6 research outputs found
MOESM2 of Shift work and the risk of cardiovascular disease among workers in cocoa processing company, Tema
Additional file 2. Strobe checklist
MOESM1 of Shift work and the risk of cardiovascular disease among workers in cocoa processing company, Tema
Additional file 1. Questionnaire
MOESM4 of Impact of exercise intensity on oxidative stress and selected metabolic markers in young adults in Ghana
Additional file 4: Table S1. Association between antioxidant concentration, oxidative stress and exercise intensity of study population
Homotypic cell contact enhances insulin but not glucagon secretion
Intra-islet interactions influence ?-cell function, and disruption of islet architecture results in a reduction in glucose-induced insulin secretion, whereas re-aggregation improves secretory responsiveness. Our studies on MIN6 cells have shown that by configuring ?-cells as three-dimensional islet-like structures there is a marked improvement in glucose-induced insulin secretion compared to that of their monolayer equivalents. In the present study, we have used the mouse glucagon-secreting ?TC1 cell line to see whether homotypic interactions are important in the regulation of glucagon secretion from ?-cells. We found no significant difference in the secretory responses of ?TC1 cells maintained as monolayers or as cell clusters. We also found that different cell adhesion molecules are involved in cell interactions between ?- and ?-cells; MIN6 cells express ECAD, whereas ?TC1 cells express NCAM. ECAD is necessary for cell cluster formation by MIN6 cells but not by ?TC1 cells, whereas NCAM is not needed for the formation of cell clusters in either cell line.</p
Homotypic cell contact enhances insulin but not glucagon secretion
Intra-islet interactions influence ?-cell function, and disruption of islet architecture results in a reduction in glucose-induced insulin secretion, whereas re-aggregation improves secretory responsiveness. Our studies on MIN6 cells have shown that by configuring ?-cells as three-dimensional islet-like structures there is a marked improvement in glucose-induced insulin secretion compared to that of their monolayer equivalents. In the present study, we have used the mouse glucagon-secreting ?TC1 cell line to see whether homotypic interactions are important in the regulation of glucagon secretion from ?-cells. We found no significant difference in the secretory responses of ?TC1 cells maintained as monolayers or as cell clusters. We also found that different cell adhesion molecules are involved in cell interactions between ?- and ?-cells; MIN6 cells express ECAD, whereas ?TC1 cells express NCAM. ECAD is necessary for cell cluster formation by MIN6 cells but not by ?TC1 cells, whereas NCAM is not needed for the formation of cell clusters in either cell line.</p
Activation of the extracellular calcium-sensing receptor initiates insulin secretion from human islets of Langerhans: involvement of protein kinases
The extracellular calcium-sensing receptor (CaR) is usually associated with systemic Ca2+ homeostasis, but the CaR is also expressed in many other tissues, including pancreatic islets of Langerhans. In the present study, we have used human islets and an insulin-secreting cell line (MIN6) to investigate the effects of CaR activation using the calcimimetic R-568, a CaR agonist that activates the CaR it physiological concentrations of extracellular Ca2+. CaR activation initiated a marked but transient insulin secretory response from both human islets and MIN6 cells at a sub-stimulatory concentration of glucose, and further enhanced glucose-induced insulin secretion. CaR-induced insulin secretion was reduced by inhibitors of phospholipase C or calcium-calmodulin-dependent kinases, but not by a protein kinase C inhibitor. CaR activation was also associated with an activation of p42/44 mitogen-activated protein kinases (MAPK), and CaR-induced insulin secretion was reduced by an inhibitor of p42/44 MAPK activation. We suggest that the P-cell CaR is activated by divalent cations co-released with insulin, and that this may be an important mechanism of intra-islet communication between beta-cells.</p
