ABSTRACT Objective: In this study, we aimed to evaluate subclinical atherosclerosis in patients with obesity who had cardiovascular disease risk indicators such as arterial stiffness, which is evaluated using pulse wave velocity (PWV), carotid intima-media thickness (CIMT), and biomarkers of endothelial dysfunction such as endocan, ADAMTS97, and ADAMTS9. Subjects and methods: Sixty obese subjects, including 23 subjects with body mass index (BMI) ≥ 40, 37 subjects with BMI ≥ 30 but < 40, and 60 age-and sex-matched control subjects, were included in our study. Serum endocan, ADAMTS97, and ADAMTS9 levels as well as PWV and CIMT measurements of the subjects in the obese and control groups were performed. Results: In the obesity group, PWV levels were significantly higher than they were in the control group and endocan levels were significantly lower than they were in the control group. When we compared the obese group with BMI ≥ 40 and the control group, the BMI ≥ 40 group had significantly higher PWV and CIMT levels than the control group had, whereas endocan, ADAMTS7, and ADAMTS9 levels were similar to those of the control group. When we compared the obese group with BMI ≥ 30 < 40 to the control group, endocan levels were lower in the group with BMI ≥ 30 < 40, and PWV and CIMT levels were similar to the control group. Conclusions: We found that arterial stiffness and CIMT increased in obese patients with BMI ≥ 40 and that increased arterial stiffness was associated with age, systolic blood pressure, and HBA1C. In addition, we found that the endocan levels were lower in obese patients than they were in nonobese control individuals.

RESUMO Objetivo A acrilamida é um químico potencialmente neurotóxico e carcinogênico, sendo naturalmente criada durante o processo de aquecimento de alimentos ricos em carboidratos, como batatas fritas e cereais matinais. Dado que o composto pode ser ingerido através do consumo de alimentos, o presente trabalho teve por objetivo investigar o seu efeito, quando administrado oralmente a ratos, medindo-se os níveis plasmáticos de ácido retinoico e α-tocoferol, bem como os níveis séricos de ácido siálico e malondialdeído Métodos Foram utilizados cinquenta ratos Wistar, sendo metade de cada sexo, com idade entre três e quatro semanas. Os animais foram divididos em dois grupos, os quais receberam diferentes doses diárias de acrilamida, via água potável, durante noventa dias: o primeiro ingeriu 2mg/kg/dia; e o segundo, 5mg/kg/dia. Ao final do tratamento, os animais foram eutanasiados por meio de luxação cervical. Amostras de sangue foram coletadas através de punção cardíaca, assim como amostras de soro e plasma foram medidas usando-se a técnica de cromatografia líquida de alta performance com detector de Ultravioleta. Resultados A análise das amostras de plasma e soro revelou que os níveis de ácido siálico e malondialdeído, em ratos de ambos os sexos tratados com acrilamida de 5mg/kg/dia, foram significativamente aumentados, ao passo que os níveis séricos de ácido siálico foram maiores em ratas tratadas com 2mg/kg/dia de acrilamida. Já os níveis plasmáticos de ácido retinoico e α-tocoferol diminuíram significativamente em ratos de ambos os sexos, quando tratados com a dose mais elevada.Concl Conclusão Os resultados mostram que a acrilamida causa um aumento no estresse oxidativo e leva a uma diminuição nos níveis de ácido retinoico e α-tocoferol, que desempenham um papel no mecanismo de defesa contra esse estresse.

ABSTRACT Objective Acrylamide is a potentially neurotoxic and carcinogenic chemical and naturally creates during the heating process of carbohydrate-rich foods, such as potato chips and breakfast cereals. Acrylamide might be ingested by people via consuming food that contains it. Therefore, we investigated the effect of acrylamidegiven orally to male and female rats on plasma retinoic acid and α-tocopherol and serum sialic acid and malondialdehyde levels. Method A total of 50 Wistar rats were used (25 female and 25 male, three-four weeks old). The rats of each sex were given 2 and 5mg/kg/day acrylamide via drinking water for 90 days. At the end of the treatment, the animals were euthanized by cervical dislocation. Blood specimens were collected through cardiac puncture, and serum and plasma samples were analysed using the high-performance liquid chromatography technique with a Ultraviolet detector. Results The analysis of the plasma and serum samples revealed that serum sialic acid and malondialdehyde levels in both sexes given 5mg/kg/day acrylamide were significantly increased, and the serum sialic acid levels were higher in female rats given 2mg/kg/day acrylamide. The plasma retinoic acid and α-tocopherol levels significantly decreased in both sexes given only the highest dose. Conclusion The results show that acrylamide causes an increase in oxidative stress and leads to a decrease in the levels of retinoic acid and α-tocopherol which play a role in the defense mechanism against this stress.

RESUMO Objetivo Doenças nutricionais, como síndrome metabólica, distúrbios cardiovasculares, inflamação crônica ou mesmo câncer, são observadas em pessoas que sustentam seu estilo de vida na dieta ocidental, caracterizada pela alta ingestão de calorias. Dado que a origem dessas doenças é a estrutura degradada do ácido desoxirribonucleico, o presente estudo investigou se a dieta ocidental produzia dano oxidativo endógeno ao ácido desoxirribonucleico, apoptose ou inflamação. Métodos Foram utilizados 28 ratos Wistar machos, com idade entre 10-12 semanas, divididos em quatro grupos. Os ratos do grupo controle receberam a dieta padrão, ao passo que os ratos restantes receberam uma das três dietas seguintes por quatro semanas: uma dieta rica em gordura contendo 35% de gordura; uma dieta rica em sacarose contendo 69% de sacarose; e dieta ocidental compreendendo os dois tipos de dietas. Após o tratamento soro 8-hidroxi-2-desoxiguanosina, poli (adenosina difosfato ribose) polimerase-1, quitinase-3-like proteína 1, uroquinase solúvel tipo de receptor ativador de plasminogênio, os níveis do ligante Fas e do citocromo c foram medidos. Resultados Não foram observadas alterações nos níveis séricos de uroquinase solúvel tipo de receptor ativador de plasminogênio, ligante Fas e citocromo c, enquanto um aumento estatisticamente significativo nos níveis séricos de 8-hidroxi-2-desoxiguanosina, poli (adenosina difosfato ribose) polimerase-1 e quitinase-3-like proteína 1 foi encontrado apenas em ratos que receberam dieta ocidental. Conclusão Os resultados mostram que a dieta ocidental produziu danos no ácido desoxirribonucleico oxidativo endógeno, o que aumentou os níveis séricos de poli (adenosina difosfato ribose) polimerase-1, levando à inflamação.

ABSTRACT Objective Nutritional diseases such as metabolic syndrome, cardiovascular disorder, chronic inflammation or even cancer are observed in people who sustain their lifestyle by Western diet due to high calorie intake. The origin of these diseases are the degraded deoxyribonucleic acid structure. In this study, we investigated whether Western diet produced endogenous oxidative deoxyribonucleic acid damage, apoptosis or inflammation. Methods Twenty-eight male Wistar rats, aged 10-12 weeks, were divided into four groups. The rats in control group received the standard diet and the remaining rats were given one of the following three diets for four weeks: a high-fat diet containing 35% fat, a high-sucrose diet containing 69% sucrose and Western diet comprising both two types of diets. After treatment the serum 8-hydroxy-2-deoxyguanosine, poly (adenosine diphosphate ribose) polymerase-1, chitinase-3-like protein 1, soluble urokinase-type plasminogen activator receptor, Fas ligand and cytochrome c levels were measured. Results It was observed no changes in the serum soluble urokinase-type plasminogen activator receptor, Fas ligand and cytochrome c levels whereas a statistically significant increase in the serum 8-hydroxy-2-deoxyguanosine, poly (adenosine diphosphate ribose) polymerase-1 and chitinase-3-like protein 1 levels were found only in rats that were given Western diet. Conclusion The findings show that Western diet produced endogenous oxidative deoxyribonucleic acid damage, which then increased serum poly (adenosine diphosphate ribose) polymerase-1 levels, eventually leading to inflammation.