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RISS 인기검색어
- 검색키워드
- 저자 : Pratleyd, Richard E. (검색결과 2 건)
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Kima, Jinil,Jeonga, Ja In,Kim, Kwang Min,Choi, Inho,Pratleyd, Richard E.,Lee, Yong-Ho 한국통합생물학회 2014 Animal cells and systems Vol.18 No.3
This study examined the effects of long-term consumption of a high-fat diet (HFD) on glucose metabolism in C57BL/6 mice. A total of 95 male 6-week-old mice were divided into normal diet (ND) and HFD groups until 16, 26, 36, 47, or 77 weeks of age. Plasma and blood glucose and insulin levels and area under the glucose curve ($AUC_{glucose}$) during an intraperitoneal glucose tolerance test were measured. Quantitative real-time PCR was performed to determine the mRNA expression levels of glucose transporter 4 (GLUT4) in adipose tissue. $AUC_{glucose}$ levels in HFD mice at 16, 26, and 36 weeks were significantly higher than those in ND mice (p < 0.001) and significantly reduced in HFD mice at 47 and 77 weeks. Nonfasting plasma glucose concentrations in both groups were significantly decreased at 47 and 77 weeks ($p{\leq}0.05$). Insulin levels in HFD mice at 47 and 77 weeks were 12.5% lower than those at 36 weeks. Relative GLUT4 mRNA expression in adipose tissue of HFD mice was significantly decreased at 26 and 36 weeks and increased at 47 and 77 weeks. These data suggest that the glucose tolerance was impaired by relatively short-term high-fat feeding and significantly improved by very long periods of high-fat feeding with restored GLUT4 expression in adipose tissue in HFD mice. The differential effects of short-and long-term HFD on glucose metabolism must be considered for recharacterizing the diet-induced obesity and clarify the pathogenesis of metabolic disorders in this animal model.
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Jeong, Ja In,Kim, Jinil,Kim, Kwang Min,Choi, Inho,Pratleyd, Richard E.,Lee, Yong-Ho 한국통합생물학회 2014 Animal cells and systems Vol.18 No.4
Mid-life obesity is associated with increased risk of Alzheimer's disease (AD). Amyloid precursor protein (APP) and its processing are centrally involved in the etiology of AD. Our previous studies demonstrated that human APP is expressed in adipocytes, up-regulated with obesity, and correlated with adipokine expression. This study was to determine whether APP expression is also dysregulated in mouse models of obesity and diabetes. Six-week-old C57BL/6 mice were fed normal or high-fat diets (HFD) until 16, 26, 36, 47, or 77 weeks of age. We measured gene expression of APP and adipokines, levels of glucose and insulin, and area under the glucose curve ($AUC_{glucose}$) during the glucose tolerance test. Using quantitative real-time polymerase chain reaction (PCR), we demonstrated that APP expression in subcutaneous adipose tissue (SAT) significantly increased in all HFD mice groups, and that it correlated with the levels of $AUC_{glucose}$, insulin, and expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-6 (IL-6) and chemokine (C-C motif) ligand 2 (CCL2) genes. Thiazolidinedione treatment significantly reduced plasma insulin levels and APP expression in SAT and epididymal adipose tissue. APP expression in the SAT and brain also decreased significantly in streptozotocin-induced diabetic mice, indicating an important role of insulin in the regulation of APP gene expression. These results demonstrate that adipose tissue APP expression is increased with obesity and regulated by insulin levels, suggesting that the regulation and role of APP are similar in humans and mice. Insights into APP regulation and processing in the adipose tissue may improve our understanding of obesity-related adipose-tissue inflammation and the increased risk of AD in obese individuals.
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