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Type 2 diabetes disease progression ...

Xue, Bai.

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Type 2 diabetes disease progression and gene array analysis in adipose tissue of Goto-Kakizaki rats.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Type 2 diabetes disease progression and gene array analysis in adipose tissue of Goto-Kakizaki rats./
作者:	Xue, Bai.
面頁冊數:	381 p.
附註:	Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 1961.
Contained By:	Dissertation Abstracts International72-04B.
標題:	Biology, Endocrinology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3440365
ISBN:	9781124476179

Type 2 diabetes disease progression and gene array analysis in adipose tissue of Goto-Kakizaki rats.
Xue, Bai.

Type 2 diabetes disease progression and gene array analysis in adipose tissue of Goto-Kakizaki rats. - 381 p.

Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 1961.

Thesis (Ph.D.)--State University of New York at Buffalo, 2011.

Type 2 diabetes is an epidemic disease involving disrupted glucose homeostasis and is characterized by hyperglycemia. The common form of this disease involves both polygenetic components and environmental contributors, including dietary fat intake diet. However, the precise etiology of type 2 diabetes remains elusive. The Goto-Kakizaki (GK) rat is a non-obese, polygenetic, spontaneous diabetic model, widely used in diabetes related studies, while the Wistar-Kyoto (WKY) rat is its inbreed normoglycemic control. To investigate the interaction of genetic background and fat content of diet, a population study of disease progression and high-fat diet effect in GK rats was conducted with an emphasis on gene expression in adipose tissue along with phenotypic indices relevant to diabetes and adipose tissue function.

ISBN: 9781124476179Subjects--Topical Terms:

1682242
Biology, Endocrinology.

Type 2 diabetes disease progression and gene array analysis in adipose tissue of Goto-Kakizaki rats.
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100 1 $a Xue, Bai. $3 727369
245 1 0 $a Type 2 diabetes disease progression and gene array analysis in adipose tissue of Goto-Kakizaki rats.
300 $a 381 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: 1961.
500 $a Advisers: Richard R. Almon; Debra C. DuBois.
502 $a Thesis (Ph.D.)--State University of New York at Buffalo, 2011.
520 $a Type 2 diabetes is an epidemic disease involving disrupted glucose homeostasis and is characterized by hyperglycemia. The common form of this disease involves both polygenetic components and environmental contributors, including dietary fat intake diet. However, the precise etiology of type 2 diabetes remains elusive. The Goto-Kakizaki (GK) rat is a non-obese, polygenetic, spontaneous diabetic model, widely used in diabetes related studies, while the Wistar-Kyoto (WKY) rat is its inbreed normoglycemic control. To investigate the interaction of genetic background and fat content of diet, a population study of disease progression and high-fat diet effect in GK rats was conducted with an emphasis on gene expression in adipose tissue along with phenotypic indices relevant to diabetes and adipose tissue function.
520 $a Male GK and WKY rats fed on a rodent normal diet (ND) or a high fat (HF) diet were sacrificed at 4, 8, 12, 16 and 20 weeks of age. Body weights and food consumption were recorded throughout the study period. At the time of sacrifice, plasma and fat pads were harvested. Glucose and hormones (insulin, corticosterone, adiponectin and leptin), lipid profiles and blood cell counts were measured. RNA samples prepared from abdominal fat were used for Affymetrix 230-2 gene array analyses to explore differential gene expression in these animals.
520 $a The most prominent difference between GK and WKY rats is that GK rats exhibit an age-specific failure to accumulate body fat starting from 8 weeks of age, despite their relatively higher calorie consumption, which indicates a mild lipoatrophy in these animals. Another novel observation is the significantly elevated total white blood cell (WBC) counts in GK rats which occurred throughout the entire experimental period, indicating chronic systemic inflammation. Gene expression analysis reflects the failure of GK rats to accumulate adipose tissue, suggesting that the molecular mechanisms of lipoatrophy involve 3 aspects: a defect in lipogenesis, decreased lipid storage and accumulation, and impaired preadipocyte differentiation. In addition, array results support the presence of chronic inflammation in GK adipose tissue. Moreover, several diabetes biomarkers were differentially expressed only in animals fed a high fat diet, suggesting that exposure to HF diet subclinically exacerbates type 2 diabetes or accelerates the disease progression in GK rats.
520 $a Increased dietary fat did result in increased fat accumulation and plasma FFAs in these animals. Combined with food consumption data, we conclude that WKY rats are more efficient in energy use than GK animals, and that GK animals may be more efficient in the use of lipid energy sources than carbohydrates. The microarray analysis on the data comparing diet effects within strains supports the conclusion that HF induces an adaptive increase in lipid utilization as well as adipose tissue macrophage infiltration accompanying increased adiposity in both strains. HF diet also induces adaptive responses of decreased fatty acid synthesis and lipogenesis in WKY rats, but increased lipid elimination and suppressed inflammation in GK animals.
520 $a This study evaluated the influence of genetic background interacting with increased dietary fat as an environmental contributor to diabetes disease progression in the polygenetic spontaneous diabetic inbred GK rat model, providing insights into the underlying molecular mechanisms and aiding in the identification of potential biomarkers useful in development of new anti-diabetic drugs.
590 $a School code: 0656.
650 4 $a Biology, Endocrinology. $3 1682242
650 4 $a Biology, Systematic. $3 1676856
650 4 $a Biology, Bioinformatics. $3 1018415
690 $a 0409
690 $a 0423
690 $a 0715
710 2 $a State University of New York at Buffalo. $b Biological Sciences. $3 1025373
773 0 $t Dissertation Abstracts International $g 72-04B.
790 1 0 $a Almon, Richard R., $e advisor
790 1 0 $a DuBois, Debra C., $e advisor
790 1 0 $a Free, Stephen J. $e committee member
790 1 0 $a Loretz, Christopher A. $e committee member
790 1 0 $a Yu, Michael C. $e committee member
790 $a 0656
791 $a Ph.D.
792 $a 2011
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3440365