• 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

高脂饮食喂养的 Goto-Kakizaki 大鼠胰岛 β 细胞质量增加减少及其被匹伐他汀治疗抑制。

Augmented reduction of islet β-cell mass in Goto-Kakizaki rats fed high-fat diet and its suppression by pitavastatin treatment.

机构信息

Department of Pathology and Molecular Medicine, Hirosaki University Graduate School of Medicine, Hirosaki.

Tokyo New Drug Research Laboratories, Pharmaceutical Division, Kowa Company Ltd., Higashimurayama, Tokyo, Japan.

出版信息

J Diabetes Investig. 2012 Jun 6;3(3):235-44. doi: 10.1111/j.2040-1124.2011.00173.x.

DOI:10.1111/j.2040-1124.2011.00173.x
PMID:24843571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4014944/
Abstract

UNLABELLED

Aims/Introduction:  High fat diet (HFD) is known to be a risk for development of type 2 diabetes. It is unclear, however, how it affects the glucose tolerance or the islet structure in type 2 diabetes. The aim of this study is: (i) to examine the effects of HFD on the islet in GK rats, non-obese type 2 diabetic model; and (ii) to explore if pitavastatin treatment influences the change.

MATERIALS AND METHODS

To see the effects of HFD on islet changes in type 2 diabetes, 4-week old male GK and Wistar rats were fed HFD for 16 weeks and subjected to glucose tolerance tests and pathological studies of the islet. The effects of pitavastatin (3 mg/kg/day for 16 weeks, oral), one of the lipophilc statins, were also examined in both GK and Wistrar rats fed with or without HFD.

RESULTS

The HFD induced hyperlipidemia and aggravated glucose intolerance in both GK and Wistar rats. Pitavastatin treatment did not influence the glucose tolerance in HFD-fed animals. HFD caused an increase in hepatic lipid contents in all the animals, which was partially suppressed by pitavastatin treatment. GK rats showed reduced β-cell mass, and fibrosis and macrophage migration in the islets. HFD feeding in GK rats augmented these changes which were associated with enhanced expression of 8-hydroxydeoxyguanosine and an increase in apoptotic cells. Pitavastatin treatment improved the HFD-induced islet pathology, and pancreatic insulin contents paralleled the structural changes.

CONCLUSIONS

HFD feeding worsened the islet pathology in GK rats which was suppressed by pitavastatin treatment. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00173.x, 2011).

摘要

目的/引言：高脂肪饮食（HFD）已知是 2 型糖尿病的发病风险因素。然而，它如何影响 2 型糖尿病患者的葡萄糖耐量或胰岛结构尚不清楚。本研究的目的是：（i）检查 HFD 对非肥胖 2 型糖尿病模型 GK 大鼠胰岛的影响；（ii）探讨匹伐他汀治疗是否会影响这种变化。

材料和方法

为了观察 HFD 对 2 型糖尿病患者胰岛变化的影响，4 周龄雄性 GK 和 Wistar 大鼠给予 HFD 喂养 16 周，并进行葡萄糖耐量试验和胰岛病理研究。还在给予或不给予 HFD 的 GK 和 Wistar 大鼠中，检查了亲脂性他汀类药物之一匹伐他汀（3mg/kg/天，16 周，口服）的作用。

结果

HFD 可引起高脂血症，并加重 GK 和 Wistar 大鼠的葡萄糖耐量异常。匹伐他汀治疗对 HFD 喂养动物的葡萄糖耐量没有影响。HFD 引起所有动物的肝脂质含量增加，匹伐他汀治疗部分抑制了这种增加。GK 大鼠的胰岛β细胞质量减少，纤维化和巨噬细胞迁移增加。HFD 喂养加剧了这些变化，与 8-羟基脱氧鸟苷表达增强和凋亡细胞增加有关。匹伐他汀治疗改善了 HFD 诱导的胰岛病理学，胰腺胰岛素含量与结构变化平行。

结论

HFD 喂养可加重 GK 大鼠的胰岛病理学，而匹伐他汀治疗可抑制这种变化。（J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00173.x, 2011）。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/282913036733/jdi-3-235-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/484046c0a1c9/jdi-3-235-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/ee44f0254cf3/jdi-3-235-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/6b55a1664ef3/jdi-3-235-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/c107e8ca5303/jdi-3-235-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/f8cef2420444/jdi-3-235-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/80afbb948b23/jdi-3-235-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/b585f428827f/jdi-3-235-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/282913036733/jdi-3-235-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/484046c0a1c9/jdi-3-235-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/ee44f0254cf3/jdi-3-235-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/6b55a1664ef3/jdi-3-235-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/c107e8ca5303/jdi-3-235-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/f8cef2420444/jdi-3-235-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/80afbb948b23/jdi-3-235-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/b585f428827f/jdi-3-235-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a7a1/4014944/282913036733/jdi-3-235-g8.jpg

相似文献

1
Augmented reduction of islet β-cell mass in Goto-Kakizaki rats fed high-fat diet and its suppression by pitavastatin treatment.高脂饮食喂养的 Goto-Kakizaki 大鼠胰岛 β 细胞质量增加减少及其被匹伐他汀治疗抑制。
J Diabetes Investig. 2012 Jun 6;3(3):235-44. doi: 10.1111/j.2040-1124.2011.00173.x.
2
Accelerated loss of islet beta cells in sucrose-fed Goto-Kakizaki rats, a genetic model of non-insulin-dependent diabetes mellitus.蔗糖喂养的Goto-Kakizaki大鼠（非胰岛素依赖型糖尿病的遗传模型）胰岛β细胞加速丢失。
Am J Pathol. 1998 Aug;153(2):537-45. doi: 10.1016/s0002-9440(10)65596-4.
3
Structural lesions and changing pattern of expression of genes encoding cardiac muscle proteins are associated with ventricular myocyte dysfunction in type 2 diabetic Goto-Kakizaki rats fed a high-fat diet.结构损伤和编码心肌蛋白的基因表达模式的改变与 2 型糖尿病 Goto-Kakizaki 大鼠高脂饮食喂养时心室肌细胞功能障碍有关。
Exp Physiol. 2011 Aug;96(8):765-77. doi: 10.1113/expphysiol.2011.058446. Epub 2011 Jun 10.
4
A prescribed Chinese herbal medicine improves glucose profile and ameliorates oxidative stress in Goto-Kakisaki rats fed with high fat diet.一种规定的中草药可改善高脂肪饮食喂养的 Goto-Kakisaki 大鼠的血糖谱并改善氧化应激。
PLoS One. 2013;8(4):e60262. doi: 10.1371/journal.pone.0060262. Epub 2013 Apr 2.
5
Enhanced Glucose Tolerance and Pancreatic Beta Cell Function by Low Dose Aspirin in Hyperglycemic Insulin-Resistant Type 2 Diabetic Goto-Kakizaki (GK) Rats.低剂量阿司匹林改善高血糖胰岛素抵抗2型糖尿病Goto-Kakizaki（GK）大鼠的葡萄糖耐量和胰岛β细胞功能
Cell Physiol Biochem. 2015;36(5):1939-50. doi: 10.1159/000430162. Epub 2015 Jul 17.
6
High dietary fat-induced obesity in Wistar rats and type 2 diabetes in nonobese Goto-Kakizaki rats differentially affect retinol binding protein 4 expression and vitamin A metabolism.高膳食脂肪诱导的Wistar大鼠肥胖和非肥胖Goto-Kakizaki大鼠的2型糖尿病对视黄醇结合蛋白4表达和维生素A代谢有不同影响。
Nutr Res. 2016 Mar;36(3):262-70. doi: 10.1016/j.nutres.2015.11.018. Epub 2015 Nov 26.
7
Effects of long-term treatment with the dipeptidyl peptidase-4 inhibitor vildagliptin on islet endocrine cells in non-obese type 2 diabetic Goto-Kakizaki rats.长期应用二肽基肽酶-4 抑制剂维格列汀对非肥胖型 2 型糖尿病 Goto-Kakizaki 大鼠胰岛内分泌细胞的影响。
Eur J Pharmacol. 2012 Sep 15;691(1-3):297-306. doi: 10.1016/j.ejphar.2012.07.030. Epub 2012 Jul 20.
8
Asiatic acid mitigates hyperglycemia and reduces islet fibrosis in Goto-Kakizaki rat, a spontaneous type 2 diabetic animal model.齐墩果酸可减轻自发性2型糖尿病动物模型——Goto-Kakizaki大鼠的高血糖症状，并减少胰岛纤维化。
Chin J Nat Med. 2015 Jul;13(7):529-34. doi: 10.1016/S1875-5364(15)30047-9.
9
Improved glucose-stimulated insulin secretion by intra-islet inhibition of protein-tyrosine phosphatase 1B expression in rats fed a high-fat diet.高脂饮食喂养的大鼠胰岛内蛋白酪氨酸磷酸酶 1B 表达抑制可改善葡萄糖刺激的胰岛素分泌。
J Endocrinol Invest. 2012 Jan;35(1):63-70. doi: 10.3275/7766. Epub 2011 May 30.
10
Effect of high dietary fat on insulin secretion in genetically diabetic Goto-Kakizaki rats.高膳食脂肪对遗传性糖尿病Goto-Kakizaki大鼠胰岛素分泌的影响。
Pancreas. 2002 Nov;25(4):393-9. doi: 10.1097/00006676-200211000-00012.

引用本文的文献

1
Pathological evaluation of the pathogenesis of diabetes mellitus and diabetic peripheral neuropathy.糖尿病发病机制及糖尿病周围神经病变的病理学评价。
Pathol Int. 2024 Aug;74(8):438-453. doi: 10.1111/pin.13458. Epub 2024 Jun 18.
2
Prevalence and Risk Factors of Type 2 Diabetes and Prediabetes Among 53,288 Middle-Aged and Elderly Adults in China: A Cross-Sectional Study.中国53288名中老年人2型糖尿病和糖尿病前期的患病率及危险因素：一项横断面研究
Diabetes Metab Syndr Obes. 2021 May 3;14:1975-1985. doi: 10.2147/DMSO.S305919. eCollection 2021.
3
MIF May Participate in Pathogenesis of Polycystic Ovary Syndrome in Rats through MAPK Signalling Pathway.

本文引用的文献

1
The spontaneous-diabetes rat: a model of noninsulin dependent diabetes mellitus by Yoshio Goto and Masaei Kakizaki (1981).自发性糖尿病大鼠：由 Yoshio Goto 和 Masaei Kakizaki（1981 年）建立的非胰岛素依赖型糖尿病模型。
Proc Jpn Acad Ser B Phys Biol Sci. 2024;100(9):500-507. doi: 10.2183/pjab.100.036.
2
Components of metabolic syndrome and their combinations as predictors of cardiovascular disease in Japanese patients with type 2 diabetes. Implications for improved definition. Analysis from Japan Diabetes Complications Study (JDCS).日本2型糖尿病患者代谢综合征的组成成分及其组合作为心血管疾病预测指标。对改进定义的启示。来自日本糖尿病并发症研究（JDCS）的分析
J Atheroscler Thromb. 2009 Aug;16(4):380-7. doi: 10.5551/jat.no117. Epub 2009 Aug 11.
3
MIF 可能通过 MAPK 信号通路参与多囊卵巢综合征大鼠的发病机制。
Curr Med Sci. 2018 Oct;38(5):853-860. doi: 10.1007/s11596-018-1953-7. Epub 2018 Oct 20.
4
Increases in bioactive lipids accompany early metabolic changes associated with β-cell expansion in response to short-term high-fat diet.生物活性脂质的增加伴随着与β细胞扩张相关的早期代谢变化，这是对短期高脂肪饮食的反应。
Am J Physiol Endocrinol Metab. 2018 Dec 1;315(6):E1251-E1263. doi: 10.1152/ajpendo.00001.2018. Epub 2018 Aug 14.
5
Statins and New-Onset Diabetes Mellitus: LDL Receptor May Provide a Key Link.他汀类药物与新发糖尿病：低密度脂蛋白受体可能提供关键联系。
Front Pharmacol. 2017 Jun 13;8:372. doi: 10.3389/fphar.2017.00372. eCollection 2017.
6
Age-associated changes of islet endocrine cells and the effects of body mass index in Japanese.胰岛内分泌细胞的年龄相关性变化及体重指数的影响（日本人）。
J Diabetes Investig. 2014 Feb 12;5(1):38-47. doi: 10.1111/jdi.12118. Epub 2013 Aug 4.
Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters.瘦而非肥胖的个体中，脂肪富含一群独特的调节性T细胞，这些细胞会影响代谢参数。
Nat Med. 2009 Aug;15(8):930-9. doi: 10.1038/nm.2002. Epub 2009 Jul 26.
4
Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein.瑞舒伐他汀预防C反应蛋白升高的男性和女性发生血管事件。
N Engl J Med. 2008 Nov 20;359(21):2195-207. doi: 10.1056/NEJMoa0807646. Epub 2008 Nov 9.
5
Influence of pitavastatin on glucose tolerance in patients with type 2 diabetes mellitus.匹伐他汀对2型糖尿病患者糖耐量的影响。
J Atheroscler Thromb. 2008 Oct;15(5):269-75. doi: 10.5551/jat.e562.
6
Suppression of post-prandial hyperglycaemia by pioglitazone improved islet fibrosis and macrophage migration in the Goto-Kakizaki rat.
Diabetes Obes Metab. 2008 Sep;10(9):791-4. doi: 10.1111/j.1463-1326.2008.00893.x.
7
Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet.自噬在胰岛内环境稳定以及胰岛β细胞质量对高脂饮食的代偿性增加中发挥重要作用。
Cell Metab. 2008 Oct;8(4):325-32. doi: 10.1016/j.cmet.2008.08.009.
8
Effect of pitavastatin on type 2 diabetes mellitus nephropathy in KK-Ay/Ta mice.匹伐他汀对KK-Ay/Ta小鼠2型糖尿病肾病的影响。
Metabolism. 2008 May;57(5):691-7. doi: 10.1016/j.metabol.2008.01.007.
9
Augmented beta cell loss and mitochondrial abnormalities in sucrose-fed GK rats.蔗糖喂养的GK大鼠中β细胞损失增加及线粒体异常
Virchows Arch. 2008 Apr;452(4):383-92. doi: 10.1007/s00428-007-0508-2. Epub 2008 Jan 31.
10
The replication of beta cells in normal physiology, in disease and for therapy.β细胞在正常生理状态下、疾病状态下以及治疗过程中的复制。
Nat Clin Pract Endocrinol Metab. 2007 Nov;3(11):758-68. doi: 10.1038/ncpendmet0647.