The effect of lifestyle change and metformin therapy on serum arylesterase and paraoxonase activity in obese children

Author(s):  
Atilla Çayır ◽  
Mehmet İbrahim Turan ◽  
Fatih Gurbuz ◽  
Nezahat Kurt ◽  
Abdulkadir Yildirim

AbstractObesity is known to be associated with many diseases in the long and short terms. Elevated oxidative stress contributes to the development of such obesity-related diseases as dyslipidemia, diabetes mellitus and hypertension. Levels of the endogenous antioxidants paraoxonase and arylesterase have been shown to decrease in such diseases. The purpose of this study was to investigate whether or not changes in lifestyle and metformin therapy would affect serum paraoxonase and arylesterase levels.The study was performed with 25 overweight, 26 obese and 25 morbidly obese patients aged 6–15 years as well as 27 healthy children. Serum paraoxonase (PON1) and arylesterase (ARE) activity levels and total cholesterol, triglyceride, low-density protein, high-density protein, very low-density protein, glucose, aspartate amino transferase and alanine amino transferase levels were measured. Enrolled patients were assessed at initial presentation and again at 6 months. No procedure was performed in the control group, while the overweight, obese and morbidly obese groups were recommended diet and exercise and given metformin therapy (insulin-resistant subjects only).Serum PON1 activity levels in patients with metabolic syndrome were significantly lower than those in individuals without metabolic syndrome (p<0.05), while lipid concentrations were significantly higher (p<0.05). Metabolic syndrome patients had higher serum glucose, total cholesterol, low-density protein, very low-density protein and triglyceride values compared to those of the control group but significantly lower high-density protein values (p<0.05). No difference was determined between the groups in terms of PON1 and ARE levels following diet and exercise and metformin therapy.Measurement of PON1 and ARE enzyme levels may be useful in monitoring the effectiveness of treatment aimed at reducing oxidative stress in obese children.

Author(s):  
Eman A. Al-Rekabi ◽  
Dheyaa K. Alomer ◽  
Rana Talib Al-Muswie ◽  
Khalid G. Al-Fartosi

The present study aimed to investigate the effect of turmeric and ginger on lipid profile of male rats exposed to oxidative stress induced by hydrogen peroxide H2O2 at a concentration of 1% given with consumed drinking water to male rats. Methods: 200 mg/kg from turmeric and ginger were used, and the animals were treatment for 30 days. Results: the results showed a significant increase in cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), whereas it explained a significant decrease in high density lipoprotein (HDL) of male rats exposed to oxidative stress when compared with control group. the results showed a significant decrease in cholesterol, triglycerides, (LDL), (VLDL), whereas it explained a significant increase in (HDL) of rats treated with turmeric and ginger at dose 200 mg/kg when compared with male rats exposed to oxidative stress.


2021 ◽  
Vol 68 (1) ◽  
pp. 222-228
Author(s):  
Ahmet Özkaya ◽  
Kenan Türkan

In this study, the effects of 3-benzoyl-7-hydroxy coumarin molecule on mineral and antioxidant enzymes were investigated in rat liver exposed to oxidative stress with aluminium chloride (AlCl3). Adult male Wistar albino rats were divided into four groups as Control, Coumarin, AlCl3, and Coumarin + AlCl3. Coumarin at the dose of 10 mg/kg and AlCl3 at the dose of 8.3 mg/kg were administered for 30 days every other day. In AlCl3 group, malondialdehyde (MDA), iron (Fe), aluminium (Al) and copper (Cu) levels increased compared to the control group, while glutathione (GSH) level, glutathione S-transferase (GST), and carboxylesterase (Ces) enzyme activity levels decreased. In Coumarin + AlCl3 group, MDA, Fe, Al and Cu levels decreased with the effect of coumarin compared to AlCl3 group, while GSH level, and GST enzyme activity levels increased. According to our results, AlCl3 generates oxidative stress in rat livers, and we believe that 3-benzoyl-7-hydroxy coumarin has an ameliorative effect on antioxidant enzyme system, Al, Fe and Cu levels.


2020 ◽  
Vol 8 (1) ◽  
pp. e001426
Author(s):  
Wei Wu ◽  
Jinna Yuan ◽  
Yu Shen ◽  
Yunxian Yu ◽  
Xuefeng Chen ◽  
...  

IntroductionThis study was performed to investigate the role of iron overload in the early stage of hyperglycemia-induced vascular functional impairment.Research design and methodsA total of 196 obese children were enrolled, and data regarding ferritin levels, blood glucose levels, intima-media thickness of carotid arteries, liver function and fibrosis index, hemoglobin, blood pressure, blood lipids, and inflammation indicators were collected. Ferritin levels were compared with a control group, which consisted of 148 healthy non-obese children who were age-matched and gender-matched. Endothelial cells were cultured in high glucose medium and supplemented with ferric citrate with or without iron remover (deferoxamine), a reducing agent (N-acetyl-cysteine), or a nuclear factor-κB (NF-κB) inhibitor (BAY 11-7082). Apoptosis, oxidative stress, nitric oxide levels, and endothelin content were evaluated. DNA microarray analysis was performed to analyze the expression of genes in the NF-κB signaling pathway.ResultsObese children have significantly higher ferritin levels compared with the control group. Ferritin level was positively correlated with hemoglobin and was related to metabolic disorders, including impaired glucose tolerance, higher blood pressure, dyslipidemia, and impaired hepatic function. Endothelial cells treated with ferric citrate showed a significantly higher rate of apoptosis, higher levels of oxidative stress, and impaired vasomotor function under high glucose conditions. The above effects were rescued by treatment with an iron remover, reducing agent, or NF-κB inhibitor. Further, detection of phosphorylated-p65 distribution in cells confirmed activation of the NF-κB pathway. DNA microarrays and subsequent gene oncology enrichment analyses revealed the main processes activated in cells.ConclusionIncreased ferritin levels are related to impaired glucose tolerance and other metabolic disorders in obese children. At the cellular level, iron overload aggravated the endothelial cell dysfunction caused by high glucose.


Author(s):  
И.Л. Гуляева ◽  
И.А. Булатова ◽  
Л.Д. Пестренин

Цель исследования - изучение роли васкулоэндотелиального фактора роста в патогенезе неалкогольного стеатоза печени и дислипидемии при метаболическом синдроме. Методика. Обследовано 35 пациентов с неалкогольным стеатозом печени, в том числе 22 женщины и 13 мужчин. Группу контроля составили 12 сопоставимых по полу и возрасту лиц без патологии печени и признаков метаболического синдрома. Наличие жирового гепатоза подтверждали методом ультразвукового исследования. У пациентов с патологией печени рассчитывали индексы-предикторы стеатоза: Fatty Liver Index (FLI) и Hepatic Steatosis Index (HSI). У всех участников исследования определяли уровни провоспалительных цитокинов и васкулоэндотелиального фактора роста (ВЭФР), оценивали также липидный спектр крови и функциональные печеночные пробы. Результаты. У пациентов со стеатозом печени наблюдалось значимое увеличение уровней провоспалительных цитокинов, ВЭФР, общего холестерина и липопротеинов низкой и очень низкой плотности. Индекс атерогенности также был значимо выше, чем в контрольной группе. Концентрация ВЭФР положительно коррелировала с показателями окружности талии, тимоловой пробы, уровнями общего холестерина, липопротеинов низкой плотности и индексом атерогенности. Чувствительность FLI составила 91,4%, HSI - 97,1%. При этом, значения FLI и HSI значимо коррелировали с уровнем ВЭФР. Заключение. Полученные данные позволяют предположить, что ВЭФР, один из основных маркеров эндотелиальной дисфункции, может играть немаловажную роль в патогенезе неалкогольного стеатоза печени и дислипидемии у пациентов с метаболическомим синдромом The aim of the study was to assess the role of vascular endothelial growth factor (VEGF) in the pathogenesis of nonalcoholic hepatic steatosis and dyslipidemia in patients with signs of metabolic syndrome. Methods. 35 patients with nonalcoholic fatty liver disease, including 22 women and 13 men, were evaluated. The sex- and age-matched control group consisted of 12 people without liver pathology and metabolic syndrome criteria. Presence of hepatic steatosis was confirmed by an ultrasound examination. The Fatty Liver Index (FLI) and the Hepatic Steatosis Index (HSI) were calculated for patients with hepatic steatosis. Concentrations of proinflammatory cytokines and VEGF were measured for all participants. Also, blood biochemistry, including the lipid profile and liver function tests, was analyzed. Results. In patients with hepatic steatosis, levels of proinflammatory cytokines and VEGF were significantly increased. Also, concentrations of total cholesterol, low-density lipoproteins, and very low-density lipoproteins were higher in patients with the liver pathology than in the control group. Atherogenic coefficient was increased in hepatic steatosis. Significant correlations were observed between VEGF and waist circumference, thymol test, total cholesterol, low-density lipoproteins, very low-density lipoproteins, and atherogenic coefficient. Sensitivity of FLI and HIS was 91.4% and 97.1%, respectively. Also, FLI significantly correlated with HSI and VEGF level. Conclusion. The study suggested that VEGF, of the main markers of endothelial dysfunction, plays an important role in the pathogenesis of nonalcoholic hepatic steatosis and dyslipidemia in patients with signs of metabolic syndrome.


2020 ◽  
Vol 3 (2) ◽  
pp. 76-86
Author(s):  
Mahmoud M. Farag ◽  
Ehab H. Ashour ◽  
Wessam F. El-Hadidy

Background: The use of high-fructose (Fr) corn sweeteners and sucrose in manufactured food has markedly increased recently. This excessive Fr intake has been proposed in the etiology of the metabolic syndrome, which shows an increasing prevalence throughout the world. Objective: In this study, we questioned whether fenofibrate (FF), a peroxisome proliferator-activated receptor (PPAR)-α agonist, and pioglitazone (PG), a PPAR-γ agonist, might be effective in ameliorating the metabolic syndrome in a rat model. Materials and Methods: The metabolic syndrome was induced by feeding rats a high-Fr (60%) diet for 10 weeks. The rats were divided into 5 groups: control group, fed a normal rat chow; Fr + vehicle group; Fr + FF group; Fr + PG group; and Fr + (FF + PG) group (treated with both drugs). Drug or vehicle treatment was given daily for 6 weeks (from weeks 5 to 10). Thereafter, blood and liver samples were obtained for biochemical studies. Results: Rats fed a high-Fr diet developed hyperglycemia, hyperinsulinemia, hyperuricemia, hypertriglyceri­demia, and hypercholesterolemia, and had increased serum alanine aminotransferase, hepatic tumor necrosis factor-α, and malondialdehyde levels but decreases in both glutathione content and superoxide dismutase activity. Rat treatment with FF and/or PG attenuated these alterations. The improvement was greater with the combined treatment than with either drug alone, and normalization of insulin sensitivity was observed only in rats treated with the combination therapy. Conclusion: Acting on the 2 main PPAR subfamilies, the combination of FF and PG provides a more efficacious therapy for modulating the changes in serum insulin, uric acid, and lipids, as well as the accompanying hepatic inflammation and oxidative stress that characterize the Fr-induced metabolic syndrome.


Author(s):  
Huseyin Gungor ◽  
Haki Kara

AbstractBackgroundThe aim of this study was to investigate the effects of selenium, zinc, insulin, and metallothionein on oxidative damage and metallothionein (MT) gene expression levels in streptozotocin (STZ)-induced type 1 diabetic rats exposed to Cd.MethodsRats were categorized under eight groups (control, STZ, Cd, STZ + Cd, Group 5, Group 6, Group 7, and STZ + Cd + MT [n:8/group]) were used. After diabetes was induced by STZ (55 mg/kg, i.p.), Cd was administered (1 mg/kg CdCl, orally) for 4 weeks. In cadmium-treated groups selenium (Na2SeO3 1.5 mg/kg, i.p.), zinc (ZnSO4 10 mg/kg via oral gavage), insulin (insulin glargine, 2U/day, s.c.), and MT (1mg/kg, every other 10 days, s.c.) were administered. MT gene expression levels, MDA levels, GPx, SOD, and CAT activity levels were determined in liver and kidney tissues.ResultsMT gene expression and MDA levels increased (p < 0.05) while GPx and SOD activity levels decreased (p < 0.05) in STZ, Cd, and STZ + Cd groups. In Group 5, Group 6, Group 7, and Group 8 groups MT gene expression and MDA levels were decreased while GPx and SOD activity levels were increased (p < 0.05). CAT activity significantly increased (p < 0.05) in STZ + Cd group while there were no significance in other groups (p > 0.05). Compared to the control, Group 5, Group 6, Group 7, and Group 8 groups provided no difference for alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen and creatinine levels (p > 0.05).ConclusionsOur results suggest that Se, insulin, Zn and MT may have protective effects against hepatotoxicity and nephrotoxicity caused by Cd exposure in diabetic rats by reducing oxidative stress and MT gene expression levels.


2021 ◽  
Vol 34 (4) ◽  
pp. 495-502
Author(s):  
Esra Aktağ ◽  
Kadriye Yurdakök ◽  
Siddika Songül Yalçın ◽  
Nurgün Kandemir

Abstract Objectives Recent studies have shown a potential link between chronic exposure to Bisphenol A (BPA) and exogenous obesity, the prevalence of which has been increasing dramatically in all age groups and particularly among children in the last decades. In this study, we aimed at comparing BPA exposure levels between controls and otherwise healthy, drug-naive, pre-pubertal children having exogenous obesity with/without metabolic syndrome. Methods A total of 63 pre-pubertal children with exogenous obesity whom 27 of them having metabolic syndrome attending Hacettepe University Ihsan Dogramaci Children’s Hospital were included in this study. The control group consisted of 34 age- and sex-matched healthy children with no significant underlying medical conditions. Urinary BPA levels were measured using LC-MS/MS (high-performance liquid chromatography coupled with tandem mass spectrometry) methodology. Results Urinary BPA levels among obese children were significantly higher than those of the control group (median: 22.9 μg/g-creatinine and 6.9 μg/g-creatinine, respectively; p=0.0001). When adjusted with generalized linear models for age, gender and z scores of body mass index, obese children having metabolic syndrome had significantly higher urinary BPA levels than obese children without metabolic syndrome and both obese groups had considerably elevated levels of urinary BPA than the controls (estimated marginal mean ± standard error: 42.3 ± 7.4 μg/g-creatinine, 22.6 ± 3.5 μg/g-creatinine and 12.1 ± 2.5 μg/g-creatinine, respectively, p=0.0001) Conclusions This study shows much higher BPA exposure among obese children with metabolic syndrome during the prepubertal period.


Sign in / Sign up

Export Citation Format

Share Document