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je propose , que quand vous allez voir vos medecins pour des maladies , acheter les medicaments et envoyer les en Algerie , il ya a des malades qui en besoins et vous envoies les plantes pour soigner vol mal .
Recemment, des chercheurs Americains ont demontre que l'effet hypoglycemiant de la metformine est le resultat du changement dans la microbiote des intestins. Ils admettent qu'on ne sait meme pas que ces medicaments utilises depuis longtemps marchent.
New mechanisms of metformin action: Focusing on mitochondria and the gut
Kyu Yeon Hur and Myung-Shik Lee*
Division of Endocrinology & Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
* Correspondence Myung-Shik Lee, Tel.: +82-2-3410-3436, Fax: +82-2-3410-6491, E-mail address: ude.ukks@3290eelsm
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Abstract
The most well-known mechanism of metformin action, one of the most commonly prescribed antidiabetic drugs, is adenosine monophosphate-activated protein kinase activation; however, recent investigations have shown that adenosine monophosphate-activated protein kinase-independent pathways can explain some of metformin's beneficial metabolic effects as well as undesirable side-effects. Such novel pathways include induction of mitochondrial stress, inhibition of mitochondrial shuttles, alteration of intestinal microbiota, suppression of glucagon signaling, activation of autophagy, attenuation of inflammasome activation, induction of incretin receptors and reduction of terminal endoplasmic reticulum stress. Together, these studies have broadened our understanding of the mechanisms of antidiabetic agents as well as the pathogenic mechanism of diabetes itself. The results of such investigations might help to identify new target molecules and pathways for treatment of diabetes and metabolic syndrome, and could also have broad implications in diseases other than diabetes. Accordingly, new antidiabetic drugs with better efficacy and fewer adverse effects will likely result from these studies.
Kyu Yeon Hur and Myung-Shik Lee*
Division of Endocrinology & Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea
* Correspondence Myung-Shik Lee, Tel.: +82-2-3410-3436, Fax: +82-2-3410-6491, E-mail address: ude.ukks@3290eelsm
Author information ▼ Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
Go to:
Abstract
The most well-known mechanism of metformin action, one of the most commonly prescribed antidiabetic drugs, is adenosine monophosphate-activated protein kinase activation; however, recent investigations have shown that adenosine monophosphate-activated protein kinase-independent pathways can explain some of metformin's beneficial metabolic effects as well as undesirable side-effects. Such novel pathways include induction of mitochondrial stress, inhibition of mitochondrial shuttles, alteration of intestinal microbiota, suppression of glucagon signaling, activation of autophagy, attenuation of inflammasome activation, induction of incretin receptors and reduction of terminal endoplasmic reticulum stress. Together, these studies have broadened our understanding of the mechanisms of antidiabetic agents as well as the pathogenic mechanism of diabetes itself. The results of such investigations might help to identify new target molecules and pathways for treatment of diabetes and metabolic syndrome, and could also have broad implications in diseases other than diabetes. Accordingly, new antidiabetic drugs with better efficacy and fewer adverse effects will likely result from these studies.
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