obesus islets have low oxidative capacity, probably resulting in limited ability to generate ATP to initiate and drive the insulin secretion 2) insulin response potentiated by cyclic AMP-dependent protein kinase is intact in P. Immunohistochemical analysis indicated that hyperglycemia was associated with reduced expression ofα-protein kinase C (PKC) and diminished translocation of λ-PKC. obesus for 18 h in low (3.3 mmol/l) glucose in the presence of diazoxide (375 μmol/l) dramatically improved the insulin response to glucose and restored the responsiveness to PMA. Maintenance of islets from hyperglycemic P. obesus but had no effect on islets from hyperglycemic P. At the maximal stimulatory glucose concentration, PMA potentiated insulin response in islets from normoglycemic prediabetic and diabetes-resistant P. The phorbol ester phorbol myristic acid (PMA) potentiated basal insulin release in islets from prediabetic animals, but not those from hyperglycemic or diabetes-resistant P. GLP-1 and forskolin potentiated the insulin response to maximal (11.1 mmol/l) glucose in islets from all groups. obesus was unaffected by glucagon-like peptide 1 (GLP-1) or forskolin, whereas that of islets of the diabetic line was augmented by the drugs. Basal insulin release in islets from diabetes-resistant P. The mitochondrial substrates α-ketoisocaproate and monomethyl succinate had no effect on insulin secretion in P. Fractional oxidation of glucose was constant in control islets over a range of concentrations, whereas islets from hyperglycemic P. Islets from hyperglycemic animals utilized twice as much glucose as islets from normoglycemic diabetes-prone or diabetes-resistant controls but exhibited similar rates of glucose oxidation. We examined the major signaling pathways for insulin release in P. Psammomys obesus is a model of type 2 diabetes that displays resistance to insulin and deranged β-cell response to glucose.
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