcription factors peroxisome proliferator-activated receptor gamma coactivator 1,forkhead box protein O1 and hepatocyte nuclear factor 4 and of gluconeogenic genes.RESULTS In the adipose tissue,we observed a transitory(i.e.,at 30 d)downregulation of pyruvate dehydrogenase kinase 4,citrate synthase and carnitine palmitoyl transferase 1b gene expression.Such transcriptional changes did not persist in adult LP rats(90 d),but we observed a tendency towards a decreased gene expression of leptin(P=0.052).The liver featured some gene expression alterations comparable to the adipose tissue,such as pyruvate dehydrogenase kinase 4 downregulation at 30 d and displayed other tissue-specific changes,including citrate synthase and fatty acid synthase upregulation,but pyruvate kinase downregulation at 30 d in the LP group and carnitine palmitoyl transferase 1b downregulation at 90 d.These gene alterations,together with previously described changes in gene expression in skeletal muscle,may account for the metabolic adaptations in response to maternal LP diet and highlight the occurrence of persistent transcriptional defects in key metabolic genes that may contribute to the development of metabolic alterations during the adult life as a consequence of perinatal malnutrition.CONCLUSION We conclude that perinatal malnutrition relays long-lasting transcriptional alterations in metabolically active organs,i.e.,liver and adipose tissue. | Allan de Oliveira Lira JoséLuiz de Brito Alves Mariana Pinheiro Fernandes Diogo Vasconcelos David Filipe Santana João Henrique da Costa-Silva Béatrice Morio Carol Góis Leandro Luciano Pirola | 2020 | World Journal of Diabetes2020,11,5: | 0 |