Sökning: "IRS-1"

Visar resultat 1 - 5 av 28 avhandlingar innehållade ordet IRS-1.

  1. 1. Fat cell insulin resistance : an experimental study focusing on molecular mechanisms in type 2 diabetes

    Författare :Frida Renström; Jan Eriksson; Anna Krook; Umeå universitet; []
    Nyckelord :LANTBRUKSVETENSKAPER; AGRICULTURAL SCIENCES; adipocyte; insulin signaling; insulin; glucose; IRS-1; glucose uptake; insulin resistance; typ 2 diabetes; serum; Medicine; Medicin;

    Sammanfattning : The aim of the present thesis was to further increase our understanding of mechanisms contributing to and maintaining cellular insulin resistance in type 2 diabetes (T2D). For this reason, the effects of high glucose and insulin levels on glucose transport capacity and insulin signaling, with emphasis on insulin receptor substrate 1 (IRS-1) were assessed in fat cells. LÄS MER

  3. 2. Molecular characterization of insulin resistance in the adipose tissue and the effects of thiazolidinediones

    Författare :Ann Hammarstedt; Göteborgs universitet; []
    Nyckelord :IRS-1; PGC-1; adiponectin; insulin resistance; TZD;

    Sammanfattning : Type 2 diabetes is the most common metabolic disorder today and has reached epidemic proportions in many contries. Insulin resistance plays a central role in the pathogenesis of Type 2 diabetes and can be present for a decade or more before onset of the disease. LÄS MER

  4. 3. Identification of abnormally expressed genes in skeletal muscle contributing to insulin resistance and type 2 diabetes

    Författare :Xudong Huang; Malmö Institutionen för kliniska vetenskaper; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Endocrinology; secreting systems; diabetology; Endokrinologi; gene expression; high-fat intake; RT-PCR; mitochondrial genes; cathepsin L; Shc; IRS-2; IRS-1; GS; cDNA differential display; Insulin resistance; type 2 diabetes; sekretion; diabetologi;

    Sammanfattning : The metabolic defects of insulin resistance and type 2 diabetes can result from changes in gene expression and protein functions due to genetic and environmental influences. The aim of this study was to identify abnormally expressed genes associated with insulin resistance or type 2 diabetes, and further to test whether possible defects are inherited or acquired. LÄS MER

  5. 4. Molecular mechanisms of insulin resistance with special emphasis on IRS-1 and PKB/Akt

    Författare :Eugénia Carvalho; Göteborgs universitet; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Insulin; insulin resistance; diabetes; protein kinase B; insulin receptor substrate-1; insulin signalin; Glute-4; PI 3-kinase; glucose transport; adipose tissue;

    Sammanfattning : .... LÄS MER

  7. 5. Molecular Mechanism of Growth Hormone - Involvement of Janus Kinase 2, Insulin Receptor Substrate-1 and -2 and Phosphatidylinositol 3-Kinase In the Acute Insulin-Like Effects of Growth Hormone In Primary Rat Adipocytes

    Författare :Martin Ridderstråle; Diabetes - klinisk obesitasforskning; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; insulin receptor substrate-1; insulin receptor substrate-2 phosphatidylinositol 3-kinase; signal transducer and activator of transcription 5; janus kinase 2; phosphotyrosine; receptor; phosphorylation; Growth hormone; Metabolism; Biochemistry; rat; adipocyte; lipolysis; lipogenesis; Biokemi; metabolism; Pharmacological sciences; pharmacognosy; pharmacy; toxicology; Farmakologi; farmakognosi; farmaci; toxikologi; Endocrinology; secreting systems; diabetology; Endokrinologi; sekretion; diabetologi;

    Sammanfattning : Originally studying the molecular mechanisms for the insulin-like effects of growth hormone (GH), lipogenesis and antilipolysis, in isolated rat adipocytes we found that the GH receptor (GHR) was tyrosine phosphorylated in response to GH in cells that were responsive to these effects. Then, as Janus kinase 2 (JAK2) was described as a GH-stimulated and GHR-associated tyrosine kinase, we found that JAK2 was tyrosine phosphorylated in response to GH in responsive cells. LÄS MER