Immunocytochemical changes in the fetal pancreatic islet following fetal administration of streptozotocin in the rat

Yamamoto, Masayuki; Kudoh, Ayako; Arishima, Kazuyoshi; Eguchi, Yawara

doi:10.1002/(sici)1097-0185(199702)247:2<248::aid-ar11>3.0.co;2-p

Cited by 10 publications

(6 citation statements)

References 21 publications

(20 reference statements)

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“…Direct administration of STZ at 1/10 the dose in our previous study (Yamamoto et al, 1997) reduced the total volume of pancreatic B-cells to about 35% of that in the control group 3 hr after the administration. However, the total volume of B-cells exceeded the 3-hr level 6 hr after the administration and increased to about 50% of that in the control group after 12 hr.…”

Section: Discussionmentioning

confidence: 72%

“…Conversely, in rats treated with STZ at birth (Portha et al, 1974), after 2 (BonnerWeir et al, 1981) or 3 days (Ferrand et al, 1995), a loss of B-cell mass triggered acute diabetes followed by a rapid regression and the reappearance of a large B-cell mass and normal insulin content. In a previous study, we demonstrated that fetal rats injected with STZ exhibit regenerative activity of the pancreatic B-cells using histological, immunochemical, and ultrastructural techniques (Yamamoto et al, 1997). However, in these experimental models, although regeneration of B-cells and the presence of insulin in the pancreas were demonstrated, whether the new B-cell masses possess insulin secretion ability has not yet been completely demonstrated.…”

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confidence: 93%

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Recovery in the fetal pancreatic islet following fetal administration of streptozotocin in the rat in vivo and in vitro

et al. 2004

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In our previous study, after direct administration of streptozotocin (STZ; 400 g/g) to fetuses on day 19 of gestation, the B-cell volume in fetal pancreatic islets showed a marked decrease, but gradually recovered with electron microscopic confirmation of B-cell regeneration. However, STZ at this dose often caused fetal death. In this study, therefore, we determined whether B-cells are newly generated after treatment with STZ at a smaller dose in vivo and in vitro. For in vivo experiment, fetuses were administered STZ at 40 g/g on day 19 of gestation. The B-cell volume in pancreatic islets decreased markedly 3 hr after the administration of STZ, but it began to increase after 6 hr. The fetal plasma insulin concentration decreased from 6 to 12 hr after the administration, but recovered after 48 hr. The cell division index in fetal pancreatic islets of the STZ-treated group began to be significantly larger after 6 hr. For in vitro experiment, fetal pancreases on day 18 of gestation were pretreated with 10 mM STZ for 6 hr and cultured for 98 hr. B-cells were completely destroyed with STZ treatment; however, as these pancreases were cultured in a medium free of STZ, B-cells began to appear and insulin secretion was detected after 48 hr. After 72 hr, the cell division index was significantly greater. These results suggest that the fetal pancreas treated with STZ has the ability to regenerate B-cells both in vivo and in vitro.

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Section: Discussionmentioning

confidence: 72%

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confidence: 93%

Recovery in the fetal pancreatic islet following fetal administration of streptozotocin in the rat in vivo and in vitro

et al. 2004

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“…Many studies were performed to investigate changes during the progress of diabetes, and some studies were done on the morphological changes of islets by immunohistochemical staining method (17)(18)(19)(20)(21). However, studies on ultrastructure of islets during the progress of diabetes are rare (22)(23)(24).…”

Section: Introductionmentioning

confidence: 99%

Insulin and Glucagon Secretions, and Morphological Change of Pancreatic Islets in OLETF Rats, a Model of Type 2 Diabetes Mellitus

et al. 2002

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This study was performed to observe the changes of glucose-related hormones and the morphological change including ultrastructure of the pancreatic islets in the male Otsuka Long-Evans Tokushima Fatty rat. Area under the curve (AUC) of glucose at the 30th (709 plus minus 73 mg.h/dL) and at the 40th week (746 plus minus 87 mg.h/ dL) of age were significantly higher than that at the 10th week (360 plus minus 25 mg.h/ dL). AUC of insulin of the 10th week was 2.4 plus minus 0.9 ng.h/mL, increased gradually to 10.8 plus minus 8.3 ng.h/mL at the 30th week, and decreased to 1.8 plus minus 1.2 ng.h/mL at the 40th week. The size of islet was increased at 20th week of age and the distribution of peripheral alpha cells and central beta cells at the 10th and 20th weeks was changed to a mixed pattern at the 40th week. On electron microscopic examination, beta cells at the 20th week showed many immature secretory granules, increased mitochondria, and hypertrophied Golgi complex and endoplasmic reticulum. At the 40th week, beta cell contained scanty intracellular organelles and secretory granules and apoptosis of acinar cell was observed. In conclusion, as diabetes progressed, increased secretion of insulin was accompanied by increases in size of islets and number of beta-cells in male OLETF rats showing obese type 2 diabetes. However, these compensatory changes could not overcome the requirement of insulin according to the continuous hyperglycemia after development of diabetes.

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“…However, it has been reported that perinatal rats subjected to STZ treatment reversibly recover from STZinduced diabetes mellitus [2,22]. It has also been reported that the direct administration of STZ to the rat fetus immediately decreases the total mass of the islet B cells, which is markedly restored in 48 hr [30]. The purpose of this experiment was to observe how rat islet B cells recover from damage caused by treating the rat fetal pancreas with STZ in vitro, and to investigate whether EGF is involved in B cell recovery using radioimmunoassay and immunohistologic techniques.…”

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Effects of Epidermal Growth Factor (EGF) on Fetal Islet B Cells in vitro.

Yasuda

Yamamoto

Arishima

et al. 2002

The Journal of Veterinary Medical Science

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ABSTRACT. It has been reported that when the rat fetus is treated with streptozotocin (STZ) in vivo, islet B cells are destroyed but later recover. To investigate the process of the recovery of B cells after in vitro treatment of the fetal pancreas with STZ and the role of epidermal growth factor (EGF) in the recovery of B cells, we measured the level of insulin released from the cultured fetal pancreas and examined it histologically. As a result, we immunohistologically confirmed the regeneration of B cells in the pancreas that had been cultured for 48 hr after destruction of islet B cells by STZ treatment. An immunohistologic study using proliferating cell nuclear antigen (PCNA) showed that without the addition of EGF, the cell division index was significantly higher in the STZ-treated group (STZ group) than in the untreated group (intact group), whereas with the addition of EGF, the cell division index increased in both groups, but EGF did not have a significant cell division-promoting effect on the pancreas in the STZ group. The addition of EGF caused a significant decrease in the concentration of insulin in culture medium in both groups. These results indicate that EGF has a cell growth-promoting effect on intact fetal pancreas in vitro but has the effect of inhibiting the release of insulin, and thus suggest that EGF does not trigger the regeneration of islet B cells. KEY WORDS: epidermal growth factor (EGF), fetal islet B cell, insulin, proliferating cell nuclear antigen (PCNA), streptozotocin (STZ).J. Vet. Med. Sci. 64(2): 101-105, 2002 Epidermal growth factor (EGF) is a polypeptide of molecular weight 6,045 originally extracted from the submaxillary glands of mice and accelerates eyelid opening and incisor eruption in newborn mice [5]. EGF has also been reported to function in accelerating the growth of the gastrointestinal mucosal epithelium, inhibiting the secretion of gastric acid, and protecting the gastric mucosa [6,10].EGF has been shown to affect the growth and differentiation of cultured cells derived from various organs [3], and reportedly has in vivo and in vitro growth-accelerating effects on the pancreas [4]. However, these in vitro studies used the isolated exocrine part or pancreatic islets, and not intact pancreases in organ culture.EGF receptors are present in various cells [3], and their presence in the pancreas has also been confirmed [7,15,19]. From the observation that EGF occurs in pancreatic tissue and pancreatic juice [12][13][14], it is postulated that EGF has some effect on the pancreas itself.Streptozotocin (STZ) is an experimental diabetogenic agent that causes diabetes mellitus by specifically destroying islet B cells [23]. Its toxic action on islet B cells is irreversible. However, it has been reported that perinatal rats subjected to STZ treatment reversibly recover from STZinduced diabetes mellitus [2,22]. It has also been reported that the direct administration of STZ to the rat fetus immediately decreases the total mass of the islet B cells, which is markedly restored...

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Immunocytochemical changes in the fetal pancreatic islet following fetal administration of streptozotocin in the rat

Cited by 10 publications

References 21 publications

Recovery in the fetal pancreatic islet following fetal administration of streptozotocin in the rat in vivo and in vitro

Recovery in the fetal pancreatic islet following fetal administration of streptozotocin in the rat in vivo and in vitro

Insulin and Glucagon Secretions, and Morphological Change of Pancreatic Islets in OLETF Rats, a Model of Type 2 Diabetes Mellitus

Effects of Epidermal Growth Factor (EGF) on Fetal Islet B Cells in vitro.

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