Insulin resistance and oxidative stress in familial combined hyperlipidemia

Martínez-Hervás, Sergio; Fandos, Marta; Real, José T.; Espinosa, Olga; Chaves, Felipe Javier; Sáez, Guillermo; Salvador, Amparo; Cerda, C; Carmena, Rafael; Ascaso, Juan F.

doi:10.1016/j.atherosclerosis.2007.11.023

Cited by 34 publications

(24 citation statements)

References 29 publications

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“…This is due to prolonged exposure to ROS affects transcription of insulin receptor substrate-1 by involving serine/threonine phosphorylation. These data are in agreement with the observed increased OS in patients with IR versus non-IR from our study and in Martinez-Herbas et al [6]. Moreover, we have not observed an increase in OS between hypertensive subjects with and without MS.…”

Section: Resultssupporting

confidence: 94%

“…The increased oxidative stress (OS) is driven by the presence of the so-called cardiovascular (CV) risk factors and their impact on both pro-oxidant and antioxidant mechanisms. The CV risk factors, hypertension (HT), familial hypercholesterolemia (FH) and familial combined dyslipidemia (FHC), which produce and accelerate atherosclerosis also have increased OS levels [6–8]. The individual impact on the underlying OS mechanism of each CV risk factor, however, is not well known.…”

Section: Introductionmentioning

confidence: 99%

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Different Impacts of Cardiovascular Risk Factors on Oxidative Stress

Mansego

Redón

Martínez-Hervás

et al. 2011

IJMS

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The objective of the study was to evaluate oxidative stress (OS) status in subjects with different cardiovascular risk factors. With this in mind, we have studied three models of high cardiovascular risk: hypertension (HT) with and without metabolic syndrome, familial hypercholesterolemia (FH) and familial combined hyperlipidemia (FCH) with and without insulin resistance. Oxidative stress markers (oxidized/reduced glutathione ratio, 8-oxo-deoxyguanosine and malondialdehide) together with the activity of antioxidant enzyme triad (superoxide dismutase, catalase, glutathione peroxidase) and activation of both pro-oxidant enzyme (NAPDH oxidase components) and AGTR1 genes, as well as antioxidant enzyme genes (CuZn-SOD, CAT, GPX1, GSR, GSS and TXN) were measured in mononuclear cells of controls (n = 20) and patients (n = 90) by assessing mRNA levels. Activity of some of these antioxidant enzymes was also tested. An increase in OS and pro-oxidant gene mRNA values was observed in patients compared to controls. The hypertensive group showed not only the highest OS values, but also the highest pro-oxidant activation compared to those observed in the other groups. In addition, in HT a significantly reduced antioxidant activity and mRNA induction of antioxidant genes were found when compared to controls and the other groups. In FH and FCH, the activation of pro-oxidant enzymes was also higher and antioxidant ones lower than in the control group, although it did not reach the values obtained in hypertensives. The thioredoxin system was more activated in patients as compared to controls, and the highest levels were in hypertensives. The increased oxidative status in the presence of cardiovascular risk factors is a consequence of both the activation of pro-oxidant mechanisms and the reduction of the antioxidant ones. The altered response of the main cytoplasmic antioxidant systems largely contributes to OS despite the apparent attempt of the thioredoxin system to control it.

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Section: Resultssupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Different Impacts of Cardiovascular Risk Factors on Oxidative Stress

Mansego

Redón

Martínez-Hervás

et al. 2011

IJMS

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“…The aforementioned evidence leads to the idea that such fl avonoids, which are present in natural honey, could be exerting their antidiabetogenic, normoglycemic and normolipidemic properties at a molecular signaling level (Middleton et al, 2000;Havsteen, 2002;Sharma et al, 2008), mainly by decreasing the alterations caused by oxidative stress. The latter can be understood in light of the increasing acceptance by the scientifi c community that an imbalance in the oxidative state, such as that induced by abnormal ROS levels, is a phenomenon linked to cellular insulin resistance, dysglycemias and related pathologies (Evans et al, 2005;Eriksson, 2007;Martínez-Hervas et al, 2008;Choi et al, 2008). ROS accumulation can lead to the inadequate activation of stress kinases, damage in cellular membranes, dysfunction in organelles, such as the endoplasmic reticulum and mitochondria, and in the genome (Muoio and Newgard, 2004;Eriksson, 2007;Choi et al, 2008).…”

Section: How Could Honey Be Exerting Regulatory Effects On Glycemimentioning

confidence: 99%

The medicinal value of honey: a review on its benefits to human health, with a special focus on its effects on glycemic regulation

2011

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M.E. Cortés, P. Vigil, and G. Montenegro. 2011. The medicinal value of honey: a review on its benefits to human health, with a special focus on its effects on glycemic regulation. Cien. Inv. Agr. 38(2): 303-317. Honey, a natural substance produced by honeybees, is composed of a complex mixture of carbohydrates, water, and a small amount of proteins, vitamins, minerals, and phenolic compounds. Fructose, glucose and maltose are among the various types of sugars present in honey. Used for millennia as both food and medicine, honey has been associated with improved antioxidant capacity, modulation of the immune system, antimicrobial activities, influence on lipid values (through antihypercholesterolemic effects) and regulation of glycemic responses, among other benefits. The aim of this article was to review the effects of natural honey intake on human health, with particular reference to its influence on glycemic regulation. Several studies have focused on the potential use of honey as a nutritional supplement for healthy individuals and for those with impaired glucose tolerance, diabetes, and their related comorbidities. Such investigations have found that, compared to glucose and sucrose, the consumption of honey decreases glycemic levels and blood lipids in healthy, diabetic and hyperlipidemic individuals. Moreover, long periods of honey intake seem to reduce fasting glucose levels in humans, suggesting that honey consumption influences plasma glucose regulation, mainly through a normo-or hypoglycemic effect. Therefore, honey may be proposed as a nutritional dietary supplement for healthy individuals and for those suffering from alterations in glycemic regulation.

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“…Under oxidative stress, BH4 is oxidized to form 7,8-dihydropterin (BH2) and biopterin, both incapable of eNOS catalysis. The redox regulation of BH4 and BH2 seems clinically important, although, the precise mechanism is not clear 6,7) …”

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confidence: 99%

Roles of Oxidative Stress and Redox Regulation in Atherosclerosis

Kondo

Hirose

Kageyama

2009

JAT

120

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Oxidative stress is believed to be a cause of aging and cardiovascular disorders. In response to inflammation or endothelial cell injury, production of reactive oxygen species (ROS) is enhanced in vascular cells. These changes contribute to the initiation of atherosclerosis. Vascular cells possess anti-oxidant systems to protect against oxidative stress, in addition to the redox system. The redox status of protein thiols is important for cellular functions. The Akt signaling pathway exerts effects on survival and apoptosis, and is regulated by the glutathione (GSH)/glutaredoxin (GRX)-dependent redox system. Sex hormones such as estrogens protect against oxidative stress by protecting the Akt signaling pathway but the physiological role of the extracellular GSH/GRX system has not been clarified, although found an increase in the levels of S-glutathionylated serum proteins in patients with atherosclerosis obliterans. The results suggested that impaired serum redox potential is a marker of the development vascular dysfunction and estrogen has a possible role in the prevention of atherosclerosis. eNOS and its level is regulated by guanosine triphosphate cyclohydrolase 1, a rate-limiting enzyme in BH4 synthesis, and the redox state of BH4. Under oxidative stress, BH4 is oxidized to form 7,8-dihydropterin (BH2) and biopterin, both incapable of eNOS catalysis. The redox regulation of BH4 and BH2 seems clinically important, although, the precise mechanism is not clear 6,7)

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Insulin resistance and oxidative stress in familial combined hyperlipidemia

Cited by 34 publications

References 29 publications

Different Impacts of Cardiovascular Risk Factors on Oxidative Stress

Different Impacts of Cardiovascular Risk Factors on Oxidative Stress

The medicinal value of honey: a review on its benefits to human health, with a special focus on its effects on glycemic regulation

Roles of Oxidative Stress and Redox Regulation in Atherosclerosis

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