Influence of CYP2C9 gene polymorphisms on response to glibenclamide in type 2 diabetes mellitus patients

Pradhan, S.C.; Agrawal, Alpna; Subrahmanyam, D. K. S.; Rajan, S; Anichavezhi, D.; Chandrasekaran, Adithan

doi:10.1007/s00228-011-1013-8

Cited by 42 publications

(39 citation statements)

References 19 publications

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“…Of importance was the observation that insulin inhibits increased expression of CYP4A in diabetic rats. There are a number of studies associating sEH polymorphisms with insulin resistance in T2DM; however, there seems to be no association of variant alleles of CYP2C9, CYP2C8 or CYP2CJ2 in humans with either T1DM or T2DM (Surendiran et al, 2011). Further studies are necessary to determine the role of CYP2C and CYP4A AA metabolites in the function of β-cells and exocrine islet function in GSIS in hyperglycemia.…”

Section: Eicosanoids and Mets Diseasesmentioning

confidence: 99%

Eicosanoids in Metabolic Syndrome

Hardwick

Eckman

Lee

et al. 2013

Advances in Pharmacology

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Chronic persistent inflammation plays a significant role in disease pathology of cancer, cardiovascular disease, and metabolic syndrome (MetS). MetS is a constellation of diseases that include obesity, diabetes, hypertension, dyslipidemia, hypertriglyceridemia, and hypercholesterolemia. Nonalcoholic fatty liver disease (NAFLD) is associated with many of the MetS diseases. These metabolic derangements trigger a persistent inflammatory cascade, which includes production of lipid autacoids (eicosanoids) that recruit immune cells to the site of injury and subsequent expression of cytokines and chemokines that amplify the inflammatory response. In acute inflammation, the transcellular synthesis of antiinflammatory eicosanoids resolve inflammation, while persistent activation of the autacoid-cytokine-chemokine cascade in metabolic disease leads to chronic inflammation and accompanying tissue pathology. Many drugs targeting the eicosanoid pathways have been shown to be effective in the treatment of MetS, suggesting a common linkage between inflammation, MetS and drug metabolism.The cross-talk between inflammation and MetS seems apparent because of the growing evidence linking immune cell activation and metabolic disorders such as insulin resistance, dyslipidemia, and hypertriglyceridemia. Thus modulation of lipid metabolism through either dietary adjustment or selective drugs may become a new paradigm in the treatment of metabolic disorders. This review focuses on the mechanisms linking eicosanoid metabolism to persistent inflammation and altered lipid and carbohydrate metabolism in MetS.

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Section: Eicosanoids and Mets Diseasesmentioning

confidence: 99%

Eicosanoids in Metabolic Syndrome

Hardwick

Eckman

Lee

et al. 2013

Advances in Pharmacology

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“…CYP2C9 polymorphism displays a better response to anti-diabetic medicine in T2DM patients [150; 151], but carries a high risk of hypoglycemia, raising the possibility of a pharmacogenetic interaction [152]. Increased prevalence of the CYP2C8*4 mutation has been found in T2DM patients [153].…”

Section: Eicosanoids and Diabetesmentioning

confidence: 99%

Eicosanoids, β-cell function, and diabetes

Luo

Wang

2011

Prostaglandins & Other Lipid Mediators

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Arachidonic acid (AA) is metabolized by cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP) enzymes into eicosanoids, which are involved in diverse diseases, including type 1 and type 2 diabetes. During the last thirty years, evidence has been accumulated that suggests important functions for eicosanoids in the control of pancreatic β-cell function and destruction. AA metabolites of the COX pathway, especially prostaglandin E2 (PGE2), appear to be significant factors to β-cell dysfunction and destruction, participating in the pathogenesis of diabetes and its complications. Several elegant studies have contributed to the sorting out of the importance of 12-LOX eicosanoids in cytokine-mediated inflammation in pancreatic β cells. The role of CYP eicosanoids in diabetes is yet to be explored. A recent publication has demonstrated that stabilizing the levels of epoxyeicosatrienoic acids (EETs), CYP eicosanoids, by inhibiting or deleting soluble epoxide hydrolase (sEH) improves β-cell function and reduces β-cell apoptosis in diabetes. In this review we summarize recent findings implicating these eicosanoid pathways in diabetes and its complications. We also discuss the development of animal models with targeted gene deletion and specific enzymatic inhibitors in each pathway to identify potential targets for the treatment of diabetes and its complications.

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“…In 2011, Surendiran et al found a significant association between CYP2C9*1/*1 genotypes and the lack of control of diabetic Hindi patients receiving combined therapy with metformin and glibenclamide [4].…”

mentioning

confidence: 99%

“…This disease has a prevalence of 14%, and it is calculated that in Mexico there are 8 million diabetic patients; 85% of them are treated with oral hypoglycemics, mainly sulfonylureas, metformin, or both [3]. Hypoglycemic agents like glibenclamide are metabolized mainly by CYP2C9 [4]. Glibenclamide and a combination of this with metformin are the best-selling glycemia-control drugs in Mexico, and this particular market has shown a general rising trend, with an increase of 141% between 1999 and 2003 [5].…”

mentioning

confidence: 99%

Present status and perspective of pharmacogenetics in Mexico

Cuautle‐Rodríguez¹,

LLerena²,

Molina-Güarneros

2013

Drug Metabolism and Drug Interactions

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Drug costs account for up to 24% of the country's health expenditure and there are 13,000 registered drugs being prescribed. Diabetes is the main cause of death in the country, with over 85% of diabetic patients currently under drug treatment. The importance of knowing interindividual variability in drug metabolism on Mexican populations is thus evident. The purpose of this article is to provide an overlook of the current situation of pharmacogenetic research in Mexico, focusing on drug-metabolizing enzymes, and the possibility of developing a phenotyping cocktail for Mexican populations. So far, 21 pharmacogenetic studies on Mexican population samples (Mestizos and Amerindian) have been published. These have reported interindividual variability through phenotyping and/or genotyping cytochromes: CYP2D6, 2C19, 2C9, 2E1, and phase II enzymes UGT and NAT2. Some cytochromes with important clinical implications have not yet been phenotyped in Mexican populations. The development of a cocktail adapted to them could be a significant contribution to a larger knowledge on drug response variability at a lower price and shorter time. There are validated phenotyping cocktails that present several practical advantages, being valuable, safe, and inexpensive tools in drug metabolism characterization, which require only a single experiment to provide information on several cytochrome activities.

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Influence of CYP2C9 gene polymorphisms on response to glibenclamide in type 2 diabetes mellitus patients

Cited by 42 publications

References 19 publications

Eicosanoids in Metabolic Syndrome

Eicosanoids in Metabolic Syndrome

Eicosanoids, β-cell function, and diabetes

Present status and perspective of pharmacogenetics in Mexico

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