Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Fabri, P.J. et al.

Hypogastrinemia in streptozotocin diabetes with islet transplantation--reconstitution.

Gastrin is present in normal mammalian pancreatic islets, as well as in the antrum and duodenum. Serum gastrin levels are responsive to many physiologic and pharmacologic factors including hyperglycemia, somatostatin, and glucagon. To evaluate the effects of streptozotocin diabetes and islet transplantation on gastrin homeostasis, young, adult, male Lewis rats underwent streptozotocin diabetes alone (N = 14), diabetes plus intraperitoneal islet isografts (N = 22), or sham operation alone (N = 18). Streptozotocin reduced fasting gastrin immunoreactivity (107 pg/ml +/- 26 mean +/- SEM) compared to controls (256 pg/ml +/- 31) (P less than 0.001). Islet isotransplantation resulted in restoration of fasting gastrin immunoreactivity (230 pg/ml +/- 19) to levels significantly greater than diabetics (P less than 0.001) and comparable to control animals (P = NS). Normalization of serum gastrin levels occurred within one month of transplantation and persisted for up to 14 months. In addition, media from cultures of 4/7 dispersed neonatal rat pancreas cultures contained gastrin immunoreactivity. Streptozotocin diabetes produces hypogastrinemia; intraperitoneal islet isotransplantation normalizes fasting gastrin immunoreactivity. Rat islet culture medium contains gastrin-like immunoreactivity. Pancreatic islets would appear to produce or control a portion of circulating gastrin immunoreactivity.[1]

References

Hypogastrinemia in streptozotocin diabetes with islet transplantation--reconstitution. Fabri, P.J., Weber, C.J., Gower, W.R., Reemtsma, K. J. Surg. Res. (1983) [Pubmed]

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