Sökning: "insulin secretion"

Visar resultat 16 - 20 av 402 avhandlingar innehållade orden insulin secretion.

  1. 16. ADP regulation of insulin secretion and beta-cell apoptosis

    Författare :Chanyuan Tan; Kardiologi; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; P2Y; β-cell; ADP; insulin; apoptosis; autocrine; ectonucleotidase;

    Sammanfattning : The aims of this dissertation were to investigate the effects of extracellular purines on insulin secretion, and apoptosis in mouse pancreatic islets and β-cells; to examine if high glucose and free fatty acids induces β-cell apoptosis via autocrine effects of ADP acting on the P2Y13 receptor; and to investigate the modulation of extracellular purines in vascular smooth muscle cells (VSMCs) through ectonucleotidase or ATP release under the effect of high glucose. The expression of the ADP receptors P2Y1 and P2Y13 were shown in both mouse pancreatic islets and isolated β-cells using real-time PCR quantification. LÄS MER

  2. 17. GH, IGF-1 and insulin in the regulation of lipid and lipoprotein metabolism

    Författare :Fredrik Frick; Göteborgs universitet; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Growth-hormone; insulin-like growth factor-I; insulin; lipoprotein lipase; adipose tissue; muscle tissue; VLDL secretion;

    Sammanfattning : It is well known that growth hormone (GH) has profound effects on lipid and lipoprotein metabolism. Insulin-like growth factor-I (IGF-I) is believed to mediate some of the effects of GH via endocrine and paracrine mechanisms. Moreover, both GH and IGF-I are known to influence insulin secretion. LÄS MER

  3. 18. On Cholecystokinin and Phospholipase A2 in Insulin Secretion - an Experimental Study With Reference to the Development of Diabetes

    Författare :Erik Simonsson; Malmö Institutionen för kliniska vetenskaper; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Type 2 Diabetes; Insulin Resistance; Islet; Beta-cell; Insulin Secretion; Ca2 -Dependency; Intracellular Signalling; Phospholipase A2; Cholecystokinin; Non-glucose Secretagogues; Endocrinology; secreting systems; diabetology; Endokrinologi; sekretion; diabetologi;

    Sammanfattning : In view of unsolved issues regarding cellular events underlying the adaptation of insulin secretion to insulin resistance, together with the observation that insulin secretion induced by the gastrointestinal hormone and neuropeptide cholecystokinin (CCK) is not solely explained by phospholipase C-protein kinase C (PLC-PKC) pathway activation, this study aimed at delineate mechanisms responsible for the hyperinsulinemia in insulin resistance, with particular attention paid to the action of glucose vs. non-glucose secretagogues, such as CCK. LÄS MER

  4. 19. Signal Transduction of Glucagon Secretion

    Författare :Elaine Vieira; Erik Gylfe; Lena Eliasson; Uppsala universitet; []
    Nyckelord :NATURVETENSKAP; NATURAL SCIENCES; Cell biology; secretion; glucagon; store-operated channels; calcium; diabetes; Cellbiologi; Cell biology; Cellbiologi;

    Sammanfattning : Diabetes mellitus is a bihormonal disorder with hyperglycemia due to deficiency of insulin and hypersecretion of glucagon. To improve diabetes treatment it is important to clarify the signal transduction of glucagon secretion. LÄS MER

  5. 20. Beta Cell Function: from Human Genetics to Animal Models

    Författare :Martins Kalis; Diabetes - immunovirologi; []
    Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; animal model; Dicer1; genetics; genetic association; single nucleotide polymorphism; SNP; INS-1E; AAT; FOXP3; beta cell function; insulin secretion; FFAR1; insulin; T2D; glucose; T1D;

    Sammanfattning : Beta cell function is an important factor in the development of both Type 1 (T1D) and Type 2 (T2D) diabetes mellitus. T1D is characterized by a primary defect in insulin secretion due to the immune-mediated beta cell destruction, however, the more common T2D beside insulin resistance also include impaired beta cell function as a consequence to abnormal glucose homeostasis. LÄS MER