Search for dissertations about: "PDE3B"
Showing result 1 - 5 of 12 swedish dissertations containing the word PDE3B.
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1. Studies in beta cells and adipocytes in the context of obesity and T2D - focusing on PDE3B, OPN and SCFAs
Abstract : Type 2 diabetes (T2D) is a heterogeneous disease characterized by altered lipid parameters and elevated glucose levels, as a direct consequence of impaired insulin signaling in target tissues and reduced insulin exocytosis from pancreatic β-cells. Obesity, which dramatically increases worldwide, is associated with insulin resistance and T2D. READ MORE
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2. The Role of Phosphodiesterase 3B in the Regulation of Insulin Secretion
Abstract : Pancreatic beta-cell dysfunction and insulin resistance are the two hallmarks of type 2 diabetes. An early sign of beta-cell dysfunction is impaired nutrient-induced insulin release. Several insulin secretagogues act by increasing the formation of intracellular cAMP. READ MORE
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3. Adipocyte phosphatases and the antilipolytic action of insulin
Abstract : Adipose tissue is the main site of energy storage of the body and an important endocrine organ. Knowledge of the regulation of fat metabolism and the endocrine factors secreted by the adipocyte is crucial for the understanding of diseases such as obesity and diabetes. Insulin is the main antilipolytic hormone. READ MORE
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4. The role of phosphodiesterase 3B in energy metabolism
Abstract : Energy metabolism at the level of any particular tissue is tightly regulated by hormones, neurotransmitters and cytokines in order to maintain overall energy homeostasis. Any dysfunctions in energy metabolism may lead to more or less severe consequences, with obesity and type 2 diabetes being the most prevalent ones. READ MORE
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5. THE ROLE OF PHOSPHODIESTERASE 3B IN CAMP-MEDIATED REGULATION OF INSULIN SECRETION
Abstract : Type 2 diabetes mellitus (T2DM) is characterized by various combinations of ?-cell failure and insulin resistance leading to hyperglycemia and glucose intolerance. In order to maintain glucose tolerance in the insulin resistance state, increased insulin secretion is a requirement and it is because of inadequate islet adaptation that glucose intolerance develops in T2DM. READ MORE