Search for dissertations about: "STXBP1"
Found 5 swedish dissertations containing the word STXBP1.
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1. Effects of Ca2+, microRNAs, and rosuvastatin on insulin-secreting beta cell function
Abstract : Type 2 diabetes (T2D) is a condition of high blood glucose levels due to insulin resistance and defective insulin secretion. Impaired insulin secretion plays a major role in the pathophysiology of T2D, it is mainly attributed to beta cell function i.e. failure to secrete insulin or reduced beta cell mass. READ MORE
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2. Exocytosis in Type 2 Diabetes- Functional and genetic studies of hormone secretion
Abstract : Type 2 Diabetes (T2D) is characterized by dysregulated beta-and alpha-cell hormone secretion leading to elevated blood glucose levels. Several proteins are crucial in maintaining exocytosis of the hormone-containing granules such as Syntaxin1A (Stx1A), SNAP25, Munc-18 (Stxbp1) and the family of Synaptotagmins (Syts). READ MORE
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3. Non-coding RNAs in beta cell insulin secretion - emerging players in Type 2 Diabetes pathogenesis
Abstract : Type 2 diabetes (T2D) is a complex polygenic disease influenced by both environmental and genetic factors resulting in impaired insulin release from pancreatic beta cells and insulin resistance in target tissues. The incidence of T2D is escalating and it is projected that over 640 million people will be affected by 2040. READ MORE
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4. Dissecting the role of micro-RNAs in diabetes
Abstract : The role of miRNAs in pancreatic islets and β-cell function and in the development of diabetes in human and rodents have been investigated in this thesis. Dicer1 was specifically deleted in vivo in pancreatic β-cells under the RIP-promoter in mice. READ MORE
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5. The role of cocaine- and amphetamine-regulated transcript in endocrine cells
Abstract : Type 2 diabetes (T2D) is a metabolic disease characterized by insufficient insulin secretion and insulin resistance. Disturbed beta-cell function is the final culprit that leads to the development of T2D. In addition, impaired incretin effect is likely a part of the pathogenesis of T2D. READ MORE