Exercise training decreases mitogen-activated protein kinase phosphatase-3 expression and suppresses hepatic gluconeogenesis in obese mice

When the hepatic insulin signaling is compromised, there is an inadequate suppression of gluconeogenic pathways, leading the organism to high levels of glucose. Studies with animals with obesity induced by high fat diet or genetically modified showed increased MKP-3 expression and MKP-3/Foxo1 association in liver, with a consequent increase in blood glucose concentration, development of insulin resistance and DM2. As a non-pharmacological strategy recognized and indicated for prevention and treatment of diabetes is the regular practice of physical exercise. In this study we demostrated that physical training is an important tool capable of reducing insulin resistance in the liver by reducing the inflammatory process, including the inhibition of MKP-3 and, therefore, suppress gluconeogenic program in obesity rats. The understanding of these new mechanisms by which physical training regulates glucose homeostasis has critical importance to health professionals for the understanding and prevention of diabetes. Insulin plays an important role in the control of hepatic glucose production. Insulin resistant states are commonly associated with excessive hepatic glucose production, which contributes to both fasting hyperglycaemia and exaggerated postprandial hyperglycaemia. In this regard, increased activity of phosphatases may contribute to the dysregulation of gluconeogenesis. Mitogen-activated protein kinase phosphatase-3 (MKP-3) is a key protein involved in the control of gluconeogenesis. MKP-3-mediated dephosphorylation activates FoxO1 (a member of the forkhead family of transcription factors) and subsequently promotes its nuclear translocation and binding to the promoters of gluconeogenic genes such as phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase). In this study, we investigated the effects of exercise training on the expression of MKP-3 and its interaction with FoxO1 in the livers of obese animals. We found that exercised obese mice had a lower expression of MKP-3 and FoxO1/MKP-3 association in the liver. Further, the exercise training decreased FoxO1 phosphorylation and protein levels of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha) and gluconeogenic enzymes (PEPCK and G6Pase). These molecular results were accompanied by physiological changes, including increased insulin sensitivity and reduced hyperglycaemia, which were not caused by reductions in total body mass. Similar results were also observed with oligonucleotide antisense (ASO) treatment. However, our results showed that only exercise training could reduce an obesity-induced increase in HNF-4 alpha protein levels while ASO treatment alone had no effect. These findings could explain, at least in part, why additive effects of exercise training treatment and ASO treatment were not observed. Finally, the suppressive effects of exercise training on MKP-3 protein levels appear to be related, at least in part, to the reduced phosphorylation of Extracellular signal-regulated kinases (ERK) in the livers of obese mice592613251340CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP471498/2011-42010/12091-2; 2011/14727-4; 2011/13779-

Eccentric Exercise Leads To Glial Activation But Not Apoptosis In Mice Spinal Cords.

The aim of this investigation was to evaluate the effects of 3 overtraining (OT) protocols on the glial activation and apoptosis in the spinal cords of mice. Rodents were divided into control (C; sedentary mice), overtrained by downhill running (OTR/down), overtrained by uphill running (OTR/up) and overtrained by running without inclination (OTR). The incremental load test, ambulation test, exhaustive test and functional behavioural assessment were used as performance evaluation parameters. 36 h after the exhaustive test, the dorsal and ventral parts of the lumbar spinal cord (L4-L6) were dissected for subsequent protein analysis by immunoblotting. The OT protocols led to similar responses of some performance parameters. The ventral glial fibrillary acidic protein (GFAP) protein levels were diminished in the OTR/up and OTR compared to CT and OTR/down groups. The ventral ionized calcium binding adaptor molecule 1 (Iba-1), and the dorsal GFAP and Iba-1 protein levels were increased in the OTR/down compared to the other groups. The ratio between the cleaved capase-3/caspase-3 and cleaved caspase-9/caspase-9 measured in the spinal cord were not sensitive to the OT protocols. In summary, the OTR/down activated the glial cells in the motor (i. e. Iba-1) and sensory (i. e. GFAP and Iba-1) neurons without leading to apoptosis

Draft of Cheyenne & Arapahoe Report

https://digitalcommons.assumption.edu/mallet-manuscripts/1030/thumbnail.jp

β-Hydroxy-β-methylbutyrate (HMβ) supplementation stimulates skeletal muscle hypertrophy in rats via the mTOR pathway

β-Hydroxy-β-methylbutyrate (HMβ) supplementation is used to treat cancer, sepsis and exercise-induced muscle damage. However, its effects on animal and human health and the consequences of this treatment in other tissues (e.g., fat and liver) have not been examined. The purpose of this study was to evaluate the effects of HMβ supplementation on skeletal muscle hypertrophy and the expression of proteins involved in insulin signalling. Rats were treated with HMβ (320 mg/kg body weight) or saline for one month. The skeletal muscle hypertrophy and insulin signalling were evaluated by western blotting, and hormonal concentrations were evaluated using ELISAs. HMβ supplementation induced muscle hypertrophy in the extensor digitorum longus (EDL) and soleus muscles and increased serum insulin levels, the expression of the mammalian target of rapamycin (mTOR) and phosphorylation of p70S6K in the EDL muscle. Expression of the insulin receptor was increased only in liver. Thus, our results suggest that HMβ supplementation can be used to increase muscle mass without adverse health effects

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