Mitochondrial complex I impairment in leukocytes from type 2 diabetic patients

Hernández‐Mijares, Antonio; Rocha, Milagros; Apostolova, Nadezda; Borrás, Consuelo; Jover, A; Bañuls, Celia; Solá, Eva; Víctor, Víctor M.

doi:10.1016/j.freeradbiomed.2011.01.019

Cited by 52 publications

(49 citation statements)

References 34 publications

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“…Although endothelial dysfunction and endothelial/leukocyte interactions are key features of diabetes and are thought to be a major cause of diabetes-associated vascular complications, the underlying molecular mechanisms remain unclear [14,15]. In the present study, we observed that serum myeloperoxidase levels were significantly increased in type 2 diabetic patients and also positively correlated with ACR indicating its relevance for diagnosis of vascular dysfunction.…”

Section: Discussionsupporting

confidence: 48%

Myeloperoxidase levels predicts the vascular dysfunction in patients with Type 2 Diabetes Mellitus

Santhi¹,

K²,

Shaik³

2017

IOSR JDMS

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Section: Discussionsupporting

confidence: 48%

Myeloperoxidase levels predicts the vascular dysfunction in patients with Type 2 Diabetes Mellitus

Santhi¹,

K²,

Shaik³

2017

IOSR JDMS

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“…UCP1 is expressed primarily in brown adipose tissue, UCP2 is ubiquitous, and UCP3 is present in skeletal muscle. 27 UCPs play important roles in decreasing ROS production and regulating mitochondrial apoptosis signals by hyperpolarizing the inner mitochondrial membrane. It has been demonstrated that ''mild uncoupling'' of the mitochondrial respiratory chain due to UCP2 activity allows a more rapid flux of electrons through the mitochondrial inner membrane, reducing membrane potential and decreasing ROS production.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of uncoupling protein-2 by genipin exacerbates diabetes-induced kidney proximal tubular cells apoptosis

Chen

Tang

et al. 2014

Renal Failure

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Renal tubular epithelial cell injury is a major pathological event that contributes to the development of diabetic kidney disease (DKD). Uncoupling protein-2 (UCP2), a mitochondrial membrane protein, has been reported to participate in the regulation of reactive oxygen species (ROS) generation, which contributes to tubular cell apoptosis induced by hyperglycemia. In this study, we found that genipin, a UCP2 inhibitor, dramatically boosted oxidative stress, attenuated antioxidative capacity, and exacerbated cell apoptosis accompanied with caspase-3 activation in rat renal proximal tubular cells (NRK-52E) incubated with high glucose. The present study results suggest that manipulation of UCP2 could be important in the prevention of oxidative stress damage in renal tubular epithelial cells induced by hyperglycemia in vitro.

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“…First we monitored the rate of O 2 consumption in PMNs from blood samples in an O 2 -tight chamber, as previously described (19,29). The O 2 requirement of the tissue was found to be mainly mitochondrial, since addition of sodium cyanide resulted in an almost complete (95-99%) inhibition of O 2 consumption (not shown).…”

Section: Mitochondrial O 2 Consumptionmentioning

confidence: 99%

Effects of metformin on mitochondrial function of leukocytes from polycystic ovary syndrome patients with insulin resistance

Víctor

Rovira‐Llopis

Bañuls

et al. 2015

European Journal of Endocrinology

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Objective: Oxidative stress and mitochondrial dysfunction are implicated in polycystic ovary syndrome (PCOS). The present study assesses the effect of metformin treatment on mitochondrial function in polymorphonuclear cells from PCOS subjects. Additionally, we evaluate endocrine parameters and levels of interleukin 6 (IL6) and tumour necrosis factor alpha (TNFa). Design and methods: Our study population was comprised of 35 women of reproductive age diagnosed with PCOS and treated with metformin for 12 weeks, and their corresponding controls (nZ41), adjusted by age and BMI. We evaluated the alteration of endocrinological and anthropometrical parameters and androgen levels. Mitochondrial O 2 consumption (using a Clark-type O 2 electrode), membrane potential, mitochondrial mass, and levels of reactive oxygen species (ROS) and glutathione (GSH) (by means of fluorescence microscopy) were assessed in poymorphonuclear cells. H 2 O 2 was evaluated with the Amplex Red R H 2 O 2 /Peroxidase Assay kit. IL6 and TNFa were measured using the Luminex 200 flow analyser system.Results: Metformin had beneficial effects on patients by increasing mitochondrial O 2 consumption, membrane potential, mitochondrial mass and glutathione levels, and by decreasing levels of reactive oxygen species and H 2 O 2 . In addition, metformin reduced glucose, follicle-stimulating hormone, IL6 and TNFa levels and increased dehydroepiandrosterone sulfate levels. HOMA-IR and mitochondrial function biomarkers positively correlated with ROS production (rZ0.486, PZ0.025), GSH content (rZ0.710, PZ0.049) and H 2 O 2 (rZ0.837, PZ0.010), and negatively correlated with membrane potential (rZK0.829, PZ0.011) at baseline. These differences disappeared after metformin treatment.Conclusions: Our results demonstrate the beneficial effects of metformin treatment on mitochondrial function in leukocytes of PCOS patients.

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Mitochondrial complex I impairment in leukocytes from type 2 diabetic patients

Cited by 52 publications

References 34 publications

Myeloperoxidase levels predicts the vascular dysfunction in patients with Type 2 Diabetes Mellitus

Myeloperoxidase levels predicts the vascular dysfunction in patients with Type 2 Diabetes Mellitus

Downregulation of uncoupling protein-2 by genipin exacerbates diabetes-induced kidney proximal tubular cells apoptosis

Effects of metformin on mitochondrial function of leukocytes from polycystic ovary syndrome patients with insulin resistance

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