Pub. Date : 2008 Jun 21
PMID : 18570670
10 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Important genetic checkpoints for insulin resistance in salt-sensitive (S) Dahl rats. | Salts | insulin | Homo sapiens |
| 2 | Insulin resistance is a multifactorial disease with both genetic and environmental factors (such as high salt) involved in its pathogenesis. | Salts | insulin | Homo sapiens |
| 3 | High salt triggers insulin resistance in genetically susceptible patients and animal models of insulin resistance. | Salts | insulin | Homo sapiens |
| 4 | High salt triggers insulin resistance in genetically susceptible patients and animal models of insulin resistance. | Salts | insulin | Homo sapiens |
| 5 | One of the mechanisms by which high salt might precipitate insulin resistance is through its ability to enhance an oxidative stress-induced inflammatory response that disrupts the insulin signaling pathway. | Salts | insulin | Homo sapiens |
| 6 | One of the mechanisms by which high salt might precipitate insulin resistance is through its ability to enhance an oxidative stress-induced inflammatory response that disrupts the insulin signaling pathway. | Salts | insulin | Homo sapiens |
| 7 | The aim of this hypothesis is to discuss two complementary approaches to find out how high salt might interact with genetic defects along the insulin signaling and inflammatory pathways to predispose to insulin resistance in a genetically susceptible model of insulin resistance. | Salts | insulin | Homo sapiens |
| 8 | The aim of this hypothesis is to discuss two complementary approaches to find out how high salt might interact with genetic defects along the insulin signaling and inflammatory pathways to predispose to insulin resistance in a genetically susceptible model of insulin resistance. | Salts | insulin | Homo sapiens |
| 9 | The aim of this hypothesis is to discuss two complementary approaches to find out how high salt might interact with genetic defects along the insulin signaling and inflammatory pathways to predispose to insulin resistance in a genetically susceptible model of insulin resistance. | Salts | insulin | Homo sapiens |
| 10 | The second approach will consist of studying the over-expressed genes along the inflammatory pathway whose respective activation might be predictive of high salt-induced insulin resistance in Dahl S rats. | Salts | insulin | Homo sapiens |