Insulin Receptor Substrates
Mostrando 1-12 de 57 artigos, teses e dissertações.
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1. Trans fatty acid intake is associated with insulin sensitivity but independently of inflammation
High saturated and trans fatty acid intake, the typical dietary pattern of Western populations, favors a proinflammatory status that contributes to generating insulin resistance (IR). We examined whether the consumption of these fatty acids was associated with IR and inflammatory markers. In this cross-sectional study, 127 non-diabetic individuals were alloc
Brazilian Journal of Medical and Biological Research. Publicado em: 2012-07
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2. Organization of the ventral tegmental area projections to the VTA-nigral complex and to the hypothalamus in the rat and VTA neurons projecting to the accumbens express insulin receptor substrates. / Organização das projeções da área tegmental ventral para o complexo VTA-substância negra e para o hipotálamo no rato e estudo da expressão dos substratos do receptor de insulina em neurônios da VTA que se projetam para o estriado
Numa primeira etapa, estudamos as conexões da VTA para o complexo VTA-substância negra (SN) utilizando a leucoaglutinina do Phaseolus vulgaris (PHA-L). Estas conexões são substanciais, topograficamente organizadas, com destaque para o pólo caudal da VTA que inerva bilateralmente toda a extensão deste complexo. Numa segunda etapa, estudamos as projeçõ
Publicado em: 2010
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3. Inter-relação entre as vias de transmissão do sinal de insulina e leptina em hipotalamo e figado de ratos
Insulin and leptin have overlapping effects in the control of energy homeostasis and glucose metabolism, but the molecular basis of this synergism is unknown. Insulin signals through a receptor tyrosine kinase that phosphorylates and activates the docking proteins IRSs (insulin receptor substrates), whereas the leptin receptor and its associated protein tyro
Publicado em: 2002
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4. Efeito da hiperinsulinemia cronica na regulação das etapas iniciais da ação insulinica em tecidos de ratos
Insulin resistance, defined as subnormal response to a given concentration of insulin, is an important component in the pathophysiology of diseases with high prevalence in the population as obesity, diabetes mellitus type 2 and hypertension. The chronic euglycemic hyperinsulinemiafor as 3-5 days can induce insulinresistance. Insulin initiates its growth and
Publicado em: 2001
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5. Angiotensina II induz resistencia a insulina associada com alteração do sinal insulinico em figado e musculo esqueletico de ratos
We have examine the influence of long-term infusion of angiotensin II (AII) on insulin sensitivity and action on liver and skeletal muscle of rats. Rats were continuously infused with saline or AlI-lO and 40 ng/kg/min for 6 consecutive days. Arterial pressure (AP) was daily monitored with a computer system (1 hour, beat-to-beat). Insulin sensitivity was eval
Publicado em: 2001
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6. Regulação do IRS-2 e da AKT em modelos animais de resistencia a insulina
Insulin induced a wide variety of growth and metabolic responses in many cell types. These actions are initiated by insulin binding to its receptor, and involves a series of alternative and complementary p athways created by the multiple substrates of the insulin receptor (IRSs). In this study we investigated IRS-2 tyrosine phosphorylation, its association w
Publicado em: 2001
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7. A high-fructose diet induces changes in pp185 phosphorylation in muscle and liver of rats
Insulin stimulates the tyrosine kinase activity of its receptor resulting in the tyrosine phosphorylation of pp185, which contains insulin receptor substrates IRS-1 and IRS-2. These early steps in insulin action are essential for the metabolic effects of insulin. Feeding animals a high-fructose diet results in insulin resistance. However, the exact molecular
Brazilian Journal of Medical and Biological Research. Publicado em: 2000-12
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8. Insulin rapidly stimulates phosphorylation of a 46-kDa membrane protein on tyrosine residues as well as phosphorylation of several soluble proteins in intact fat cells.
It is speculated that the transmission of an insulin signal across the plasma membrane of cells occurs through activation of the tyrosine-specific receptor kinase, autophosphorylation of the receptor, and subsequent phosphorylation of unidentified substrates in the cell. In an attempt to identify possible substrates, we labeled intact rat fat cells with [32P
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9. Replacement of insulin receptor tyrosine residues 1162 and 1163 does not alter the mitogenic effect of the hormone.
Chinese hamster ovary transfectants that express insulin receptors in which tyrosine residues 1162 and 1163 were replaced by phenylalanine exhibit a total inhibition of the insulin-mediated tyrosine kinase activity toward exogenous substrates [histone, casein, and poly(Glu/Tyr)]; this latter activity is associated with total inhibition of the hypersensitivit
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10. Monoclonal antibodies to the human insulin receptor that activate glucose transport but not insulin receptor kinase activity.
Three mouse monoclonal antibodies were produced that reacted with the alpha subunit of the human insulin receptor. All three both immunoprecipitated 125I-labeled insulin receptors from IM-9 lymphocytes and competitively inhibited 125I-labeled insulin binding to its receptor. Unlike insulin, the antibodies failed to stimulate receptor autophosphorylation in b
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11. Hepatic protein phosphotyrosine phosphatase. Dephosphorylation of insulin and epidermal growth factor receptors in normal and alloxan diabetic rats.
Polypeptide hormone signal transmission by receptor tyrosine kinases requires the rapid reversal of tyrosine phosphorylation by protein phosphotyrosine phosphatases (PPTPases). We studied hepatic PPTPases in the rat with emphasis on acute and chronic regulation by insulin. PPTPase activity with artificial substrates ([32P]Tyr-reduced, carboxyamidomethylated,
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12. Stearoyl-CoA desaturase 1 deficiency elevates insulin-signaling components and down-regulates protein-tyrosine phosphatase 1B in muscle
We have shown previously that mice with a targeted disruption in the stearoyl-CoA desaturase 1 gene (SCD1-/-) have increased insulin sensitivity compared with control mice. Here we show that the SCD1-/- mice have increased insulin signaling in muscle. The basal tyrosine phosphorylation of the insulin receptor and insulin receptor substrates 1 and 2 are eleva
National Academy of Sciences.