MOTIVASI ATLET UNTUK MENGIKUTI KEJUARAAN TINGKAT INTERNASIONAL PADA MAHASISWA FAKULTAS ILMU KEOLAHRAGAAN UNY

Penelitian ini membahas tentang motivasi dalam ranah olahraga yang begitu sengit dan perlu kerja keras serta konsistensi di dalamnya. Adapun tujuan yang ingin dicapai adalah untuk mengetahui motivasi atlet untuk mengikuti kejuaraan tingkat Internasional pada mahasiswa Fakultas Ilmu Keolahragaan UNY. Di samping itu, penelitian ini dimaksudkan untuk mengetahui seberapa besar motivasi intrinsik dan ekstrinsik atlet Fakultas Ilmu Keolahragaan Universitas Negeri Yogyakarta. Penelitian ini merupakan penelitian deskriptif kuantitatif dengan menggunakan satu variabel, yaitu motivasi. Sampel yang digunakan dalam penelitian ini adalah atlet Fakultas Ilmu Keolahragaan Universitas Negeri Yogyakarta. Peneliti menggunakan teknik purposive sampling. Instrumen yang digunakan untuk mengumpulkan data adalah angket. Untuk menganalisis data yang terkumpul, peneliti menggunakan teknik deskriptif kuantitatif dengan persentase. Hasil penelitian menunjukkan bahwa nilai rata-rata motivasi atlet FIK UNY untuk mengikuti kejuaraan tingkat Internasional berada pada kategori kurang baik dengan jumlah 25 atlet atau 41,66%. Motivasi instrinsik atlet FIK UNY untuk mengikuti kejuaraan tingkat Internasional berada pada kategori kurang baik dengan jumlah 21 atlet atau 35%. Motivasi ekstrinsik atlet motivasi atlet FIK UNY untuk mengikuti kejuaraan tingkat Internasional berada pada kategori kurang baik dengan jumlah 24 atlet atau 40%

Physical Exercise Reduces Circulating Lipopolysaccharide and TLR4 Activation and Improves Insulin Signaling in Tissues of DIO Rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)OBJECTIVE-Insulin resistance in diet-induced obesity (DIO) is associated with a chronic systemic low-grade inflammation, and Toll-like receptor 4 (TLR4) plays an important role in the link among insulin resistance, inflammation, and obesity. The current study aimed to analyze the effect of exercise on TLR4 expression and activation in obese rats and its consequences on insulin sensitivity and signaling. RESEARCH DESIGN AND METHODS-The effect of chronic and acute exercise was investigated on insulin sensitivity, insulin signaling, TLR4 activation, c-Jun NH(2)-terminal kinase (JNK) and I kappa B kinase (IKK beta) activity, and lipopolysaccharide (LPS) serum levels in tissues of DIO rats. RESULTS-The results showed that chronic exercise reduced TLR4 mRNA and protein expression in liver, muscle, and adipose tissue. However, both acute and chronic exercise blunted TLR4 signaling in these tissues, including a reduction in JNK and IKK beta phosphorylation and IRS-1 serine 307 phosphorylation, and, in parallel, improved insulin-induced IR, IRS-1 tyrosine phosphorylation, and Akt serine phosphorylation, and reduced LPS serum levels. CONCLUSIONS-Our results show that physical exercise in DIO rats, both acute and chronic, induces an important suppression in the TLR4 signaling pathway in the liver, muscle, and adipose tissue, reduces LPS serum levels, and improves insulin signaling and sensitivity. These data provide considerable progress in our understanding of the molecular events that link physical exercise to an improvement in inflammation and insulin resistance. Diabetes 60:784-796, 2011603784796Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de PesquisaINCT-Obesidade e DiabetesFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP

Blocking inos and endoplasmic reticulum stress synergistically improves insulin resistance in mice

Recent data show that iNOS has an essential role in ER stress in obesity. However, whether iNOS is sufficient to account for obesity-induced ER stress and Unfolded Protein Response (UPR) has not yet been investigated. In the present study, we used iNOS knockout mice to investigate whether high-fat diet (HFD) can still induce residual ER stress-associated insulin resistance. Methods: For this purpose, we used the intraperitoneal glucose tolerance test (GTT), euglycemic-hyperinsulinemic clamp, western blotting and qPCR in liver, muscle, and adipose tissue of iNOS KO and control mice on HFD. Results: The results of the present study demonstrated that, in HFD fed mice, iNOS-induced alteration in insulin signaling is an essential mechanism of insulin resistance in muscle, suggesting that iNOS may represent an important target that could be blocked in order to improve insulin sensitivity in this tissue. However, in liver and adipose tissue, the insulin resistance induced by HFD was only partially dependent on iNOS, and, even in the presence of genetic or pharmacological blockade of iNOS, a clear ER stress associated with altered insulin signaling remained evident in these tissues. When this ER stress was blocked pharmacologically, insulin signaling was improved, and a complete recovery of glucose tolerance was achieved. Conclusions: Taken together, these results reinforce the tissue-specific regulation of insulin signaling in obesity, with iNOS being sufficient to account for insulin resistance in muscle, but in liver and adipose tissue ER stress and insulin resistance can be induced by both iNOS-dependent and iNOS-independent mechanisms62206218FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCAPES - COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL E NÍVEL SUPERIORCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO2012/15009-0; 2016/07122-2sem informaçãosem informaçã

The role of gut-liver axis in the restriction of intrauterine growth in a model of experimental gastroschisis

PURPOSE: To evaluate the intrauterine growth restriction (IUGR) by the expression of IR-&#946;, IRS-1, IRS-2, IGF-IR&#946; and Ikappa&#946; in experimental model of gastroschisis. METHODS: Pregnant rats at 18.5 days of gestation were submitted to surgery to create experimental fetal gastroschisis (term = 22 days) were divided in three groups: gastroschisis (G), control (C) and sham (S). Fetuses were evaluated for body weight (BW), intestinal (IW), liver (LW) and their relations IW/BW and LW/BW. IR-&#946; and IGF-IR&#946; receptors, IRS-1 and IRS-2 substrates and Ikappa&#946; protein were analyzed by western blotting. RESULTS: BW was lower in G, the IW and IW / BW were greater than C and S (p<0.05) groups. The liver showed no differences between groups. In fetuses with gastroschisis, compared with control fetuses, the expression of IGF-IR&#946; (p<0.001) and Ikappa&#946; (p<0.001) increased in the liver and intestine, as well as IR-&#946; (p<0.001) which decreased in both. In contrast to the intestine, IRS-1 (p<0.001) increased in the liver and IRS-2 decreased (p<0.01). CONCLUSION: The axis of the intestine liver has an important role in inflammation, with consequent changes in the metabolic pathway of glucose can contribute to the IUGR in fetuses with gastroschisis

Insulin Resistance in HIV-Patients: Causes and Consequences

Here we review how immune activation and insulin resistance contribute to the metabolic alterations observed in HIV-infected patients, and how these alterations increase the risk of developing CVD. The introduction and evolution of antiretroviral drugs over the past 25 years has completely changed the clinical prognosis of HIV-infected patients. The deaths of these individuals are now related to atherosclerotic CVDs, rather than from the viral infection itself. However, HIV infection, cART, and intestinal microbiota are associated with immune activation and insulin resistance, which can lead to the development of a variety of diseases and disorders, especially with regards to CVDs. The increase in LPS and proinflammatory cytokines circulating levels and intracellular mechanisms activate serine kinases, resulting in insulin receptor substrate-1 (IRS-1) serine phosphorylation and consequently a down regulation in insulin signaling. While lifestyle modifications and pharmaceutical interventions can be employed to treat these altered metabolic functions, the mechanisms involved in the development of these chronic complications remain largely unresolved. The elucidation and understanding of these mechanisms will give rise to new classes of drugs that will further improve the quality of life of HIV-infected patients, over the age of 50

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

Atorvastatin Improves Survival in Septic Rats: Effect on Tissue Inflammatory Pathway and on Insulin Signaling

The aim of the present study was to investigate whether the survival-improving effect of atorvastatin in sepsis is accompanied by a reduction in tissue activation of inflammatory pathways and, in parallel, an improvement in tissue insulin signaling in rats. Diffuse sepsis was induced by cecal ligation and puncture surgery (CLP) in male Wistar rats. Serum glucose and inflammatory cytokines levels were assessed 24 h after CLP. The effect of atorvastatin on survival of septic animals was investigated in parallel with insulin signaling and its modulators in liver, muscle and adipose tissue. Atorvastatin improves survival in septic rats and this improvement is accompanied by a marked improvement in insulin sensitivity, characterized by an increase in glucose disappearance rate during the insulin tolerance test. Sepsis induced an increase in the expression/activation of TLR4 and its downstream signaling JNK and IKK/NF-κB activation, and blunted insulin-induced insulin signaling in liver, muscle and adipose tissue; atorvastatin reversed all these alterations in parallel with a decrease in circulating levels of TNF-α and IL-6. In summary, this study demonstrates that atorvastatin treatment increased survival, with a significant effect upon insulin sensitivity, improving insulin signaling in peripheral tissues of rats during peritoneal-induced sepsis. The effect of atorvastatin on the suppression of the TLR-dependent inflammatory pathway may play a central role in regulation of insulin signaling and survival in sepsis insult

Estudo da filtração glomerular e da manipulação tubular renal de sodio em animais normotensos e hipertensos submetidos a injeção intracerebroventricular de solução salina hipertonica : influencia da denervação renal bilateral

Orientador: Jose Antonio Rocha GontijoDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias MedicasResumo: o mecanismo pelo qual o aumento da pressão sanguínea em grupos de ratos espontaneamente hipertensos (SHR) se estabelece, não foi totalmente esclarecido. Além disso, há uma surpreendente falta de dados experimentais sobre os mecanismos natriuréticos induzidos pela injeção intracerebroventricular (i.c.v.) de salina hipertônica em SHR. No presente estudo, realça-se a hipótese de que a hipertensão em SHR pode ser resultado, pelo menos em parte, da contínua superatividade do nervo simpático renal, causada pela menor resposta central frente ao aumento da concentração de sódio no fluido cerebroespinal. Para testar esta hipótese, o estudo foi projetado para avaliar a influência da atividade nervosa renal, após injeção i.c.v. de salina hipertônica de concentrações crescentes sobre o manuseio renal de sódio urinário em SHR submetidos à denervação renal bilateral comparados a seus respectivos controles Wistar Kyoto (WKy). A presente investigação confirmou estudos anteriores, mostrando pronunciada resposta natriurética renal pós-injeção central de salina hipertônica, mas também demonstrou redução na taxa de filtração glomerular, estimado pelo "Clearance" de Creatinina endógena (Cer) associada à menor fração de excreção de sódio (FENa)relacionados à concentração administrada em ratos WKy, mas não nos SHR. Nos SHR, a elevação da FENafoi obtida somente pela administração central de NaCI na concentração de O.90M.Este resultado foi conseqüência da rejeição à reabsorção de sódio nos segmentos tubulares proximais (FEPNa) e pósproximais (FEPPNa) do nefro, sem entretanto, qualquer modificação do Ccr. Estes resultados indicam que os mecanismos envolvidos em tal resposta estão relacionados ao efeito direto sobre os segmentos tubulares do nefro. A denervação renal causou um significante efeito antinatriurético secundário, possivelmente, à diminuição do Ccr e à elevada reabsorção de sódio na porção proximal dos túbulos (FEPNa)renais em ratos WKy, mas não em SHR. Um aspecto novo do presente estudo mostrou que em animais normotensos, a natriurese está diretamente associada ao aumento do Ccr e à menor reabsorção proximal de sódio, resultando em maior aporte de íons aos segmentos distais no nefro. A reabsorção desta elevada carga dista! de íons, e fluxo dos segmentos proximais, não é completamente compensada por estes segmentos pós-proximais do nefro. Adicionalmente, a elevação da FENaem SHR somente após injeção i.c.v. de elevada concentração de salina (O.90MNaCI), com um desvio para a direita da curva concentraçãoresposta, sugere a possibilidade de que estes animais apresentem atenuação da resposta, via receptores centrais circunventriculares, à concentrações de sódio em SHR, quando comparados a ratos WKy. Estes resultados poderiam estar relacionados à diminuição do número e/ou ao "downregulation" na área de sinalização de receptores de sódio em regiões periventriculares. Conseqüentemente, esta menor sensibilidade central estaria relacionada com a resposta pressórica inadequada e atenuada resposta neuro-humoral na linhagem SHRAbstract: The mechanism by which blood pressure has risen in the spontaneously hypertensive rats (SHR) strain remains to be elucidated. Besides, there is a surprising lack of experimental data on the natriuretic mechanisms induced by intracerebroventricular (i.c.v.) injection of hypertonic saline in SHR. In the current study, we have hypothesized that SHR hypertension may result, at least in part, :ITom sustained renal sympathetic nerve overactivity caused by decreased central response to elevated cerebrospinal fluid sodium concentration. To test this hypothesis, the study was designed to evaluate the influence of renal denervation activity after i.c.v. hypertonic saline injection at increasing concentration on renal urinary sodium handling in SHR compared with appropriate age-matched Wistar Kyoto (WKy) control subjects. The present investigation has confirmed previous data showing pronounced renal natriuretic response to i.c.v. hypertonic saline stimuli but, also, it has demonstrated a decreased creatinine clearance (Cer) and :ITactionalsodium excretion (FENa)in a concentration-dependent manner in WKy rats but not in SHR. In SHR, it has increased FENaobtained by centrally administration of concentration of O.90MNaCI. This result was produced by increases in proximal (FEPNa) and post-proximal (FEPPNa) fractional urinary sodium rejection without presenting changes in CCr, indicating a direct tubular effect. Renal denervation has caused significant antinatriuresis by decreased Ccr and increased FEPNareabsorption in WKy but not in SHR. The novel finding of the present research has shown that natriuresis is associated with an increased Cer and ion delivery :ITomthe proximal tubule and that is incompletely compensated by more distal nephron segments. And, an enhanced FENaonly after higher i.c.v. hypertonic saline (O.90MNaCI) injection with shift to right of dose-response curve provides evidence of a small response of sodium sensor receptors in periventricular areas of SHR compared to WKy rats. This may be interpretedas a down-regulation of target organ responsiveness to small concentrations of NaCI and/or that inappropriately decrease in the responsiveness would be related to impairment ofblood pressure response and neuro-humoral factors release in SHR strainMestradoMedicina ExperimentalMestre em Fisiopatologia Médic