O papel da enfermagem e sua contribuição para a promoção do envelhecimento saudável e ativo

A longevidade adquirida por meio de melhor qualidade de vida da população tem obrigado o setor saúde a enfrentar alguns desafios para proporcionar aos idosos longos anos de vida saudáveis, o que tem levado as equipes de enfermagem das unidades básicas a não conseguir realizar uma assistência de modo adequada, uma vez que os profissionais se prendem apenas aos aspectos biológicos do envelhecimento, esquecendo que a população da terceira idade também possui uma vida social e afetiva. Esta pesquisa trata-se de uma revisão bibliográfica, e para sua elaboração foram pesquisados diversos artigos científicos na BIREME, SCIELO e LILACS (Literatura Latino Americana da Ciência da Saúde e do Caribe), além de condutas e diretrizes do ministério da saúde. Seu principal objetivo foi conhecer a atuação do enfermeiro na atenção básica que favoreça o envelhecimento saudável e ativo. Considerando a importância da promoção da saúde em nosso meio, o enfermeiro, enquanto membro de uma equipe multiprofissional possui um papel de extrema responsabilidade, o qual deverá estar devidamente qualificado para atender qualitativa e quantitativamente as necessidades individuais e coletivas de todas as pessoas, e em especial os da população idosa

Effects of prolonged fasting on cardiac muscle metabolism and cardiac function in rats.

O presente estudo teve por objetivo investigar os efeitos do jejum de 48 horas sobre o metabolismo do músculo cardíaco e sobre a função cardíaca. Para isso, ratos machos com 60 dias foram separados em dois grupos: jejuados por 48 h (grupo experimental) e alimentados (grupo controle). Após eutanásia, sangue e coração foram coletados. O coração foi excisado e a aurícula do átrio direito (AAD), a aurícula do átrio esquerdo (AAE), parede do ventrículo direito (PVD), septo interventricular (SIV) e parede do ventrículo esquerdo (PVE) foram separadas e analisadas individualmente. Análises de parâmetros bioquímicos plasmáticos, dosagem de metabólitos, atividade máxima de enzimas, assim como expressão gênica e proteica foram realizadas. O jejum promoveu alterações metabólicas em todas as regiões, sendo mais intensas na PVE. Registros ventriculares e hemodinâmicos também foram obtidos. O jejum diminuiu a força de contração (dP/dt+), a força de relaxamento (dP/dt-) e a frequência cardíaca (FC), aumentou o tempo de enchimento diastólico e o hematócrito. Apesar de observamos aumento do potencial oxidativo e aumento da concentração disponível de ATP, é possível que 48h de jejum comprometa a volemia e por consequência a função cardíaca.The present study aimed to investigate the effects of 48-hour fasting on cardiac muscle metabolism and cardiac function. For this, male rats with 60 days were separated into two groups: fasted for 48 h (experimental group) and fed (control group). After euthanasia, blood and heart were collected. The heart was excised and the right atrial atrium (RAA), left atrial atrium (LAA), right ventricular wall (RVW), interventricular septum (IVS) and left ventricular wall (LVW) were separated and analyzed individually. Analyzes of plasma biochemical parameters, dosage of metabolites, maximum activity of enzymes, as well as gene and protein expression were performed. Fasting promoted metabolic alterations in all regions, being more intense in PVE. Ventricular and hemodynamic records were also obtained. Fasting decreased contraction force (dP / dt +), relaxation force (dP / dt-) and heart rate (HR), increased diastolic filling time and hematocrit. Although we observed an increase in the oxidative potential and an increase in the available ATP concentration, it is possible that 48h-fasting compromises blood volume and, consequently, cardiac function

Low Birth Weight Intensifies Changes in Markers of Hepatocarcinogenesis Induced by Fructose Consumption in Rats.

Peer reviewed: TrueFunder: Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Intrauterine growth restriction (IUGR) due to fetal exposure to glucocorticoid excess results in metabolic inflexibility and hepatic steatosis upon nutritional stress during adulthood. We previously demonstrated that rats born to dexamethasone (DEX)-treated mothers developed hepatic steatosis when exposed to 10% fructose solution during adult life. Persistent triacylglyceride (TAG) accumulation in the liver, in turn, is a feature of non-alcoholic fatty liver disease (NAFLD), which serves as a risk factor for non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC). In the present study, we demonstrate that the combination of IUGR and fructose treatment during adulthood also results in increased hepatic myeloperoxidase (MPO) activity, AKT phosphorylation and serum aspartate transaminase. Growth-restricted rats also presented reduced hepatic TRIB3 and GADD45a after fructose treatment. Other markers of cell proliferation, such as Cyclin D, PCNA, Hgf and Hspa4/Hsp70 expression and the number of Ki-67 positive cells, were all increased in the liver of growth- restricted rats treated with fructose. On the other hand, the combination of IUGR and fructose treatment during adult life reduced the levels of IGF-1. In conclusion, our data indicate that after exposure to fructose, adult rats subjected to dexamethasone-induced IUGR display exacerbated molecular changes in markers of NASH and HCC

The absence of lactation after pregnancy induces long-term lipid accumulation in maternal liver of mice

The present investigation evaluated whether pregnancy followed by lactation exerts long-term impacts on maternal hepatic lipid metabolism. Female mice were subjected to two pregnancies, after which they were either allowed to breastfeed their pups for 21 days (L21) or had their litter removed (L0). Age-matched virgin mice were used as controls (CTL). Three months after the second delivery, serum was collected for lipid profiling, and fragments of liver were used to assess lipid content and to evaluate the key steps of de novo non-esterified fatty acid (NEFA) synthesis, esterification and β-oxidation, very low density lipoprotein (VLDL) assembly and secretion and autophagy. L0 exhibited a significant increase in hepatic TG and reduced apolipoprotein B-100 (ApoB-100) expression. L21 mice had increased ATP citrate lyase (ACLY) activity and reduced acetyl-CoA carboxylase (ACC) phosphorylation but no increased hepatic TG. On the other hand, L21 mice had reduced hepatic sequestosome 1 (SQSTM1/p62) levels. Increased high density lipoprotein (HDL) cholesterol and hepatic apolipoprotein A-1 (ApoA-1) expression were found exclusively in L21. The present study reveals that long-term hepatic lipid accumulation is induced by the history of pregnancy without lactation. On the other hand, reduced SQSTM1/p62 levels indicate that increased autophagic flux during life may prevent hepatic fat in dams subjected to lactation. Lactation after pregnancy is also obligatory for a long-term increase in maternal HDL. The present data may contribute to the understanding of the mechanisms leading to elevated cardiometabolic risk in women limited to short periods of lactation217261270CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPNão tem2015/12680-1; 2013/07607-

Changes in PGC-1α-Dependent Mitochondrial Biogenesis Are Associated with Inflexible Hepatic Energy Metabolism in the Offspring Born to Dexamethasone-Treated Mothers

In the present study we investigated the participation of hepatic peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) in the metabolic programming of newborn rats exposed in utero to dexamethasone (DEX). On the 21st day of life, fasted offspring born to DEX-treated mothers displayed increased conversion of pyruvate into glucose with simultaneous upregulation of PEPCK (phosphoenolpyruvate carboxykinase) and G6Pase (glucose-6-phosphatase). Increased oxidative phosphorylation, higher ATP/ADP ratio and mitochondrial biogenesis and lower pyruvate levels were also found in the progeny of DEX-treated mothers. On the other hand, the 21-day-old progeny of DEX-treated mothers had increased hepatic triglycerides (TAG) and lower CPT-1 activity when subjected to short-term fasting. At the mechanistic level, rats exposed in utero to DEX exhibited increased hepatic PGC-1α protein content with lower miR-29a-c expression. Increased PGC-1α content was concurrent with increased association to HNF-4α and NRF1 and reduced PPARα expression. The data presented herein reveal that changes in the transcription machinery in neonatal liver of rats born to DEX-treated mothers leads to an inflexible metabolic response to fasting. Such programming is hallmarked by increased oxidative phosphorylation of pyruvate with impaired FFA oxidation and hepatic TAG accumulation