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Studies of the effects of pancreatic...

Chen, Hainan.

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Studies of the effects of pancreatic beta cell antioxidant transgenes on experimental models of diabetes.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Studies of the effects of pancreatic beta cell antioxidant transgenes on experimental models of diabetes./
作者:	Chen, Hainan.
面頁冊數:	158 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0170.
Contained By:	Dissertation Abstracts International65-01B.
標題:	Health Sciences, Pharmacology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3120057
ISBN:	0496674291

Studies of the effects of pancreatic beta cell antioxidant transgenes on experimental models of diabetes.
Chen, Hainan.

Studies of the effects of pancreatic beta cell antioxidant transgenes on experimental models of diabetes. - 158 p.

Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0170.

Thesis (Ph.D.)--University of Louisville, 2003.

Pancreatic beta cells are extremely vulnerable to the destruction of Reactive Oxygen Species (ROS). In both type 1 and type 2 diabetes ROS are involved in the loss of beta-cells. We hypothesized that the deficiency in ROS detoxifying system of beta-cells resulted in beta-cell vulnerability and enhanced ROS protection would protect from diabetes. To test this hypothesis, transgenic mice with overexpression of beta-cell antioxidant protein metallothionein (MT), manganese superoxide dismutase (MnSOD) and catalase were produced on an FVB background. Initial studies demonstrated that these transgenes did not affect beta-cell normal function and morphology. But those transgenes significantly protected pancreatic islets or mice from ROS induced beta-cell damage and diabetes. The transgenic islet cells had high efficacy in scavenging most forms of ROS, and generally survived and functioned better than control cells when exposed to various ROS insults. The transgenic mice were highly resistant to STZ induced diabetes.

ISBN: 0496674291Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Studies of the effects of pancreatic beta cell antioxidant transgenes on experimental models of diabetes.
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500 $a Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0170.
500 $a Adviser: Paul N. Epstein.
502 $a Thesis (Ph.D.)--University of Louisville, 2003.
520 $a Pancreatic beta cells are extremely vulnerable to the destruction of Reactive Oxygen Species (ROS). In both type 1 and type 2 diabetes ROS are involved in the loss of beta-cells. We hypothesized that the deficiency in ROS detoxifying system of beta-cells resulted in beta-cell vulnerability and enhanced ROS protection would protect from diabetes. To test this hypothesis, transgenic mice with overexpression of beta-cell antioxidant protein metallothionein (MT), manganese superoxide dismutase (MnSOD) and catalase were produced on an FVB background. Initial studies demonstrated that these transgenes did not affect beta-cell normal function and morphology. But those transgenes significantly protected pancreatic islets or mice from ROS induced beta-cell damage and diabetes. The transgenic islet cells had high efficacy in scavenging most forms of ROS, and generally survived and functioned better than control cells when exposed to various ROS insults. The transgenic mice were highly resistant to STZ induced diabetes.
520 $a However, inconsistent with studies on insulin secreting tumor cell lines in which antioxidants were shown to be protective, all these antioxidant transgenes failed to prevent cytokine toxicities in the cultured islets. We employed a speed congenic strategy to produce two lines of congenic NOD mice containing beta-cell specific expression of MT and catalase. NOD mice spontaneously develop type 1 diabetes, and cyclophosphamide (CYP) injection accelerates NOD diabetes onset. But very unexpectedly, either transgene MT or catalase dramatically hastened diabetes onset in NOD mice. In addition, no antioxidant transgene was found to be able to protect from type 2 diabetes in an Agouti obese diabetic model. But the MT transgene also unexpectedly caused severe diabetes on a normal C57BL/KsJ mouse which can be made to develop type 2 diabetes by producing obesity and insulin resistance.
520 $a The data from this project indicate that the overexpression of antioxidant transgenes protects beta-cells from ROS damaging stimuli but sensitizes beta-cells to some other insults. Some of these data are at odds with the long term favored concept that antioxidant treatment is always beneficial for treatment of diabetes. These results imply that oxidative stress may not only be harmful, but it may also be necessary to activate self-protective mechanisms in the beta-cells.
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