• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

维持体重减轻的大鼠的脂肪组织脂蛋白脂肪酶活性。

Adipose tissue lipoprotein lipase activity in rats maintained at a reduced body weight.

作者信息

Hamilton J M, Heller H W, Wade G N

出版信息

Physiol Behav. 1984 Sep;33(3):373-8. doi: 10.1016/0031-9384(84)90156-2.

DOI:10.1016/0031-9384(84)90156-2
PMID:6514826
Abstract

Male rats fed a cellulose-diluted diet maintained a reduced body weight. Adipose tissue lipoprotein lipase (LPL) activity decreased after two days of cellulose feeding, but was not different from chow-fed control levels with weight stabilized at 90% or 70% of the control group. Plasma triglyceride concentration decreased with weight loss and remained depressed with stabilized reduced weight. Regaining lost weight had no effect on LPL activity when compared with chow-fed controls or with levels obtained for the weight-reduced group. However, plasma triglyceride concentration returned to chow-fed control levels with weight gain. The disparity between these results and those obtained in obese human beings lends support to the hypothesis that the increase in adipose tissue LPL activity in weight-reduced obese human beings is indicative of a defect in regulation of adipose tissue metabolism.

摘要

喂食纤维素稀释饮食的雄性大鼠体重持续减轻。喂食纤维素两天后,脂肪组织脂蛋白脂肪酶(LPL)活性降低,但当体重稳定在对照组的90%或70%时,该活性与喂食普通饲料的对照组水平并无差异。血浆甘油三酯浓度随体重减轻而降低,且在体重稳定减轻时仍保持较低水平。与喂食普通饲料的对照组或体重减轻组的水平相比,体重恢复对LPL活性没有影响。然而,随着体重增加,血浆甘油三酯浓度恢复到喂食普通饲料的对照组水平。这些结果与在肥胖人群中获得的结果之间的差异支持了这样一种假设,即体重减轻的肥胖人群脂肪组织LPL活性的增加表明脂肪组织代谢调节存在缺陷。

相似文献

1
Adipose tissue lipoprotein lipase activity in rats maintained at a reduced body weight.维持体重减轻的大鼠的脂肪组织脂蛋白脂肪酶活性。
Physiol Behav. 1984 Sep;33(3):373-8. doi: 10.1016/0031-9384(84)90156-2.
2
Diet composition and lipoprotein lipase (EC 3.1.1.34) activity in human obesity.人类肥胖症中的饮食组成与脂蛋白脂肪酶(EC 3.1.1.34)活性
Br J Nutr. 1987 Jul;58(1):13-21. doi: 10.1079/bjn19870064.
3
The influence of starvation and refeeding on the lipoprotein lipase activity of skeletal muscle and adipose tissue of lean and obese Zucker rats.饥饿和再喂养对瘦型和肥胖型 Zucker 大鼠骨骼肌及脂肪组织脂蛋白脂肪酶活性的影响。
J Nutr. 1983 Jun;113(6):1150-6. doi: 10.1093/jn/113.6.1150.
4
Adipose tissue lipoprotein lipase (LPL) and triglyceride uptake in zucker rats.肥胖 Zucker 大鼠的脂肪组织脂蛋白脂肪酶(LPL)与甘油三酯摄取
Physiol Behav. 1982 Dec;29(6):1147-52. doi: 10.1016/0031-9384(82)90312-2.
5
Response of adipose tissue lipoprotein lipase to the cephalic phase of insulin secretion.脂肪组织脂蛋白脂肪酶对胰岛素分泌头期的反应。
Diabetes. 1999 Mar;48(3):452-9. doi: 10.2337/diabetes.48.3.452.
6
Maternal and early dietary fatty acid intake: changes in lipid metabolism and liver enzymes in adult rats.母体及早期膳食脂肪酸摄入量:成年大鼠脂质代谢及肝脏酶的变化
J Nutr. 2000 Feb;130(2):146-51. doi: 10.1093/jn/130.2.146.
7
Regulation of lipoprotein lipase and hormone-sensitive lipase activity and gene expression in adipose and muscle tissue by growth hormone treatment during weight loss in obese patients.肥胖患者体重减轻期间生长激素治疗对脂肪和肌肉组织中脂蛋白脂肪酶及激素敏感性脂肪酶活性和基因表达的调节作用
Metabolism. 2000 Jul;49(7):906-11. doi: 10.1053/meta.2000.6738.
8
Relationship of organ lipoprotein lipase activity and ketonuria to hypertriglyceridemia in starved and streptozocin-induced diabetic rats.饥饿和链脲佐菌素诱导的糖尿病大鼠器官脂蛋白脂肪酶活性和酮尿症与高甘油三酯血症的关系。
Diabetes. 1987 Apr;36(4):485-90. doi: 10.2337/diab.36.4.485.
9
Resistance of adipose tissue lipoprotein lipase to insulin action in rats fed an obesity-promoting diet.喂食促肥胖饮食的大鼠脂肪组织脂蛋白脂肪酶对胰岛素作用的抵抗
Am J Physiol Endocrinol Metab. 2002 Feb;282(2):E412-8. doi: 10.1152/ajpendo.00307.2001.
10
Adipose tissue lipoprotein lipase in chronic hemodialysis: role in plasma triglyceride metabolism.慢性血液透析中的脂肪组织脂蛋白脂肪酶:在血浆甘油三酯代谢中的作用
J Clin Endocrinol Metab. 1978 Dec;47(6):1173-82. doi: 10.1210/jcem-47-6-1173.