Nitric oxide production is increased in severely obese children and related to markers of oxidative stress and inflammation

Codoñer‐Franch, Pilar; Tavárez-Alonso, Sandra; Murria-Estal, R.; Megías-Vericat, Javier; Tortajada‐Girbés, Miguel; Alonso‐Iglesias, Eulalia

doi:10.1016/j.atherosclerosis.2010.12.035

Cited by 111 publications

(90 citation statements)

References 29 publications

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“…Despite the increase in oxidative stress, plasma NO x levels were elevated in rats fed a highfructose diet for 5 weeks. Plasma NO x levels are increased in obese children with metabolic syndrome and in New Zealand Obese mice, 29,30 whereas they are decreased in obese teenagers with metabolic syndrome. 31 Other laboratories have observed that plasma NO x was increased in rats that were fed a highfructose diet for 8 and 13 weeks.…”

Section: Discussionmentioning

confidence: 99%

Role of T Regulatory Lymphocytes in the Pathogenesis of High-Fructose Diet–Induced Metabolic Syndrome

et al. 2013

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Abstract-We recently showed that T regulatory lymphocytes (Treg), which are immune suppressors of inflammatory responses, play a role blunting the development of hypertension-induced injury. Treg are unchanged or decreased in children with metabolic syndrome, and therefore, their role in metabolic syndrome remains unclear. We hypothesized that Treg number or function would be depressed in a high-fructose diet-induced metabolic syndrome-like model in rats. Sprague-Dawley rats were fed normal chow or a high-fructose diet for 5 weeks. The high-fructose diet-induced a 3.8-fold increase in plasma triglycerides and a 14% reduction in high-density lipoprotein cholesterol (P<0.001). The high-fructose diet increased reactive oxygen species in aorta and periaortic adipose tissue 2.8-fold (P<0.05), and reduced nicotinamide adenine dinucleotide phosphate oxidase activity 1.9-fold in aorta, and 2.5-fold in the heart (P<0.05). It also increased plasma nitric oxide metabolite levels 6.4-fold (P<0.001). Western blots showed that the high-fructose diet increased ≥2.3-fold vascular and in platelet endothelial cell adhesion molecule 1 in aorta (P<0.01). It did not affect monocyte/macrophage aortic infiltration but caused a 2.4-fold increase in collagen deposition in the aortic media (P<0. 01 FoxP3+ cells was observed in children with metabolic syndrome (2.5 versus 3.1%). 15To determine the role of Treg in the metabolic syndrome, vascular oxidative stress and inflammation and the number and function of Treg were studied in high-fructose diet-fed SpragueDawley rats, a well-established model mimicking some features of the western diet-induced metabolic syndrome. 16,17 These rats exhibit hypertension, insulin resistance, and abnormal lipid profile resembling the human metabolic syndrome better than a monogenic model. We hypothesized that vascular oxidative stress and inflammation and changes in the immune response, including Treg activity and response, participate in the mechanisms leading to the metabolic syndrome. Materials and MethodsAdditional materials and methods are described in the online-only Data Supplement. Experimental DesignEight-week-old Sprague-Dawley male rats (Harlan Laboratories, Indianapolis, IN) were fed a high-fructose diet (TD.89247, Harlan Laboratories) composed of 60% fructose, 21% protein, 5% fat, 8% cellulose, and standard vitamins and mineral mix or normal chow diet (control) for 5 weeks. Systolic BP (SBP) was measured by the tailcuff method after 4 weeks on the diet. SBP was also determined by telemetry together with heart rate and animal activity every 5 minutes for 10 seconds for 2 consecutive days at baseline and at the end of every week during the 5 weeks of treatment. Three days before the end of the protocol, blood was collected from the saphenous vein on heparin for triglycerides, and high-density lipoprotein cholesterol was determined after 5 hours of fasting. At the end of the protocol, body weight was evaluated, and rats were anesthetized with 3% isoflurane mixed with O 2 at 1 L/min (depth of ane...

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Section: Discussionmentioning

confidence: 99%

Role of T Regulatory Lymphocytes in the Pathogenesis of High-Fructose Diet–Induced Metabolic Syndrome

et al. 2013

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“…(26) obez ve hipertansif çocuklarda nitrit seviyesini etkileyen NOS 3 gen mutasyonu bakılmış, ancak NOS3 tagSNP rs3918226 mutasyonu NO sentezi ile ilişkili olsa da obez hipertansiyonlu grup ile kontrol grubu arasında fark yada kan basıncı ile korelasyon saptanmamıştır. Codoñer-Franch ve ark.nın (27) yaptıkları çalışmada ise oksidatif stres göstergesi olan NO seviyesinin obez çocuklarda yüksek olduğu ve obez çocuklarda NO seviyesinin hipertansiyon ve metabolik risk faktörleri ile ilişkili bulunmuştur. Çalışmamızda, hipertansiyonu olan obez grupta plazma renin düzeyi ve NO düzeyi normal kilolu çocuklara ve kontrol grubuna göre anlamlı yüksek saptanırken, serum aldosteron, ET-1 düzeyleri iki grup arasında benzer saptanmıştır.…”

Section: Discussionunclassified

Hypertension and Renal Damage in Obese Children

Girişgen¹,

Sönmez²,

Yenisey³

et al. 2016

Turk Neph Dial Transpl

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ÖZ AMAÇ:Obezite ve hipertansiyon arasındaki ilişki iyi bilinmektedir. Çalışmamızda amacımız, hipertansiyon saptanan obez ve obez olmayan çocuklarda 24 saatlik kan basıncı değerlendirmesi, obez ve hipertansiyonlu çocuklarda kan basıncı yüksekliğine sebep olan faktörleri ve obezitenin hipertansiyonla birlikte böbreğe olan etkisini incelemektir. GEREÇ ve YÖNTEMLER:Çalışma grubunu 18 i obez, 38 normal kilolu kan basıncı 90 persentil üzerinde saptanan 56 çocuk, kontrol grubunu kan basıncı normal saptanan normal kilolu 27 çocuk oluşturdu. Tüm çocuklara 24 saatlik kan basıncı izlemi yapıldı. Tüm çocuklardan alınan serum örneklerinden renin, aldosteron, endothelin-1, NO (nitrik oksit) düzeyleri ve 24 saatlik idrarda NAG (N asetil glükozamin), mikroalbümin, Na ve K atılımlarına bakıldı. BULGULAR:Hipertansiyonlu obez çocuklarda sistolik kan basıncı yükü normal kilolu çocuklara göre yüksek, kontrol grubuna göre sistolik, diyastolik kan basıncı ortalamaları, gündüz ve gece sistolik kan basıncı yükleri yüksek ölçülmüştür. Gece sistolik kan basıncı ortalaması vücut kitle indeksi ile bağlantılı bulunmuştur. Obez hipertansiyonlu grupta normal kilolu gruba göre kan renin ve NO düzeyleri yüksek saptanmıştır. SONUÇ:Sonuç olarak obezitenin sistolik kan basıncına etkili olduğunu ve obezitede hipertansiyon etyopatogenezinde renin ve nitrik oksitin rolü olabileceği ve hipertansiyona bağlı böbrek hasarlanmasına ek olarak obezitenin tübülleri etkileyerek böbrek hasarlanmasına ek katkıda bulunmadığı düşünülmüştür.ANAhTAR SÖZcÜKLER: Obezite, Hipertansiyon, Renin, Nitrik oksit ABSTRAcT OBJEcTIVE: The relationship between obesity and essential hypertension is well known. The aim of our study was to evaluate ambulatory blood pressure of obese and non-obese patients diagnosed with hypertension, and to investigate factors causing hypertension and the effect of obesity and hypertension on kidneys. MATERIAL and METhODS:Eighteen obese-hypertensive children, thirty-eight non-obese hypertensive children and twenty-seven healthy control group subjects were enrolled in the study. Twenty-four hour blood pressure measurements were recorded for all the patients. Plasma renin activity, serum aldosterone, nitric oxide, endothelin levels and microalbumin, N-acetyl-β-D-glucosaminidase, Na, K in the 24-hour urine were investigated in all patients and in the control groups. RESULTS:According to the results of ambulatory blood pressure measurements, the systolic blood pressure loads were higher in the hypertensive and obese group when compared with the hypertensive non-obese group. Nighttime systolic blood pressure was correlated with the body mass index. Plasma renin activity and serum nitric oxide levels were higher in the hypertensive and obese group when compared with the hypertensive non-obese group.cONcLUSION: In conclusion, we believe that blood renin and NO levels may have important roles in the pathogenesis of childhood obesity and hypertension and obesity has no effect on tubular renal damage.

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“…Oxidative stress is essential in the progress of periodontal diseases while antioxidants such as flavonoids or vitamin C can prevent such progresses. NO is an important signaling molecule responsible for various inflammatory responses in vivo [22,23]. It is generated by the activation of iNOS enzyme induced by inflammation.…”

Section: Discussionmentioning

confidence: 99%

Methanol Extract of <i>Codonopsis pilosula</i> Inhibits Inducible Nitric Oxide Synthase and Protein Oxidation in Lipopolysaccharide-Stimulated Raw Cells

Yoo¹,

Kim²

2013

Trop. J. Pharm Res

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Purpose: To evaluate the mechanism of antioxidant activity of the methanol extract of Codonopsis pilosula. (p < 0.05) Methods: Anti-oxidative properties were assessed by measuring free radical scavenging activity, nitric oxide (NO) levels, protein oxidation and reducing power, while the mechanism of antioxidative effect of Codonopsis pilosula extract was determined by measuring iNOS and COX-2 expression in lipopolysaccharide (LPS)-stimulated raw cells. Results: Codonopsis pilosula extract (CPE) exerted significant DPPH free radical and NO-scavenging activities. Protein oxidation was decreased by 30 % by the CPE (1mg/ml). The extract (1mg/ml) enhanced reducing power 16-fold (compared with control). LPS-induced production of iNOS was significantly inhibited by the extract (60 %), suggesting that it inhibits NO production by suppressing iNOS expression. However, LPS-induced production of COX-2 was not significantly

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Nitric oxide production is increased in severely obese children and related to markers of oxidative stress and inflammation

Cited by 111 publications

References 29 publications

Role of T Regulatory Lymphocytes in the Pathogenesis of High-Fructose Diet–Induced Metabolic Syndrome

Role of T Regulatory Lymphocytes in the Pathogenesis of High-Fructose Diet–Induced Metabolic Syndrome

Hypertension and Renal Damage in Obese Children

Methanol Extract of <i>Codonopsis pilosula</i> Inhibits Inducible Nitric Oxide Synthase and Protein Oxidation in Lipopolysaccharide-Stimulated Raw Cells

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