O que influencia o desejo de ter um filho nos jovens adultos

Enquadramento: O Índice Sintético de Fecundidade (ISF) português é dos mais baixos da Europa. No entanto, o desejo de cada individuo jovem ter um filho, sem qualquer restrição é superior ao valor de referência para a substituição de gerações. Objectivos: Compreender a relação entre as variáveis sociodemográficas, as variáveis de contexto sexual e reprodutivo e as variáveis psicológicas com o desejo de ter um filho. Métodos: Estudo quantitativo, descritivo-correlacional. A amostra é não probabilistica por conveniência com uma média de idade de 20,79 anos (dp=2,785). O protocolo de investigação foi um questionário que caracteriza o perfil sociodemográfico, sexual e reprodutivo da amostra. Foi incluído o “QVPM” (Matos& Costa, 2001), “QVA” (Matos& Costa, 2001), “Questionário de desejo de ter um filho” (Leal, 1999) e escala de Auto estima de (Rosenberg, 1965, adaptado 1999). Resultados: É no sexo feminino e no grupo etário ≤ 19 anos que o desejo de ter um filho é maior. O desejo de ter um filho diminui com a idade. Ter namorado(a), pertencer a uma família alargada, não ter irmãos e ser proveniente de uma zona rural estão relacionados com maior desejo de ter um filho, no entanto sem diferenças estatísticas significativas. Os estudantes do primeiro ano apresentam maior desejo de ter um filho no futuro e este diminui conforme a progressão no ensino (ano de curso) e aproximação do mercado de trabalho. Os que apresentam maior desejo de ser pais com base em sentimentos relativos à parentalidade frequentam menos a consulta de planeamento familiar. Observaram-se diferenças estatísticas significativas entre o número de filhos desejado no futuro e o desejo de ter um filho. O nível de conhecimento sobre fertilidade não influencia o desejo de ter um filho. Quanto maior a ansiedade de separação da mãe (vinculação à mãe), a dependência da vinculação amorosa, a ansiedade de separação do pai (vinculação ao pai) e a auto estima, maior é o desejo de ter um filho. Conclusões: O desejo de ter um filho é um construto ao longo da vida, pelo que os enfermeiros acompanhando o ciclo vital do individuo contribuem para a promoção e capacitação da parentalidade nomeadamente através da: avaliação e promoção do vinculo parental e promoção da saúde sexual e reprodutiva. Palavras chave: Jovem adulto, parentalidade, vinculação amorosa, auto estima.Abstract: Framework: The Portuguese Synthetic Fertility Index (ISF) is among the lowest in Europe. However, the desire of each young individual to have a child without any restriction is higher than the reference value for the replacement of generations. Objective: Understand the relationship between sociodemographic variables, sexual and reproductive health variables, and psychological variables with the desire to have a child. Methods: Quantitative, descriptive-correlational study. A non-probabilistic for convenience sampling with an average age of 20.79 years (sd = 2.785). The research protocol was a questionnaire that characterizes the sociodemographic, sexual and reproductive profile of the sample and includes the “QVPM” (Matos& Costa, 2001), “QVA” (Matos& Costa, 2001), “Questionário de desejo de ter um filho” (Leal, 1999) and Rosenberg Self – esteem scale (Rosenberg, 1965, adap.1999). Results: It is in the female sex and in the age group ≤ 19 years that the desire to have a child is higher. The desire to have a child decreases with age. Having a boyfriend, belonging to an extended family, not having siblings and being from the countryside are related to higher desire to have a child, however without significant statistical differences. In the first year students the desire to have a child is higher and this decreases with the progression in school’s year and the approaching of labor market. Those who are more likely to be parents based on feelings about parenting are less likely to attend family planning visits. Significant statistical differences were observed between the number of children desired in the future and the desire to have a child. The level of knowledge about fertility does not influence the desire to have a child. The greater the separation anxiety of the mother (attachment to the mother), the dependence of the love bond, the separation anxiety of the father (attachment to the father) and the self esteem, the greater is the desire to have a child. Conclusions: The desire to have a child is a lifelong construct, so the nurses by accompanying the individual's life cycle contribute to the promotion and training of parenting, namely through: evaluation and promotion of parental attachment and promotion of sexual and reproductive health. Descriptors: Young adult, parenting, attachment, self esteem

Exercise Counterbalances Rho/ROCK2 Signaling Impairment in the Skeletal Muscle and Ameliorates Insulin Sensitivity in Obese Mice

Physical exercise is considered a fundamental strategy in improving insulin sensitivity and glucose uptake in skeletal muscle. However, the molecular mechanisms underlying this regulation, primarily on skeletal muscle glucose uptake, are not fully understood. Recent evidence has shown that Rho-kinase (ROCK) isoforms play a pivotal role in regulating skeletal muscle glucose uptake and systemic glucose homeostasis. The current study evaluated the effect of physical exercise on ROCK2 signaling in skeletal muscle of insulin-resistant obese animals. Physiological (ITT) and molecular analysis (immunoblotting, and RT-qPCR) were performed. The contents of RhoA and ROCK2 protein were decreased in skeletal muscle of obese mice compared to control mice but were restored to normal levels in response to physical exercise. The exercised animals also showed higher phosphorylation of insulin receptor substrate 1 (IRS1 Serine 632/635) and protein kinase B (Akt) in the skeletal muscle. However, phosphatase and tensin homolog (PTEN) and protein-tyrosine phosphatase-1B (PTP-1B), both inhibitory regulators for insulin action, were increased in obesity but decreased after exercise. The impact of ROCK2 action on muscle insulin signaling is further underscored by the fact that impaired IRS1 and Akt phosphorylation caused by palmitate in C2C12 myotubes was entirely restored by ROCK2 overexpression. These results suggest that the exercise-induced upregulation of RhoA-ROCK2 signaling in skeletal muscle is associated with increased systemic insulin sensitivity in obese mice and further implicate that muscle ROCK2 could be a potential target for treating obesity-linked metabolic disorders

Targeted disruption of inducible nitric oxide synthase protects against aging, S-nitrosation, and insulin resistance in muscle of male mice

Accumulating evidence has demonstrated that S-nitrosation of proteins plays a critical role in several human diseases. Here, we explored the role of inducible nitric oxide synthase (iNOS) in the S-nitrosation of proteins involved in the early steps of the insulin-signaling pathway and insulin resistance in the skeletal muscle of aged mice. Aging increased iNOS expression and S-nitrosation of major proteins involved in insulin signaling, thereby reducing insulin sensitivity in skeletal muscle. Conversely, aged iNOS-null mice were protected from S-nitrosation–induced insulin resistance. Moreover, pharmacological treatment with an iNOS inhibitor and acute exercise reduced iNOS-induced S-nitrosation and increased insulin sensitivity in the muscle of aged animals. These findings indicate that the insulin resistance observed in aged mice is mainly mediated through the S-nitrosation of the insulin-signaling pathway

High-Fat Diet Induces Apoptosis of Hypothalamic Neurons

Consumption of dietary fats is amongst the most important environmental factors leading to obesity. In rodents, the consumption of fat-rich diets blunts leptin and insulin anorexigenic signaling in the hypothalamus by a mechanism dependent on the in situ activation of inflammation. Since inflammatory signal transduction can lead to the activation of apoptotic signaling pathways, we evaluated the effect of high-fat feeding on the induction of apoptosis of hypothalamic cells. Here, we show that consumption of dietary fats induce apoptosis of neurons and a reduction of synaptic inputs in the arcuate nucleus and lateral hypothalamus. This effect is dependent upon diet composition, and not on caloric intake, since pair-feeding is not sufficient to reduce the expression of apoptotic markers. The presence of an intact TLR4 receptor, protects cells from further apoptotic signals. In diet-induced inflammation of the hypothalamus, TLR4 exerts a dual function, on one side activating pro-inflammatory pathways that play a central role in the development of resistance to leptin and insulin, and on the other side restraining further damage by controlling the apoptotic activity

Hypothalamic S1P/S1PR1 axis controls energy homeostasis

Sphingosine 1-phosphate receptor 1 (S1PR1) is a G-protein-coupled receptor for sphingosine-1-phosphate (S1P) that has a role in many physiological and pathophysiological processes. Here we show that the S1P/S1PR1 signalling pathway in hypothalamic neurons regulates energy homeostasis in rodents. We demonstrate that S1PR1 protein is highly enriched in hypothalamic POMC neurons of rats. Intracerebroventricular injections of the bioactive lipid, S1P, reduce food consumption and increase rat energy expenditure through persistent activation of STAT3 and the melanocortin system. Similarly, the selective disruption of hypothalamic S1PR1 increases food intake and reduces the respiratory exchange ratio. We further show that STAT3 controls S1PR1 expression in neurons via a positive feedback mechanism. Interestingly, several models of obesity and cancer anorexia display an imbalance of hypothalamic S1P/S1PR1/STAT3 axis, whereas pharmacological intervention ameliorates these phenotypes. Taken together, our data demonstrate that the neuronal S1P/S1PR1/STAT3 signalling axis plays a critical role in the control of energy homeostasis in rats

Unsaturated Fatty Acids Revert Diet-Induced Hypothalamic Inflammation in Obesity

Background: In experimental models, hypothalamic inflammation is an early and determining factor in the installation and progression of obesity. Pharmacological and gene-based approaches have proven efficient in restraining inflammation and correcting the obese phenotypes. However, the role of nutrients in the modulation of hypothalamic inflammation is unknown. Methodology/Principal Findings: Here we show that, in a mouse model of diet-induced obesity, partial substitution of the fatty acid component of the diet by flax seed oil (rich in C18:3) or olive oil (rich in C18:1) corrects hypothalamic inflammation, hypothalamic and whole body insulin resistance, and body adiposity. In addition, upon icv injection in obese rats, both v3 and v9 pure fatty acids reduce spontaneous food intake and body mass gain. These effects are accompanied by the reversal of functional and molecular hypothalamic resistance to leptin/insulin and increased POMC and CART expressions. In addition, both, v3 and v9 fatty acids inhibit the AMPK/ACC pathway and increase CPT1 and SCD1 expression in the hypothalamus. Finally, acute hypothalamic injection of v3 and v9 fatty acids activate signal transduction through the recently identified GPR120 unsaturated fatty acid receptor. Conclusions/Significance: Unsaturated fatty acids can act either as nutrients or directly in the hypothalamus, reverting dietinduced inflammation and reducing body adiposity. These data show that, in addition to pharmacological and geneti

Central Exercise Action Increases the AMPK and mTOR Response to Leptin

AMP-activated protein kinase (AMPK) and mammalian Target of Rapamycin (mTOR) are key regulators of cellular energy balance and of the effects of leptin on food intake. Acute exercise is associated with increased sensitivity to the effects of leptin on food intake in an IL-6-dependent manner. To determine whether exercise ameliorates the AMPK and mTOR response to leptin in the hypothalamus in an IL-6-dependent manner, rats performed two 3-h exercise bouts, separated by one 45-min rest period. Intracerebroventricular IL-6 infusion reduced food intake and pretreatment with AMPK activators and mTOR inhibitor prevented IL-6-induced anorexia. Activators of AMPK and fasting increased food intake in control rats to a greater extent than that observed in exercised ones, whereas inhibitor of AMPK had the opposite effect. Furthermore, the reduction of AMPK and ACC phosphorylation and increase in phosphorylation of proteins involved in mTOR signal transduction, observed in the hypothalamus after leptin infusion, were more pronounced in both lean and diet-induced obesity rats after acute exercise. Treatment with leptin reduced food intake in exercised rats that were pretreated with vehicle, although no increase in responsiveness to leptin-induced anorexia after pretreatment with anti-IL6 antibody, AICAR or Rapamycin was detected. Thus, the effects of leptin on the AMPK/mTOR pathway, potentiated by acute exercise, may contribute to appetite suppressive actions in the hypothalamus

The role of proliferator-activated receptor γ coactivator–1α in the fatty-acid–dependent transcriptional control of interleukin-10 in hepatic cells of rodents

Interleukin-10 (IL-10) is an endogenous factor that restrains hepatic insulin resistance in diet-induced steatosis. Reducing IL-10 expression increases proinflammatory activity in the steatotic liver and worsens insulin resistance. As the transcriptional coactivator proliferator-activated receptor γ coactivator–1 α (PGC-1 α) plays a central role in dysfunctional hepatocytic activity in diet-induced steatosis, we hypothesized that at least part of the action of PGC-1 α could be mediated by reducing the transcription of the IL-10 gene. Here, we used immunoblotting, real-time polymerase chain reaction, immunocytochemistry, and chromatin immunoprecipitation assay to investigate the role of PGC-1 α in the control of IL-10 expression in hepatic cells. First, we show that, in the intact steatotic liver, the expressions of IL-10 and PGC-1 α are increased. Inhibiting PGC-1 α expression by antisense oligonucleotide increases IL-10 expression and reduces the steatotic phenotype. In cultured hepatocytes, the treatment with saturated and unsaturated fatty acids increased IL-10 expression. This was accompanied by increased association of PGC-1 α with c-Maf and p50–nuclear factor (NF) κB, 2 transcription factors known to modulate IL-10 expression. In addition, after fatty acid treatment, PGC-1 α, c-Maf, and p50-NF κB migrate from the cytosol to the nuclei of hepatocytes and bind to the IL-10 promoter region. Inhibiting NF κB activation with salicylate reduces IL-10 expression and the association of PGC-1 α with p50-NF κB. Thus, PGC-1 α emerges as a potential transcriptional regulator of the inflammatory phenomenon taking place in the steatotic liver592215223CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPNão temNão te