Effect of metformin administration on plasma advanced glycation end product levels in women with polycystic ovary syndrome

Diamanti-Kandarakis, Evanthia; Alexandraki, Krystallenia Ι.; Piperi, Christina; Aessopos, Athanasios; Paterakis, Thomas; Katsikis, Ilias; Panidis, Dimitrios

doi:10.1016/j.metabol.2006.09.006

Cited by 71 publications

(49 citation statements)

References 32 publications

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“…Metformin therapy reduced the atherogenic AGE molecules in the serum of women with polycystic ovary syndrome (Diamanti-Kandarakis et al, 2007). Our data showed that metformin attenuated the increase of HbA1c in diabetic rats (Table 1), the level of which is positively correlated with the serum level of AGEs (Jaku s et al, 2014).…”

Section: Discussionmentioning

confidence: 52%

Metformin Restores Intermediate-Conductance Calcium-Activated K⁺Channel– and Small-Conductance Calcium-Activated K⁺Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery

et al. 2014

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The present study was designed to investigate the effect of metformin on the impairment of intermediate-conductance and small-conductance Ca 21-activated potassium channels (IK Ca and SK Ca )-mediated relaxation in diabetes and the underlying mechanism. The endothelial vasodilatation function of mesenteric arteries was assessed with the use of wire myography. Expression levels of IK Ca and SK Ca and phosphorylated Thr 172 of AMPactivated protein kinase (AMPK) were measured using Western blot technology. The channel activity was observed using a whole-cell patch voltage clamp. Reactive oxygen species (ROS) were measured using dihydroethidium and 29,79-dichlorofluorescein diacetate. Metformin restored the impairment of IK Ca -and SK Camediated vasodilatation in mesenteric arteries from streptozotocininduced type 2 diabetic rats and that from normal rats incubated with advanced glycation end products (AGEs) for 3 hours. In cultured human umbilical vein endothelial cells (HUVECs), 1 mM metformin reversed AGE-induced increase of ROS and attenuated AGEand H 2 O 2 -induced downregulation of IK Ca and SK Ca after longterm incubation (.24 hours). Short-term treatment (3 hours) with 1 mM metformin reversed the decrease of IK Ca and SK Ca currents induced by AGE incubation for 3 hours without changing the channel expression or the AMPK activation in HUVECs. These results are the first to demonstrate that metformin restored IK Ca -and SK Ca -mediated vasodilatation impaired by AGEs in rat mesenteric artery, in which the upregulation of channel activity and protein expression is likely involved.

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Section: Discussionmentioning

confidence: 52%

Metformin Restores Intermediate-Conductance Calcium-Activated K⁺Channel– and Small-Conductance Calcium-Activated K⁺Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery

et al. 2014

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“…However, in the present study we have no detected differences in NO levels between control and PCOS subjects either in basal conditions or after metformin treatment. In this sense, Kandarakis et al (2007) demonstrated that metformin reduced serum advanced glycation end products (AGEs), which are oxidative mediators [37]. Metformin has also been shown to have beneficial effects by improving arterial stiffness and endothelial function in young women with PCOS [38].…”

Section: Discussionmentioning

confidence: 99%

Metformin modulates human leukocyte/endothelial cell interactions and proinflammatory cytokines in polycystic ovary syndrome patients

et al. 2015

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“…A recent study (457) was designed to evaluate the effect of metformin on AGEs. This study involved 22 patients with PCOS who undertook metformin therapy for 6 months.…”

Section: G Endothelial Impairmentmentioning

confidence: 99%

Evidence-Based and Potential Benefits of Metformin in the Polycystic Ovary Syndrome: A Comprehensive Review

et al. 2008

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Metformin is an insulin sensitizer widely used for the treatment of patients affected by type 2 diabetes mellitus. Because many women with polycystic ovary syndrome (PCOS) are insulin resistant, metformin was introduced in clinical practice to treat these patients also. Moreover, metformin's effect has other targets beside its insulin-sensitizing action. The present review was aimed at describing all evidence-based and potential uses of metformin in PCOS patients. In particular, we will analyze the uses of metformin not only for the treatment of all PCOS-related disturbances such as menstrual disorders, anovulatory infertility, increased abortion, or complicated pregnancy risk, hyperandrogenism, endometrial, metabolic and cardiovascular abnormalities, but also for the prevention of the syndrome. (Endocrine Reviews 30: 1-50, 2009)

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Effect of metformin administration on plasma advanced glycation end product levels in women with polycystic ovary syndrome

Cited by 71 publications

References 32 publications

Metformin Restores Intermediate-Conductance Calcium-Activated K⁺Channel– and Small-Conductance Calcium-Activated K⁺Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery

Metformin Restores Intermediate-Conductance Calcium-Activated K⁺Channel– and Small-Conductance Calcium-Activated K⁺Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery

Metformin modulates human leukocyte/endothelial cell interactions and proinflammatory cytokines in polycystic ovary syndrome patients

Evidence-Based and Potential Benefits of Metformin in the Polycystic Ovary Syndrome: A Comprehensive Review

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Effect of metformin administration on plasma advanced glycation end product levels in women with polycystic ovary syndrome

Cited by 71 publications

References 32 publications

Metformin Restores Intermediate-Conductance Calcium-Activated K+Channel– and Small-Conductance Calcium-Activated K+Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery

Metformin Restores Intermediate-Conductance Calcium-Activated K+Channel– and Small-Conductance Calcium-Activated K+Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery

Metformin modulates human leukocyte/endothelial cell interactions and proinflammatory cytokines in polycystic ovary syndrome patients

Evidence-Based and Potential Benefits of Metformin in the Polycystic Ovary Syndrome: A Comprehensive Review

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Metformin Restores Intermediate-Conductance Calcium-Activated K⁺Channel– and Small-Conductance Calcium-Activated K⁺Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery

Metformin Restores Intermediate-Conductance Calcium-Activated K⁺Channel– and Small-Conductance Calcium-Activated K⁺Channel–Mediated Vasodilatation Impaired by Advanced Glycation End Products in Rat Mesenteric Artery