Characteristic features of insulin secretion in the streptozotocin-induced NIDDM rat model

Tsuji, Kôzô; Taminato, Tomohiko; Usami, Masaru; Ishida, Hideyuki; Kitano, Norikazu; Fukumoto, Hirofumi; Koh, Gyohan; Kurose, Takeshi; Yamada, Yoshio; Yano, Hideki; Seino, Yutaka; Imura, Hiroo

doi:10.1016/0026-0495(88)90064-9

Cited by 74 publications

(59 citation statements)

References 19 publications

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“…This delayed deterioration probably follows from the inability of the insulin production of the pancreas to recover to the levels of control rats [14,15]. In this study, we observed a similar clinical course, characterised by the reduction of insulin production and content in the pancreases of n0-STZ rats.…”

Section: Discussionsupporting

confidence: 71%

“…This neonatal model showed more reduction of pancreatic beta cells compared with other reports, in which the reduction was approximately 50% that of controls [15,16,24]. This may be due to the different timing of STZ injection, which is known to result in type 2 diabetes models with different severity [14]. In fact, we injected STZ at 24 h after birth, while others injected within 12 h of birth [15,16,24].…”

Section: Discussionmentioning

confidence: 51%

“…Long-lasting effects of early treatment with ghrelin: studies at 10 weeks As the n0-STZ model develops hyperglycaemia after 8-10 weeks [14], we examined the long-term effects of early treatment with ghrelin in this model. The characteristics of Control, Ghrelin, n0-STZ and n0-STZ/Ghrelin animals at 10 weeks are detailed in Table 2.…”

Section: Resultsmentioning

confidence: 99%

“…Neonatal rats treated with STZ exhibit normal glycaemia at 3 weeks after birth by rapid remission, but then deteriorate gradually after 8 weeks [14][15][16]. This delayed deterioration probably follows from the inability of the insulin production of the pancreas to recover to the levels of control rats [14,15].…”

Section: Discussionmentioning

confidence: 99%

“…In this study, we examined the effects of ghrelin on the development of hyperglycaemia and the regeneration of beta cells in streptozotocin (STZ)-treated newborn rats, which show rapid remission but gradual development of diabetes in adult animals. This model has been traditionally used to study pancreatic regeneration [14][15][16]. We investigated the changes in the islets of Langerhans morphology and pancreatic insulin mRNA and protein levels following ghrelin administration in this animal model.…”

Section: Introductionmentioning

confidence: 99%

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Ghrelin prevents development of diabetes at adult age in streptozotocin-treated newborn rats

et al. 2006

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Aims/hypothesis: Ghrelin, a stomach-derived hormone, functions in multiple biological processes, including glucose metabolism and cellular differentiation and proliferation. In this study, we examined whether early treatment with ghrelin can regenerate beta cells of the pancreas in an animal model of diabetes mellitus, the n0-STZ model, in which neonatal rats are injected with streptozotocin (STZ) at birth.Methods: Following administration of ghrelin to n0-STZ rats from postnatal days 2 to 8, we examined beta cell mass, mRNA expression levels of insulin and of pancreatic and duodenal homeobox 1 (Pdx1) gene, and pancreatic morphology on days 21 and 70. In addition, we investigated the effects of ghrelin on beta cell replication. Results: By day 21, ghrelin treatment increased pancreatic expression of insulin and Pdx1 mRNA in n0-STZ rats. The number of replicating cells was also significantly increased in the ghrelin-treated n0-STZ model. At day 70, n0-STZ rats exhibited hyperglycaemia, despite slight increases in plasma insulin levels. Ghrelin treatment resulted in the improvement of plasma glucose levels, which were associated with normal plasma insulin levels. Pancreatic insulin mRNA and protein levels were significantly increased in ghrelin-treated n0-STZ model animals. Conclusions/interpretation: These findings suggest that ghrelin promotes regeneration of beta cells in STZ-treated newborn rats. Thus, early administration of ghrelin may help prevent the development of diabetes in disease-prone subjects after beta cell destruction.

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Section: Discussionsupporting

confidence: 71%