Body Weight Loss is not Different between Patients with Digestion Gastrointestinal and Accessory Organs Cancer With High or low Neutrophils to Lymphocytes Ratio / Perda de Peso Corporal não é Diferente Entre Pacientes com Câncer Gastrointestinal e de Órgãos Acessórios da Digestão com Alta ou Baixa Relação Neutrófilos/Linfócitos

This study sought to assess if patients with cancer with high neutrophils to lymphocytes ratio (NLR) leads to body weight loss. A crosssectional study was performed in a public hospital. A total of 97 patients with digestion gastrointestinal and accessory organs cancers were evaluated. Body mass index (kg/m2) was calculated using the body weight (kg) divided by square of height (m) and body weight loss was obtained by percentage of body weight loss in the last months. The systemic inflammation was measured using the NLR and ≥6.5 values were considered as a high inflammation. It was found out that 11.3% of the patients have NLR ≥6.5. The NLR group ≥6.5 was younger than the NLR group <6.5 (NLR ≥6.5: 51.7 ± 14.1 vs. NLR <6.5: 61.9 ± 11.9 y, p=0.01), but without differences among sex, alcohol consumption, smoking, physical activity, body weight, body weight loss percentage and body mass index. In conclusion, it was found out that patients with digestion gastrointestinal and accessory organs cancers with NLR ≥6.5 did not differ in body weight loss when compared to patients with NLR <6.5. (AU)

Este estudo procurou avaliar se pacientes com câncer com alta razão neutrófilos/linfócitos (RNL) apresentam maior perda de peso corporal. Foi realizado um estudo transversal em um hospital público. Foram avaliados total de 97 pacientes com cânceres gastrointestinais e de órgãos acessórios da digestão. O índice de massa corporal (kg/m2) foi calculado usando o peso corporal (kg) dividido pelo quadrado da altura (m) e a perda de peso corporal foi adquirida pela porcentagem de perda de peso corporal nos últimos meses. A inflamação sistêmica foi medida pelo RNL e valores ≥6,5 foram considerados como alta inflamação. Nós encontramos que 11,3% dos pacientes têm RNL ≥6,5. O grupo RNL ≥6,5 é composto de pacientes mais jovens do que o grupo RNL <6,5 (RNL ≥6,5: 51,7 ± 14,1 vs. RNL <6,5: 61,9 ± 11,9 anos, p=0,01), mas sem diferenças entre sexo, consumo de álcool, tabagismo, atividade física, peso corporal, porcentagem de perda de peso corporal e índice de massa corporal. Em conclusão, nós observamos que pacientes com cânceres gastrointestinais e de órgãos acessórios da digestão com RNL ≥6,5 não diferiram na perda de peso corporal quando comparados com pacientes com RNL <6,5. (AU)

Ursolic acid does not change the cytokine levels following resistance training in healthy men: A pilot balanced, double-blind and placebo-controlled clinical trial.

Ursolic acid (UA) is a natural compound that shows anti-inflammatory actions. However, no human studies have investigated the cytokine profile during the RT and UA consumption. The purpose of this study was to verify if UA is able to potentiate the anti-inflammatory activity after RT, reflecting in the reduction of blood inflammatory markers in healthy men. Twenty-seven participants were allocated to two groups: control (CON) (n = 13) and UA (n = 14). For 8weeks, each group performed RT and consumed capsules containing a placebo (400 mg/day) or UA (400 mg/day). Serum cytokine concentrations were evaluated before and after the training period. There was no difference in the serum cytokine concentrations of TNF-α, IL-10 and IL-6 (p > 0.05). In conclusion, UA supplementation for 8weeks was not able to change the blood TNF-α, IL-10, and IL-6 concentrations in healthy men undergoing RT. However, further studies are warranted to investigate other inflammatory markers.

Acute Caffeine and Coconut Oil Intake, Isolated or Combined, Does Not Improve Running Times of Recreational Runners: A Randomized, Placebo-Controlled and Crossover Study.

The aim was to evaluate the effect of caffeine (CAF) and extra virgin coconut oil (CO), isolated or combined, on running performance in runners. Methods: A randomized, placebo-controlled, and crossover study was conducted with thirteen recreational runners aged 18-40. All volunteers performed a 1600 m time trial at a 400 m track, each ingesting four different substances: (1) placebo (water), (2) decaffeinated coffee plus isolated CAF (DECAF + CAF), (3) decaffeinated coffee plus isolated CAF plus soy oil (DECAF + CAF + SO), and (4) decaffeinated coffee plus isolated CAF plus extra virgin coconut oil (DECAF + CAF + CO). The substances were ingested 60 min before the trials, the order of the situations was randomized, and there were one-week intervals between them. At the end of the trials, the Borg scale was applied to evaluate the rating of perceived exertion (RPE) and the time was measured. Results: Our data did not show differences in running time among the trials (placebo: 7.64 ± 0.80, DECAF + CAF: 7.61 ± 1.02, DECAF + CAF + SO: 7.66 ± 0.89, and DECAF + CAF + CO: 7.58 ± 0.74 min; p = 0.93), nor RPE (placebo: 6.15 ± 2.03, DECAF + CAF: 6.00 ± 2.27, DECAF + CAF + SO: 6.54 ± 2.73, and DECAF + CAF + CO: 6.00 ± 2.45 score; p = 0.99). Lactate concentrations (placebo: 6.23 ± 2.72, DECAF + CAF: 4.43 ± 3.77, DECAF + CAF + SO: 5.29 ± 3.77, and DECAF + CAF + CO: 6.17 ± 4.18 mmol/L; p = 0.55) also was not modified. Conclusion: Our study shows that ingestion of decaffeinated coffee with the addition of isolated CAF and extra virgin CO, either isolated or combined, does not improve 1600 m running times, nor influence RPE and lactate concentrations in recreational runners. Thus, combination of coffee with CO as a pre-workout supplement seems to be unsubstantiated for a short-distance race.

Quality of Life Is Influenced by Body Weight, Education, and Family Income in Adolescents with Chronic Diseases.

OBJECTIVE: To evaluate the health-related quality of life (HRQoL) of adolescents diagnosed with different chronic conditions and to identify demographic, socioeconomic, and health-status outcomes associated with the impairment in HRQoL. STUDY DESIGN: Cross-sectional study. METHODS: We evaluated 276 adolescents (50.7% male) aged 14 ± 2 years that were assisted by healthcare public service and diagnosed with cancer (CA), type 1 diabetes mellitus (DM1), overweight (OW), asthma (AS), and no chronic health condition-control group (CG). Adolescents and parent-proxy completed age-appropriate self-report and/or parent-proxy report on generic HRQoL measures using PedsQL™. RESULTS: Adolescents with CA had lower overall HRQoL as well as poorer scores in all dimensions than either healthy participants or other chronic disease sufferers. HRQoL scores reported by parent-proxy were similar to those reported by adolescents across all chronic diseases. CG members reported better scores in all dimensions. Maternal education, family income, and marital status of parents were correlated with HRQoL scores in all dimensions. The risk of having an affected HRQoL score was higher in adolescents with CA than in adolescents with other chronic diseases. CONCLUSIONS: The likelihood of cancer affecting HRQoL was higher when compared to other chronic diseases, and the OW group had a worse overall score compared to CG. Adolescents with CA, AS, and OW reported worse school dimensions when compared to healthy adolescents. The education of adolescents and their parent-proxy, body weight, and family income influence the dimensions of HRQoL in adolescents with chronic diseases.

Nuts and Human Health Outcomes: A Systematic Review.

There has been increasing interest in nuts and their outcome regarding human health. The consumption of nuts is frequently associated with reduction in risk factors for chronic diseases. Although nuts are high calorie foods, several studies have reported beneficial effects after nut consumption, due to fatty acid profiles, vegetable proteins, fibers, vitamins, minerals, carotenoids, and phytosterols with potential antioxidant action. However, the current findings about the benefits of nut consumption on human health have not yet been clearly discussed. This review highlights the effects of nut consumption on the context of human health.

Sarcopenia and chemotherapy-mediated toxicity / Sarcopenia e toxicidade mediada pela quimioterapia

ABSTRACT This narrative review focuses on the role of sarcopenia and chemotherapy-induced toxicity in cancer patients. Consistent evidence shows that sarcopenia in cancer patients leads to decreased overall survival by influencing treatment discontinuation and dose reduction. Therefore, sarcopenia should be considered a robust prognostic factor of negative outcome as well as a determinant of increased healthcare costs.

RESUMO Esta revisão narrativa descreve o papel da sarcopenia e a toxicidade mediada pela quimioterapia em pacientes com câncer. Diversas evidências consistentes mostram que a sarcopenia em pacientes com câncer induz à menor sobrevida global, por influenciar na interrupção do tratamento e na redução da dose. Portanto, a sarcopenia pode ser considerada um importante fator de prognóstico de desfecho negativo, além de um determinante de maiores custos em saúde.

Doxorubicin caused severe hyperglycaemia and insulin resistance, mediated by inhibition in AMPk signalling in skeletal muscle.

BACKGROUND: Cancer is considered the second leading cause of death in the world, and for the treatment of this disease, pharmacological intervention strategies are frequently based on chemotherapy. Doxorubicin (DOX) is one of the most widely used chemotherapeutic agents in clinical practice for treating a number of solid tumours. The treatment with DOX mimics some effects of cancer cachexia, such as anorexia, asthenia, decreases in fat and skeletal muscle mass and fatigue. We observed that treatment with DOX increased the systemic insulin resistance and caused a massive increase in glucose levels in serum. Skeletal muscle is a major tissue responsible for glucose uptake, and the positive role of AMPk protein (AMP-activated protein kinase) in GLUT-4 (Glucose Transporter type 4) translocation, is well established. With this, our aim was to assess the insulin sensitivity after treatment with DOX and involvement of AMPk signalling in skeletal muscle in this process. METHODS: We used Wistar rats which received a single dose of doxorubicin (DOX group) or saline (CT group) intraperitoneally at a dose of 15 mg/kg b.w. The expression of proteins involved in insulin sensitivity, glucose uptake, inflammation, and activity of electron transport chain was assessed in extensor digitorum longus muscle, as well as the histological evaluation. In vitro assays were performed in L6 myocytes to assess glucose uptake after treatment with DOX. Agonist of AMPk [5-aminoimidazole-4-carboxamide (AICAR)] and the antioxidant n-acetyl cysteine were used in L6 cells to evaluate its effect on glucose uptake and cell viability. RESULTS: The animals showed a significant insulin resistance, hyperglycaemia, and hyperinsulinemia. A decrease in the expression of AMKP and GLUT-4 was observed in the extensor digitorum longus muscle. Also in L6 cells, DOX leads to a decrease in glucose uptake, which is reversed with AICAR. CONCLUSIONS: DOX leads to conditions similar to cachexia, with severe glucose intolerance both in vivo and in vitro. The decrease of AMPk activity of the protein is modulated negatively with DOX, and treatment with agonist of AMPk (AICAR) has proved to be a possible therapeutic target, which is able to recover glucose sensitivity in skeletal muscle.

Impact of Doxorubicin Treatment on the Physiological Functions of White Adipose Tissue.

White adipose tissue (WAT) plays a fundamental role in maintaining energy balance and important endocrine functions. The loss of WAT modifies adipokine secretion and disrupts homeostasis, potentially leading to severe metabolic effects and a reduced quality of life. Doxorubicin is a chemotherapeutic agent used clinically because of its good effectiveness against various types of cancer. However, doxorubicin has deleterious effects in many healthy tissues, including WAT, liver, and skeletal and cardiac muscles. Our objective was to investigate the effects of doxorubicin on white adipocytes through in vivo and in vitro experiments. Doxorubicin reduced the uptake of glucose by retroperitoneal adipocytes and 3T3-L1 cells via the inhibition of AMP-activated protein kinase Thr172 phosphorylation and glucose transporter 4 content. Doxorubicin also reduced the serum level of adiponectin and, to a greater extent, the expression of genes encoding lipogenic (Fas and Acc) and adipogenic factors (Pparg, C/ebpa, and Srebp1c) in retroperitoneal adipose tissue. In addition, doxorubicin inhibited both lipogenesis and lipolysis and reduced the hormone-sensitive lipase and adipose tissue triacylglycerol lipase protein levels. Therefore, our results demonstrate the impact of doxorubicin on WAT. These results are important to understand some side effects observed in patients receiving chemotherapy and should encourage new adjuvant treatments that aim to inhibit these side effects.

Sarcopenia and chemotherapy-mediated toxicity.

This narrative review focuses on the role of sarcopenia and chemotherapy-induced toxicity in cancer patients. Consistent evidence shows that sarcopenia in cancer patients leads to decreased overall survival by influencing treatment discontinuation and dose reduction. Therefore, sarcopenia should be considered a robust prognostic factor of negative outcome as well as a determinant of increased healthcare costs. RESUMO Esta revisão narrativa descreve o papel da sarcopenia e a toxicidade mediada pela quimioterapia em pacientes com câncer. Diversas evidências consistentes mostram que a sarcopenia em pacientes com câncer induz à menor sobrevida global, por influenciar na interrupção do tratamento e na redução da dose. Portanto, a sarcopenia pode ser considerada um importante fator de prognóstico de desfecho negativo, além de um determinante de maiores custos em saúde.

Sleep pattern and locomotor activity are impaired by doxorubicin in non-tumor-bearing rats.

PURPOSE: We sought explore the effects of doxorubicin on sleep patterns and locomotor activity. To investigate these effects, two groups were formed: a control group and a Doxorubicin (DOXO) group. METHODS: Sixteen rats were randomly assigned to either the control or DOXO groups. The sleep patterns were examined by polysomnographic recording and locomotor activity was evaluated in an open-field test. RESULTS: In the light period, the total sleep time and slow wave sleep were decreased, while the wake after sleep onset and arousal were increased in the DOXO group compared with the control group (p<0.05). In the dark period, the total sleep time, arousal, and slow wave sleep were increased, while the wake after sleep onset was decreased in the DOXO group compared with the control group (p<0.05). Moreover, DOXO induced a decrease of crossing and rearing numbers when compared control group (p<0.05). CONCLUSIONS: Therefore, our results suggest that doxorubicin induces sleep pattern impairments and reduction of locomotor activity.

Hypothalamic energy metabolism is impaired by doxorubicin independently of inflammation in non-tumour-bearing rats.

We sought to explore the effects of doxorubicin on inflammatory profiles and energy metabolism in the hypothalamus of rats. To investigate these effects, we formed two groups: a control (C) group and a Doxorubicin (DOXO) group. Sixteen rats were randomly assigned to either the control (C) or DOXO groups. The hypothalamus was collected. The levels of interleukin (IL)-1ß, IL-6, IL-10, TNF-α and energy metabolism (malate dehydrogenase, complex I and III activities) were analysed in the hypothalamus. The DOXO group exhibited a decreased body weight (p < 0.01). Hypothalamic malate dehydrogenase activity was reduced when compared with control (p < 0.05). In addition, pro-inflammatory cytokine levels were unchanged. Therefore, our results demonstrate that doxorubicin leads to an impairment of \hypothalamic energy metabolism, but do not affect the inflammatory pathway. SIGNIFICANCE PARAGRAPH: The hypothalamus is a central organ that regulates a great number of functions, such as food intake, temperature and energy expenditure, among others. Doxorubicin can lead to deep anorexia and metabolic chaos; thus, we observed the effect of this chemotherapeutic drug on the inflammation and metabolism in rats after the administration of doxorubicin in order to understand the central effect in the hypothalamus. Drug treatment by doxorubicin is used as a cancer therapy; however the use of this drug may cause harmful alterations to the metabolism. Thus, further investigations are needed on the impact of drug therapy over the long term.

High-fat fish oil diet prevents hypothalamic inflammatory profile in rats.

Whether PUFA diets affect inflammatory mediators in central and peripheral sites is not clear. We investigated the effect of high-fat PUFA diets on the expression of proteins involved in inflammatory pathways in hypothalamus, muscle, and liver. Male rats were fed for 2 months with either chow or high-fat diets enriched with either soy (n-6 PUFAs) or fish oil (n-3 PUFAs). The fish group had normal body weight, low serum NEFA, reduced hypothalamic levels of TNF- α , IL-6, and TRAF6, and increased levels of IL-10 receptor. In contrast, the soy group had increased body weight and hypothalamic levels of TRAF6 and NF κ Bp65. In muscle, the fish diet reduced TNF- α and IL-6 levels. Both PUFA diets increased muscle IL-10 levels and reduced liver TNF- α and IL-6 levels. The data showed that the high-fat soy diet induced activation of the hypothalamic NF κ B inflammatory pathway, a feature predisposing to feeding and energy expenditure disturbances associated with the development of obesity. On the other hand, the high-fat fish diet improved the central and the peripheral inflammatory profile via reduction of intracellular inflammatory mediators, suggesting a protection against obesity.

Ganho de peso em gestantes adolescentes: uma revisão / Weight gain in pregnant adolescents: a review

Teenage pregnancy is regarded as a special situation because of the demands for growth and development that occur in this period, which influences the final stage of pregnancy. Weight gain adjustment is reportedin the literature as an important factor in pregnancy because it is directlyrelated to maternal nutritional status and it is consequently one of the predictors of fetal growth and development, as well as of the postnatalnutritional status of newborns. In this study, we aimed to discuss the recommendations and guidance on weight gain during teenage pregnancyand provide subsidies for health professionals working in the . To thisend, we carried out a bibliographic survey of scientific articles indexedbetween 2001 and 2011 in the following databases: Scientific ElectronicLibrary Online (SciELO), Latin American and Caribbean Health SciencesLiterature (LILACS), and Medical Literature Analysis and RetrievalSystem Online (Medline) of the National Library of Medicine. Given therelevance of appropriate weight gain for pregnant teenagers and its majordifficulties, it is suggested that these young mothers be supervised byhealth professionals, with nutritional support, in order to ensure a successful outcome for the mother-child binomial.

La gestación en la adolescencia se considera una situación especial debido a las demandas de crecimiento y desarrollo que ocurren en esta fase, lo que influye en el resultado final del embarazo. La adecuación del aumento de peso es relatada en la literatura como un factor de suma importancia en la gestación, pues está directamente relacionada con el estado nutricional materno y, en consecuencia, es uno de los factores principales del crecimiento y desarrollo del feto y del estado nutricionaldel bebe después del nacimiento. El objetivo de este artículo fue discutir las recomendaciones y orientaciones sobre la alteración del aumento depeso en la gestación adolescente y ofrecer bases a los profesionales de la salud que actúan en esta área. En ese contexto, se realizó un levantamiento bibliográfico de artículos científicos indexados en las bases de datos: Scientific Eletronic Library On-line (SciELO), Literatura Latino Americana y del Caribe en Ciencias de la Salud (LILACS), Medical Literature Analysis and Retrieval System Online (Medline) de la National Library of Medice durante el periodo de 2001 a 2011. Una vez constatada la relevancia del aumento de peso adecuado de la adolescente gestante ysus principales complicaciones, se sugiere que estas jóvenes madres sean acompañadas por profesionales de la salud, especialmente con apoyo nutricional, con el objetivo de garantizar un buen resultado para el binomio madre-hijo.

Considera-se a gestação na adolescência uma situação especial em razão das demandas de crescimento e desenvolvimento que ocorrem nesta fase, o que influencia no resultado final da gravidez. A adequação do ganho de peso é relatada na literatura como um fator de extrema importância na gestação, pois está diretamente relacionada ao estado nutricional materno e, consequentemente, é um dos fatores preditores do crescimento e do desenvolvimento do concepto e do estado nutricional da criança após onascimento. O objetivo deste artigo foi discutir as recomendações e orientações sobre a alteração ponderal na gestação na adolescência, além de fornecer subsídios para os profissionais da saúde que atuam nessa área. Nesse contexto, realizou-se levantamento bibliográfico de artigos científicos indexados nas bases de dados: Scientific Eletronic Library On-line (SciELO), Literatura Latino-Americana e do Caribe em Ciências daSaúde (LILACS), Medical Literature Analysis and Retrieval System Online (Medline) da National Library of Medice durante o período de 2001 a2011. Constatada a relevância do ganho de peso adequado da gestante adolescente e das principais complicações caso essa adequação não sejaalcançada, sugere-se que essas jovens mães sejam monitoradas por profissionais de saúde, em especial com suporte nutricional, com o objetivode garantir um bom resultado para o binômio mãe-filho.

Both adiponectin and interleukin-10 inhibit LPS-induced activation of the NF-κB pathway in 3T3-L1 adipocytes.

Adiponectin and interleukin 10 (IL-10) are adipokines that are predominantly secreted by differentiated adipocytes and are involved in energy homeostasis, insulin sensitivity, and the anti-inflammatory response. These two adipokines are reduced in obese subjects, which favors increased activation of nuclear factor kappa B (NF-κB) and leads to elevation of pro-inflammatory adipokines. However, the effects of adiponectin and IL-10 on NF-κB DNA binding activity (NF-κBp50 and NF-κBp65) and proteins involved with the toll-like receptor (TLR-2 and TLR-4) pathway, such as MYD88 and TRAF6 expression, in lipopolysaccharide-treated 3T3-L1 adipocytes are unknown. Stimulation of lipopolysaccharide-treated 3T3-L1 adipocytes for 24h elevated IL-6 levels; activated the NF-κB pathway cascade; increased protein expression of IL-6R, TLR-4, MYD88, and TRAF6; and increased the nuclear activity of NF-κB (p50 and p65) DNA binding. Adiponectin and IL-10 inhibited the elevation of IL-6 levels and activated NF-κB (p50 and p65) DNA binding. Taken together, the present results provide evidence that adiponectin and IL-10 have an important role in the anti-inflammatory response in adipocytes. In addition, inhibition of NF-κB signaling pathways may be an excellent strategy for the treatment of inflammation in obese individuals.

Associação do consumo de gorduras e do nível socioeconômico sobre as medidas antropométricas de adultos. / Association of fat intake and socioeconomic status on anthropometric measurements of adults.

O objetivo do estudo foi identificar a influência das gorduras dietéticas sobre o índice de massa corporal (IMC) e a circunferência abdominal (CA) em uma amostra populacional de adultos. O estudo tranversal foi realizado com 448 adultos, entre 35 e 85 anos, de janeiro de 2004 a dezembro de 2007. Os indivíduos foram divididos em dois grupos de acordo com a renda familiar: Grupo 1 (G1) com maior renda, e Grupo 2 (G2) com menor renda. Foram levantadas variáveis socioeconômicas e demográficas, juntamente com variáveis antropométricas, índice de alimentação saudável (IAS) e perfil dietético. Os grupos foram semelhantes quanto ao gênero, à idade, ao IMC, e à CA. O IAS foi maior no G1 em decorrência do maior consumo de proteínas (+12,8%), laticínios (p<0.001), maior consumo de hortaliças (p<0,01), frutas (p<0,001), e menor de gordura (-9,8%). A maior contribuição das gorduras foi a saturada para o G1 (+5,0%) e a polinsaturada para o G2 (+14,4%). Apesar das diferenças socioeconômicas os grupos foram similares quanto ao IMC e à adiposidade abdominal. As diferenças no perfil do consumo de gorduras foram correlacionadas com as medidas antropométricas e puderam ser explicadas pelo menor consumo de óleo entre os indivíduos de renda mais elevada.

We aimed to identify the influence of dietary fat profile on body mass index (BMI) and waist circumference (WC) in a middle-class general population sample. A cross-sectional study of 448 adults aged 35-85 years was carried out from January 2004 to December 2007. Patients were divided in two groups according to family income: Group 1 (G1) with higher income, and Group 2 (G2) with lower income. Demographic and socioeconomic status were identified, along with anthropometric data, health eating index (HEI) and dietary profile. The groups were similar with respect to gender, age, BMI and WC. HEI was higher in G1 due to a higher intake of protein (+12.8%), dairy products (p<0.001), higher intake of vegetables (p<0.01), fruit (p<0.001), and less dietary fat (-9.8%). The main contribution of fats was saturated fat for G1 (+5.0%) and polyunsaturated fat for G2 (+14.4%). Besides differences in socioeconomic status the groups had similar BMI and abdominal fatness. Only differences in fat profile were correlated with the anthropometric measures mostly explained by the lower vegetable oil intake in higher income participants.

Ácidos graxos ômega 3 e tratamento da esquizofrenia: [revisão] / Omega 3 fatty acid and schizophrenia treatment: [review]

CONTEXTO: A esquizofrenia é uma desordem psiquiátrica complexa e debilitante cujo tratamento de base é realizado com medicamentos antipsicóticos. No entanto, evidências sugerem que a suplementação dietética com ácidos graxos ômega 3 (n-3) pode ser benéfica em diversas desordens psiquiátricas. OBJETIVO: Revisar a eficácia do n-3 como coadjuvante no tratamento farmacológico da esquizofrenia. MÉTODOS: Realizou-se uma pesquisa nas bases de dados eletrônicas Medline, Lilacs e SciELO. A estratégia de busca também incluiu a busca em árvore. Todos os estudos randomizados e controlados relevantes foram incluídos nesta revisão, independentemente do ano de publicação. RESULTADOS: Até o momento, foram divulgados seis estudos randomizados, duplo-cegos placebo controlados; cinco deles apresentaram resultados positivos na melhora dos sintomas da esquizofrenia, assinalando, ainda, superioridade do ácido graxo eicosapentaenoico (EPA) em relação ao ácido graxo docosaexaenoico. Em geral, o consumo de 2 g/dia de EPA conjuntamente com a medicação antipsicótica usual parece reduzir a sintomatologia da esquizofrenia, particularmente os sintomas positivos. CONCLUSÃO: A terapia nutricional com EPA mostrou-se útil como coadjuvante no tratamento da esquizofrenia. Por conseguinte, sugere-se que os pacientes esquizofrênicos sejam encorajados a consumir refeições balanceadas e saudáveis ricas em EPA e, caso a quantidade ideal não seja atingida pela dieta, a suplementação pode ser benéfica.

BACKGROUND: Schizophrenia is a complex and debilitating psychiatric disorder, whose primary pharmacological intervention is the use of antipsychotics. There is, however, growing evidence that dietary supplementation with omega 3 fatty acids (n-3) may be beneficial in several psychiatric conditions. OBJECTIVE: To review the efficacy of n-3 as a treatment for schizophrenia. METHODS: Electronic searches of the following databases were performed: Medline, Lilacs e SciELO. The search strategy also included cited reference searching. All relevant randomized controlled trials were included in the review. RESULTS: To date, five out of six randomized, double-blind, and placebo controlled studies obtained improvement in the symptoms of the psychosis. Besides, an advantage in the intake of eicosapentaenoic fatty acid (EPA) in relation to docosahexaenoic fatty acid was designated. Essentially, the intake of 2 g/day of EPA in addition to the standard medication was effective in decreasing the symptoms of schizophrenia. DISCUSSION: The nutritional therapy with EPA revealed to be useful as coadjutant in the treatment of schizophrenia. Therefore, we suggest that the schizophrenic patients should be encouraged to consume balanced and healthy meals rich in EPA and, if the ideal amount is not reached by the diet, the supplementation is likely to be beneficial.

Oxintomodulina e obesidade / Oxyntomodulin and obesity

Desde o descobrimento da leptina, avanços consideráveis foram obtidos na caracterização dos mecanismos hipotalâmicos do controle da ingestão alimentar e, atualmente, a oxintomodulina é reconhecida como um regulador da homeostase energética. O presente artigo de revisão enfoca algumas das mais relevantes inter-relações do hormônio oxintomodulina com o apetite, a homeostase energética e aspectos de seu papel na bioquímica e fisiologia nutricional. A oxintomodulina é um peptídeo intestinal anorexígeno produzido pelas células L do intestino. Recentes estudos têm demonstrado que em longo prazo a administração de oxintomodulina reduz a ingestão alimentar e o ganho de peso. Pesquisas em humanos têm verificado que o seu uso reduz o consumo energértico em 25 por cento. Portanto, a oxintomodulina representa uma potente terapia anti-obesidade. Entretanto, o mecanismo de ação da oxintomodulina ainda é desconhecido. Atuais evidências sugerem que tem ação via receptor do peptídeo semelhante ao glucagon 1. Além disso, a literatura mostra que, juntamente com a adoção de hábitos saudáveis e a mudança do estilo de vida, a oxintomodulina pode proporcionar menor avanço da obesidade.

Since the discovery of leptin, great advances occurred in the characterization of hypothalamic mechanisms involved in the control of food intake and oxyntomodulin is currently recognized as a homeostasis energy regulator. This review discusses the most important interrelationships between the hormone oxyntomodulin and appetite, energy homeostasis and aspects of its role in nutritional biochemistry and physiology. Oxyntomodulin is an anorexigenic peptide produced by the L cells of the small intestine. Recent studies have shown that long-term use of oxyntomodulin in rats leads to reduced food intake and weight gain. Studies in humans have demonstrated that its administration reduces food intake by 25 percent. Therefore, oxyntomodulin represents a potent anti-obesity therapy. However, its mechanism of action is unknown. Current evidence suggests that it acts via the peptide receptor similar to glucagon 1. Moreover, the literature shows that together with the adoption of healthy habits and lifestyle changes, oxyntomodulin can reduce weight gain.

AMP-activated protein kinase (AMPK): the key role in metabolic regulation and control of food intake: [review] / Proteína quinase ativada por AMP (AMPK): o papel-chave na regulação metabólica e controle da ingestão alimentar: [revisão]

Obesity is a clinical condition which has been viewed as a serious and growing public health problem. Excessive body weight has been shown to predispose to several diseases, mainly cardiovascular diseases, type 2 diabetes, and metabolic syndrome. AMP-activated protein kinase (AMPK) plays a potential role in food intake control in the hypothalamus and peripheral tissues. In vivo administration of leptin, which leads to a reduction of food intake, decreases hypothalamic AMPK activity. In peripheral tissues, AMPK regulates a variety of metabolic pathways that result in the suppression of ATP consumption (anabolic pathway) and the induction of ATP production (catabolic pathway). These include stimulating fatty acid uptake and oxidation and glucose uptake in multiple tissues: stimulating mitochondrial biogenesis in the skeletal muscle, stimulating glycolysis in the heart, inhibiting fatty acid synthesis in the liver and adipocyte, inhibiting cholesterol synthesis and glucogenesis in the liver, and inhibiting insulin secretion from pancreatic β-cells. AMPK is activated in response to environmental or nutritional stress factors, including thermal shock, hypoxia, glucose deprivation, calorie restriction, fasting, epigallocatechin-3-gallate consumption, resveratrol, exercising, ethanol consumption, n-3 (PUFA), statins, or troglitazone. These outcomes demonstrate that AMPK plays a key role in the regulation of feeding, indicating AMPK as a new target in the study of the anti-metabolic syndrome. Particularly, this review with recent findings show how AMPK activation coordinates the metabolic regulations and food intake control under different metabolic and nutritional circumstances.

La obesidad es una condición clínica vista como un serio y creciente problema de salud pública. Está demostrado que el exceso de peso corporal es un factor que predispone para muchas enfermedades, particularmente las cardiovasculares, diabetes mellitus y síndrome metabólico. La proteína quinasa AMP-activada (AMPK) en los tejidos periféricos y el hipotálamo tiene un papel importante sobre el control de la ingestión de alimentos. La administración de leptina in vivo conduce a la reducción de la ingestión energética, disminuyendo la actividad hipotalámica de la AMPK. En los tejidos periféricos, la AMPK regula una variedad de vías metabólicas provocando supresión del consumo de ATP (vía anabólica) e inducción de la producción de ATP (vía catabólica). Incluyendo estimulo a la captación de ácidos grasos y oxidación y captación de glucosa en diversos tejidos: estimulación de la glucosa en el corazón, inhibición de la síntesis de ácidos grasos en hígado y en los adipocitos, inhibición de la síntesis de colesterol y de la glicogénesis en el hígado e inhibición de la secreción de insulina por las células beta del páncreas. La AMPK es activada en repuesta a factores de stress ambiental o nutricional, incluyendo: choque térmico, hipoxia, pr ivación de glucosa, restricción calórica, ayuno, epigalocatequina-3-galato, estatinas o troglitazona. Eses datos demuestran la AMPK como nuevo objeto de estudio anti-síndrome metabólico. En especial, esta revisión sobre pesquisas recientes muestra como la activación de la AMPK coordina las regulaciones metabólicas y el control de la ingestión alimentar en diferentes circunstancias metabólicas y nutricionales.

A obesidade é uma condição clínica que é vista como um sério e crescente problema de saúde pública. O excesso de peso corporal tem demonstrado ser fator predisponente para várias doenças, particularmente as doenças cardiovasculares, diabetes tipo 2 e síndrome metabólica. A proteína quinase AMP-ativada (AMPK) nos tecidos periféricos e hipotálamo tem um papel importante no controle do consumo alimentar. A administração de leptina in vivo conduz à redução da ingestão energética, diminuindo a atividade hipotalâmica da AMPK. Nos tecidos periféricos, a AMPK regula uma variedade de rotas metabólicas que resultam na supressão do consumo de ATP (rota anabólica) e na indução da produção de ATP (rota catabólica). Estas rotas incluem estimulação da captação de ácidos graxos e oxidação e captação de glicose em diversos tecidos: estimulação da biogênese mitocondrial no músculo esquelético, estimulação da glicólise no coração, inibição da síntese de ácidos graxos no fígado e nos adipócitos, inibição da síntese de colesterol e da glicogênese no fígado, e inibição da secreção de insulina pelas células β-pancreática. A AMPK é ativada em resposta a fatores de estresse ambiental ou nutricional, incluindo: choque térmico, hipóxia, privação de glicose, restrição calórica, jejum, epigalocatequina-3-galato, resveratrol, exercício físico, consumo de etanol/álcool, n-3 (PUFA), estatinas ou troglitazona. Esses dados demonstram que a AMPK tem um papel chave na regulação da alimentação, indicando a AMPK como um novo alvo no estudo da antissíndrome metabólica. Em especial, esta revisão com recentes pesquisas mostra como a ativação da AMPK coordena as regulações metabólicas e o controle da ingestão alimentar em diferentes circunstâncias metabólicas e nutricionais.