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Showing result 1 - 5 of 115 swedish dissertations matching the above criteria.
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1. Insulin signalling in human adipocytes : mechanisms of insulin resistance in type 2 diabetes
Abstract : 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. READ MORE
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2. Glucose and lipid metabolism in insulin resistance : an experimental study in fat cells
Abstract : 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. READ MORE
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3. Membrane rafts and its GPI anchored complement inhibitors regulate insulin secretion
Abstract : Type 2 diabetic patients usually exhibit an abnormal lipid profile. One such lipid that is constantly elevated in T2D is cholesterol. At the cellular level, cholesterol aids in tight packing of sphingolipids in certain regions of the plasma membrane and these specialized regions are termed ‘membrane rafts’, which act as signalling hubs. READ MORE
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4. Insulin Signalling and Regulation of Protein Kinase B in Adipocytes
Abstract : Insulin resistance is a hallmark of type 2 diabetes, an increasingly common disorder. The cause of insulin resistance is supposedly failures in the processes used by insulin to signal to the interior of its target cells. These failing steps are still unknown, most probably because of incomplete knowledge of how the insulin signals are transmitted. READ MORE
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5. Mathematical Modelling of Insulin Signalling : Effects on Glucose Metabolism in Skeletal Muscle
Abstract : The use of models to understand complex phenomena is indispensable to the scientific community. The advantage of a model is that it simplifies the phenomena under study. However, a model should be only as complex as required, no more, no less. READ MORE