Evaluation of nitric oxide metabolites in a group of subjects with metabolic syndrome

Caimi, Gregorio; Hopps, Eugenia; Montana, M.; Noto, Davide; Canino, Baldassare; Presti, Rosalia Lo; Averna, Maurizio

doi:10.1016/j.dsx.2012.09.012

Cited by 23 publications

(12 citation statements)

References 37 publications

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“…Avci et al [117] recently showed that enhanced lipid peroxidation inversely correlates with GSH content in individuals with metabolic syndrome. This was supported by others demonstrating that systemic markers of lipid peroxidation such as oxidised LDL and TBARS are elevated in individuals with metabolic syndrome compared to control subjects [118,119]. Such findings have also been supported by data from animal models of metabolic syndrome with increased liver dysfunction, muscle insulin resistance, and subsequent cardiomyocyte remodelling and apoptosis [83,84,88].…”

Section: Metabolic Syndrome and Oxidative Stressmentioning

confidence: 54%

Aspalathin from Rooibos (Aspalathus linearis): A Bioactive C-glucosyl Dihydrochalcone with Potential to Target the Metabolic Syndrome

et al. 2018

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Aspalathin is a C-glucosyl dihydrochalcone that is abundantly present in Aspalathus linearis. This endemic South African plant, belonging to the Cape Floristic region, is normally used for production of rooibos, a herbal tea. Aspalathin was valued initially only as precursor in the formation of the characteristic red-brown colour of “fermented” rooibos, but the hype about the potential role of natural antioxidants to alleviate oxidative stress, shifted interest in aspalathin to its antioxidant properties and subsequently, its potential role to improve metabolic syndrome, a disease condition interrelated with oxidative stress. The potential use of aspalathin or aspalathin-rich rooibos extracts as a condition-specific nutraceutical is hampered by the limited supply of green rooibos (i.e., “unfermented” plant material) and low levels in “fermented” rooibos, providing incentive for its synthesis. In vitro and in vivo studies relating to the metabolic activity of aspalathin are discussed and cellular mechanisms by which aspalathin improves glucose and lipid metabolism are proposed. Other aspects covered in this review, which are relevant in view of the potential use of aspalathin as an adjunctive therapy, include its poor stability and bioavailability, as well as potential adverse herb-drug interactions, in particular interference with the metabolism of certain commonly prescribed chronic medications for hyperglycaemia and dyslipidaemia.

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Section: Metabolic Syndrome and Oxidative Stressmentioning

confidence: 54%

Aspalathin from Rooibos (Aspalathus linearis): A Bioactive C-glucosyl Dihydrochalcone with Potential to Target the Metabolic Syndrome

et al. 2018

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“…In this group of subjects with MS, we observed [13] a significant increment in NOx (N = 28.07 ± 18.83; MS = 79.82 ± 29.22, p < 0.001). This finding was also present between normal subjects and MS subjects with diabetes mellitus (N = 28.07 ± 18.83; DMS = 78.10 ± 20.76, p < 0.001) and between normal subjects and MS subjects without diabetes mellitus (N = 28.07 ± 18.83; NDMS = 80.99 ± 33.93, p < 0.001).…”

Section: Metabolic Syndromementioning

confidence: 57%

Nitric oxide metabolites (nitrite and nitrate) in several clinical condition

Caimi

Hopps

Montana

et al. 2014

Clinical Hemorheology and Microcirculation

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We determined the concentration of nitric oxide metabolites (NO 2 − +NO 3 − ), expressed as NOx, in several clinical conditions. Regarding this, we have examined 25 subjects with arterial hypertension, 41 subjects with chronic kidney disease in conservative treatment, 106 subjects with metabolic syndrome subdivided according to the presence (n = 43) or not (n = 63) of diabetes mellitus, 48 subjects with obstructive sleep apnea syndrome (OSAS), 14 women with systemic sclerosis complicated with Raynaud's phenomenon, 42 dialyzed subjects and 105 young subjects with acute myocardial infarction (AMI). In subjects with arterial hypertension, chronic kidney disease, metabolic syndrome, systemic sclerosis, as well as, in dialyzed and AMI subjects, we found at baseline a NOx increase. In dyalized subjects after a standard dialysis session, we observed a decrease in NOx. The increase in NOx in juvenile AMI was significantly influenced by cigarette smoking and less by cardiovascular risk factors and the extent of coronary lesions; at 3 and 12 months later than the initial event, we observed a decrease of NOx that remains significantly higher than the control group. In subjects with OSAS no difference in NOx was noted in comparison with normal controls, although their subdivision according to the apnea/hypopnea index operates a clear distinction regarding NOx concentration. G. Caimi et al. / NOx in several clinical conditionsNO interacts with the superoxide anion (O 2 − ) to produce peroxynitrite and other oxidants involved in tissue injury. Considering this pathophysiological aspect, NOS inhibitors have been administrated in some critical conditions, such as congestive heart failure [64], refractory cardiogenic shock [21], cardiogenic shock complicating an acute myocardial infarction [26,58,70] and septic shock [44]. Among the NOS inhibitors, the L-monomethylarginine (L-NMM), a non-selective NOS inhibitor, has been investigated the most. The TRIUMPH study [70] has been conducted in 130 centers and in 8 countries in North America and Europe, enrolling 398 patients with acute myocardial infarction (AMI) and cardiogenic shock; it has demonstrated, however, that the use of tilarginine acetate has no effect on mortality of these patients. Other authors [65] have consequently suggested avoiding further trials with non-selective inhibitors of NOS in the cardiovascular area. Whereas the considerations about the possible coming of NO are interesting. As it is known, NO metabolites, such as nitrite (NO 2 − ) and nitrate (NO 3 − ), usually evaluated together and expressed as NOx, may play a positive role in stable clinical conditions, because they can be reduced to NO once again [20,49,53,54]. All the NO produced, including those generated by red blood cells subjected to several stimuli, such as mechanical and shear stress [71][72][73], act on the cardiovascular system contributing to the modulation of blood flow and vascular tone and regulating vascular relaxation without, however, recognizing the pivotal role played in this microcir...

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“…Moreover, a cross-sectional study conducted on the limited number of Japanese MetS patients and healthy subjects indicated an increase of systemic OxS, as determined by urinary 8-epiprostaglandin F2α (8-epi-PGF2α) in single urine samples, being correlated with visceral AT (VAT) accumulation [55]. MetS patients, including those with T2DM, also exhibited elevation of plasma thiobarbituric acid reactive substances (TBARS), protein carbonylation products, and NOx, where the latter indicated the phenomenon of nitrosative stress (NS) [56][57][58]. Additionally, study on MetS and healthy subjects reported raised values for advanced oxidation protein products (AOPP) and pro-oxidant-antioxidant balance (PAB), in plasma and serum, respectively [59].…”

Section: The Interplay Between Oxidative Stress and Metabolic Syndromementioning

confidence: 99%

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

Włodarski

Strycharz

Wróblewski

et al. 2020

IJMS

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Oxidative stress (OxS) is the cause and the consequence of metabolic syndrome (MetS), the incidence and economic burden of which is increasing each year. OxS triggers the dysregulation of signaling pathways associated with metabolism and epigenetics, including microRNAs, which are biomarkers of metabolic disorders. In this review, we aimed to summarize the current knowledge regarding the interplay between microRNAs and OxS in MetS and its components. We searched PubMed and Google Scholar to summarize the most relevant studies. Collected data suggested that different sources of OxS (e.g., hyperglycemia, insulin resistance (IR), hyperlipidemia, obesity, proinflammatory cytokines) change the expression of numerous microRNAs in organs involved in the regulation of glucose and lipid metabolism and endothelium. Dysregulated microRNAs either directly or indirectly affect the expression and/or activity of molecules of antioxidative signaling pathways (SIRT1, FOXOs, Keap1/Nrf2) along with effector enzymes (e.g., GPx-1, SOD1/2, HO-1), ROS producers (e.g., NOX4/5), as well as genes of numerous signaling pathways connected with inflammation, insulin sensitivity, and lipid metabolism, thus promoting the progression of metabolic imbalance. MicroRNAs appear to be important epigenetic modifiers in managing the delicate redox balance, mediating either pro- or antioxidant biological impacts. Summarizing, microRNAs may be promising therapeutic targets in ameliorating the repercussions of OxS in MetS.

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Evaluation of nitric oxide metabolites in a group of subjects with metabolic syndrome

Cited by 23 publications

References 37 publications

Aspalathin from Rooibos (Aspalathus linearis): A Bioactive C-glucosyl Dihydrochalcone with Potential to Target the Metabolic Syndrome

Aspalathin from Rooibos (Aspalathus linearis): A Bioactive C-glucosyl Dihydrochalcone with Potential to Target the Metabolic Syndrome

Nitric oxide metabolites (nitrite and nitrate) in several clinical condition

The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress

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