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Visar resultat 1 - 5 av 462 avhandlingar som matchar ovanstående sökkriterier.

  1. 1. Insulin signalling in human adipocytes : mechanisms of insulin resistance in type 2 diabetes

    Författare :Anna Danielsson; Peter Strålfors; Fredrik Nyström; Lena Stensson; Linköpings universitet; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; adipocytes; type 2 diabetes; insulin; insulin resistance; insulin signalling; phosphorylation; insulin receptor substrate 1; feedback control; Medical cell biology; Medicinsk cellbiologi;

    Sammanfattning : Prevalensen av fetma ökar drastiskt i stora delar av världen och utgör en stor riskfaktor för att utveckla insulinresistens och typ 2 diabetes. Fettväven kan bli mycket stor om för mycket energi tas upp av kroppen. LÄS MER

  2. 2. 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. 3. Glucose and lipid metabolism in insulin resistance : an experimental study in fat cells

    Författare :Jonas Burén; Umeå universitet; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Public health; adipocyte; insulin resistance; type 2 diabetes; insulin signalling; glucose uptake; insulin; glucose; dexamethasone; insulin receptor substrate; protein kinase B; GLUT4; lipoprotein lipase; Folkhälsomedicin; Public health medicine research areas; Folkhälsomedicinska forskningsområden; medicin; Medicine;

    Sammanfattning : Type 2 diabetes is usually caused by a combination of pancreatic β-cell failure and insulin resistance in target tissues like liver, muscle and fat. Insulin resistance is characterised by an impaired effect of insulin to reduce hepatic glucose production and to promote glucose uptake in peripheral tissues. LÄS MER

  4. 4. Carbohydrate-Rich Foods in the Treatment of the Insulin Resistance Syndrome : Studies of the Importance of the Glycaemic Index and Dietary Fibre

    Författare :Anette Järvi; Gabriele Riccardi; Uppsala universitet; []
    Nyckelord :Medical sciences; diabetes; insulin resistance; carbohydrates; starch; glycaemic index; dietary fibre; postprandial; second-meal; glucose; insulin; triacylglycerol; MEDICIN OCH VÅRD; MEDICINE; MEDICIN; Geriatrics; geriatrik;

    Sammanfattning : The glycaemic responses to various carbohydrate-rich foods are partly dependent on the rate at which the carbohydrate is digested and absorbed. The glycaemic index (GI) is a way of ranking foods according to their glycaemic response and is recommended as a useful tool in identifying starch-rich foods that give the most favourable glycaemic response. LÄS MER

  5. 5. Interplay between hormones, nutrients and adipose depots in the regulation of insulin sensitivity : an experimental study in rat and human adipocytes

    Författare :Magdalena Lundgren; Jan Eriksson; Jonas Burén; Eva Degerman; Umeå universitet; []
    Nyckelord :LANTBRUKSVETENSKAPER; AGRICULTURAL SCIENCES; adipose tissue; cAMP; glucocorticoids; glucose; insulin; insulin resistance; lipolysis; subcutaneous fat; type 2 diabetes; visceral fat; Medicine; Medicin;

    Sammanfattning : Obesity and specifically central obesity is related to insulin resistance, type 2 diabetes and other components of the so-called metabolic syndrome. The aim of this study was to elucidate the interplay between hormones, nutrients and adipose depots in normal and insulin-resistant fat cell metabolism. LÄS MER