Energy imbalance in Cyp11a1-/- mice

碩士 === 國立陽明大學 === 生物化學研究所 === 90 === Steroid hormones can control energy homeostasis to sustain the physiological functions under stress conditions. Imbalance of steroid hormones in human leads to many diseases that are associated with disrupted lipid and glucose metabolism. Mice lacking...

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Main Authors: Hsueh-Ping Chu, 朱雪萍
Other Authors: Bon-Chu Chung
Format: Others
Language:zh-TW
Published: 2002
Online Access:http://ndltd.ncl.edu.tw/handle/09018914603826607646
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spelling ndltd-TW-090YM0001070192016-06-24T04:15:11Z http://ndltd.ncl.edu.tw/handle/09018914603826607646 Energy imbalance in Cyp11a1-/- mice Cyp11a1基因剔除小鼠所造成能量平衡缺失的探討 Hsueh-Ping Chu 朱雪萍 碩士 國立陽明大學 生物化學研究所 90 Steroid hormones can control energy homeostasis to sustain the physiological functions under stress conditions. Imbalance of steroid hormones in human leads to many diseases that are associated with disrupted lipid and glucose metabolism. Mice lacking steroid hormone production for a null mutation in Cyp11a1 gene showed severe hypoglycemia followed by death between P1 and P8. Cyp11a1-/- mice had very low insulin levels, consistent with low blood glucose. Glycogen was also absent in the Cyp11a1-/- livers. On the other hand, lipid storage was reduced in the brown adipose tissue (BAT). It supports the glucocorticoid is required for fat buildup of BAT. Leptin, the other factor for energy balance, was severely low in circulation of Cyp11a1-/-mice. Further, triglycerides in the serum were markedly lower in Cyp11a1-/-mice, but triglycerides in the livers were enhanced that results lipid droplets accumulation. The hepatic gene expression of fatty acids catabolic enzyme, acyl-CoA oxidase, was elevated in Cyp11a1-/-mice. The mRNA of the genes involved in gluconeogenesis, glucose-6 phosphotase and phosphoenopyruvate carboxykinase, however, were not changed in 3-day old Cyp11a1-/- livers. This report demonstrates that Cyp11a1-/- mice have energy problems caused by hypoglycemia as well as shortage of glycogen and lipid storage. Bon-Chu Chung 鍾邦柱 2002 學位論文 ; thesis 57 zh-TW
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language zh-TW
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sources NDLTD
description 碩士 === 國立陽明大學 === 生物化學研究所 === 90 === Steroid hormones can control energy homeostasis to sustain the physiological functions under stress conditions. Imbalance of steroid hormones in human leads to many diseases that are associated with disrupted lipid and glucose metabolism. Mice lacking steroid hormone production for a null mutation in Cyp11a1 gene showed severe hypoglycemia followed by death between P1 and P8. Cyp11a1-/- mice had very low insulin levels, consistent with low blood glucose. Glycogen was also absent in the Cyp11a1-/- livers. On the other hand, lipid storage was reduced in the brown adipose tissue (BAT). It supports the glucocorticoid is required for fat buildup of BAT. Leptin, the other factor for energy balance, was severely low in circulation of Cyp11a1-/-mice. Further, triglycerides in the serum were markedly lower in Cyp11a1-/-mice, but triglycerides in the livers were enhanced that results lipid droplets accumulation. The hepatic gene expression of fatty acids catabolic enzyme, acyl-CoA oxidase, was elevated in Cyp11a1-/-mice. The mRNA of the genes involved in gluconeogenesis, glucose-6 phosphotase and phosphoenopyruvate carboxykinase, however, were not changed in 3-day old Cyp11a1-/- livers. This report demonstrates that Cyp11a1-/- mice have energy problems caused by hypoglycemia as well as shortage of glycogen and lipid storage.
author2 Bon-Chu Chung
author_facet Bon-Chu Chung
Hsueh-Ping Chu
朱雪萍
author Hsueh-Ping Chu
朱雪萍
spellingShingle Hsueh-Ping Chu
朱雪萍
Energy imbalance in Cyp11a1-/- mice
author_sort Hsueh-Ping Chu
title Energy imbalance in Cyp11a1-/- mice
title_short Energy imbalance in Cyp11a1-/- mice
title_full Energy imbalance in Cyp11a1-/- mice
title_fullStr Energy imbalance in Cyp11a1-/- mice
title_full_unstemmed Energy imbalance in Cyp11a1-/- mice
title_sort energy imbalance in cyp11a1-/- mice
publishDate 2002
url http://ndltd.ncl.edu.tw/handle/09018914603826607646
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AT zhūxuěpíng cyp11a1jīyīntīchúxiǎoshǔsuǒzàochéngnéngliàngpínghéngquēshīdetàntǎo
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