Metformin

Bailey, Clifford J.; Turner, R. C.

doi:10.1056/nejm199602293340906

Cited by 1,814 publications

(1,382 citation statements)

References 57 publications

Supporting

Mentioning

1,319

Contrasting

Unclassified

Order By: Relevance

“…Choosing specific diabetes interventions and their roles in treating type 2 diabetes Numerous reviews have focused on the characteristics of the specific diabetes interventions listed below [25][26][27][28][29][30][31][32][33][34]. In addition, meta-analyses and reviews have summarised and compared the glucose-lowering effectiveness and other characteristics of the medications [35][36][37].…”

Section: Non-glycaemic Effects Of Medicationsmentioning

confidence: 99%

Medical management of hyperglycaemia in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of therapy

et al. 2008

View full text Add to dashboard Cite

The consensus algorithm for the medical management of type 2 diabetes was published in August 2006 with the expectation that it would be updated, based on the availability of new interventions and new evidence to establish their clinical role. The authors continue to endorse the principles used to develop the algorithm and its major features. We are sensitive to the risks of changing the algorithm cavalierly or too frequently, without compelling new information. An update to the consensus algorithm published in January 2008 specifically addressed safety issues surrounding the thiazolidinediones. In this revision, we focus on the new classes of medications that now have more clinical data and experience.

show abstract

Section: Non-glycaemic Effects Of Medicationsmentioning

confidence: 99%

Medical management of hyperglycaemia in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of therapy

et al. 2008

View full text Add to dashboard Cite

show abstract

“…Although most of the genes in these pathways were not included in the initial list of 72 differentially expressed genes identified from comparison analysis, the derived pathways are closely related to the physiological action of metformin [1,5,8]. The pathways mentioned above were not obtained when metformin-treated animals (n=10), including both 50 and 400 mg/kg treatment conditions, were compared with the remaining animal groups, i.e.…”

Section: Metformin Causes Down-regulation Of G6pc In Vitromentioning

confidence: 99%

“…The action of metformin in ameliorating hyperglycaemia is linked to its ability to reduce hepatic gluconeogenesis and to improve peripheral insulin sensitivity [1,2]. Metformin promotes glucose uptake in muscle [3,4] and lowers hepatic glucose production [5,6].…”

Section: Introductionmentioning

confidence: 99%

Global gene expression analysis in liver of obese diabetic db/db mice treated with metformin

et al. 2006

View full text Add to dashboard Cite

Aims/hypothesis: Metformin is widely used as a hypoglycaemic reagent for type 2 diabetes. While the reduction of hepatic gluconeogenesis is thought to be a key effect, the detailed molecular mechanism of action of metformin remains to be elucidated. To gain insight into this, we performed a global gene expression profiling study. Materials and methods: We performed DNA microarray analysis to study global gene expression in the livers of obese diabetic db/db mice 2 h after a single administration of metformin (400 mg/kg). Results: This analysis identified 14 genes that showed at least a 1.5-fold difference in expression following metformin treatment, including a reduction of glucose-6-phosphatase gene expression. The mRNA levels of glucose-6-phosphatase showed one of the best correlations with blood glucose levels among 12,000 genes. Enzymatic activity of glucose-6-phosphatase was also reduced in metformin-treated liver. Moreover, intensive analysis of the expression profile revealed that metformin effected significant alterations in gene expression across at least ten metabolic pathways, including those involved in glycolysis-gluconeogenesis, fatty acid metabolism and amino acid metabolism. Conclusions/interpretation: These results suggest that reduction of glucose-6-phosphatase activity, as well as suppression of mRNA expression levels of this gene, in liver is of prime importance for controlling blood glucose levels in vivo, at least at early time points after metformin treatment. Our results also suggest that metformin not only affects expression of specific genes, but also alters the expression level of multiple genes linked to the metabolic pathways involved in glucose and lipid metabolism in the liver.

show abstract

“…Based on these pathophysiological considerations, correcting the insulin resistance and substituting insulin is the current mainstay of diabetes therapy. To achieve the former goal, metformin (Bailey and Turner 1996) and pioglitazone (Nesto et al 2003;Yki-Jarvinen 2004) are available. Insulin can be substituted either directly by (in most cases SC) injection or by indirect means to elicit liberation from stores in the pancreas.…”

mentioning

confidence: 99%

“…There are already substance classes available with this property (e.g. biguanides and thiazolidinediones; for review of their desired and undesired effects, see for example Bailey and Turner 1996;Nesto et al 2003;Yki-Jarvinen 2004). But the glucose-lowering effect of each individual compound is usually rather small so that antidiabetics of different classes are often combined.…”

mentioning

confidence: 99%

Chances and risks of SGLT2 inhibitors

Mayer

2011

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

Metformin

Cited by 1,814 publications

References 57 publications

Medical management of hyperglycaemia in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of therapy

Medical management of hyperglycaemia in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of therapy

Global gene expression analysis in liver of obese diabetic db/db mice treated with metformin

Chances and risks of SGLT2 inhibitors

Contact Info

Product

Resources

About