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The effects of a 60% partial pancreatectomy were studied in hyperglycemic GK (Goto–Kakizaki) rats. Partial pancreatectomy or a sham operation was performed on 12-week-old female Wistar rats, GK rats or hybrids between male GK rats and female Wistar rats. Measurements of pancreatic blood flow and islet blood flow were performed by a microsphere technique 2 weeks after surgery. Glucose tolerance was decreased in hybrid compared with Wistar rats, and in GK rats compared with both hybrid and Wistar rats before surgery. Partial pancreatectomy induced minor changes in glucose tolerance. Wistar rats had a decreased islet mass following partial pancreatectomy. Both hybrid and GK rats showed a significant decrease in relative islet volume, but only GK rats in total islet mass, compared with Wistar rats 2 weeks after surgery. Pancreatic blood flow and islet blood flow did not significantly differ between sham-operated Wistar, hybrid or GK rats. After partial pancreatectomy, islet blood flow in relation to islet mass increased 3-fold in Wistar rats and 2-fold in hybrid rats. In contrast, GK rats showed no increase in islet blood flow following partial pancreatectomy. It is concluded that compensatory mechanisms after partial pancreatectomy are operating less effciently in hybrid and GK rats.
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Src homology 2 domain-containing protein B (SHB) is an adapter protein involved in the regulation of β-cell and endothelial cell function. We have recently obtained the Shb knockout mouse, and consequently, the aim of this study was to assess the effect of Shb deletion upon β-cell function and blood glucose homeostasis. Shb−/− mice display an elevated basal blood glucose concentration, and this increase is maintained during insulin challenge in insulin sensitivity tests. To assess glucose-induced insulin secretion, pancreata were perfused, and it was observed that Shb−/− first phase insulin secretion was blunted during glucose stimulation. Gene expression of Shb−/− islets shortly after isolation was altered, with increased pancreatic and duodenal homeobox gene-1 (Pdx1) gene expression and reduced expression of Vegf-A. Islet culture normalized Pdx1 gene expression. The microvascular density of the Shb−/− islets was reduced, and islet capillary endothelial cell morphology was changed suggesting an altered microvascular function as a contributing cause to the impaired secretory activity. Capacitance measurements of depolarization-induced exocytosis indicate a direct effect on the exocytotic machinery, in particular a dramatic reduction in readily releasable granules, as responsible for the insulin-secretory defect operating in Shb −/− islets. Shb−/− mice exhibited no alteration of islet volume or β-cell area. In conclusion, loss of Shb impairs insulin secretion, alters islet microvascular morphology, and increases the basal blood glucose concentration. The impaired insulin secretory response is a plausible underlying cause of the metabolic impairment observed in this mutant mouse.
Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden
Department of Pharmacology, University of California, San Diego, California, USA
Diabetes Research Institute, The University of Miami School of Medicine, Miami, Florida, USA
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Pancreatic islet function and glucose homeostasis have been characterized in the transgenic YC-3.0 mouse, which expresses the yellow chameleon 3.0 (YC-3.0) protein under the control of the β-actin and the cytomegalovirus promoters. Fluorescence from the enhanced yellow fluorescent protein (EYFP), one part of the yellow chameleon protein, was used as a reporter of transgene expression. EYFP was expressed in different quantities throughout most cell types, including islet endocrine and stromal cells. No adverse effects of the transgene on animal health, growth or fertility were observed. Likewise, in vivo glucose homeostasis, mean arterial blood pressure and regional blood flow values were normal. Furthermore, the transgenic YC-3.0 mouse had a normal β-cell volume and mass as well as glucose-stimulated insulin release in vitro, compared with the C57BL/6 control mouse. Isolated islets from YC-3.0 animals continuously expressed the transgene and reversed hyperglycemia when transplanted under the renal capsule of alloxan-diabetic nude mice. We conclude that isolated pancreatic islets from YC-3.0 animals implanted into recipients without any EYFP expression, constitute a novel and versatile model for studies of islet engraftment.
