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本文引用的文献

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Effect of intensive insulin therapy on beta-cell function and glycaemic control in patients with newly diagnosed type 2 diabetes: a multicentre randomised parallel-group trial.强化胰岛素治疗对新诊断2型糖尿病患者β细胞功能及血糖控制的影响:一项多中心随机平行组试验
Lancet. 2008 May 24;371(9626):1753-60. doi: 10.1016/S0140-6736(08)60762-X.
2
Endocrine functions of adipose tissue.脂肪组织的内分泌功能。
Annu Rev Pathol. 2007;2:31-56. doi: 10.1146/annurev.pathol.2.010506.091859.
3
Insulin efficiently stores triglycerides in adipocytes by inhibiting lipolysis and repressing PGC-1alpha induction.胰岛素通过抑制脂肪分解和抑制PGC-1α的诱导,有效地将甘油三酯储存于脂肪细胞中。
Kobe J Med Sci. 2007;53(3):99-106.
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Serum visfatin increases with progressive beta-cell deterioration.随着β细胞的逐渐恶化,血清内脂素水平升高。
Diabetes. 2006 Oct;55(10):2871-5. doi: 10.2337/db06-0259.
5
Acute in vivo effects of insulin on gene expression in adipose tissue in insulin-resistant and insulin-sensitive subjects.胰岛素对胰岛素抵抗和胰岛素敏感受试者脂肪组织基因表达的急性体内效应。
Diabetologia. 2006 Jan;49(1):132-40. doi: 10.1007/s00125-005-0075-5. Epub 2005 Dec 16.
6
Elevated plasma level of visfatin/pre-B cell colony-enhancing factor in patients with type 2 diabetes mellitus.2型糖尿病患者血浆内脂素/前B细胞集落增强因子水平升高。
J Clin Endocrinol Metab. 2006 Jan;91(1):295-9. doi: 10.1210/jc.2005-1475. Epub 2005 Oct 18.
7
Aquaporin 7 deficiency is associated with development of obesity through activation of adipose glycerol kinase.水通道蛋白7缺乏通过激活脂肪甘油激酶与肥胖的发生有关。
Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):10993-8. doi: 10.1073/pnas.0503291102. Epub 2005 Jul 11.
8
Induction of long-term glycemic control in newly diagnosed type 2 diabetic patients is associated with improvement of beta-cell function.新诊断2型糖尿病患者长期血糖控制的诱导与β细胞功能改善相关。
Diabetes Care. 2004 Nov;27(11):2597-602. doi: 10.2337/diacare.27.11.2597.
9
The effect of pioglitazone on peroxisome proliferator-activated receptor-gamma target genes related to lipid storage in vivo.吡格列酮对体内与脂质储存相关的过氧化物酶体增殖物激活受体γ靶基因的影响。
Diabetes Care. 2004 Jul;27(7):1660-7. doi: 10.2337/diacare.27.7.1660.
10
Short-term intensive insulin therapy in newly diagnosed type 2 diabetes.新诊断2型糖尿病的短期强化胰岛素治疗
Diabetes Care. 2004 May;27(5):1028-32. doi: 10.2337/diacare.27.5.1028.

胰岛素治疗可刺激饮食肥胖 C57BL/6 小鼠脂肪细胞的脂质合成并改善其内分泌功能。

Insulin therapy stimulates lipid synthesis and improves endocrine functions of adipocytes in dietary obese C57BL/6 mice.

机构信息

Department of Endocrinology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

出版信息

Acta Pharmacol Sin. 2010 Mar;31(3):341-6. doi: 10.1038/aps.2010.17. Epub 2010 Feb 22.

DOI:10.1038/aps.2010.17
PMID:20173758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4002414/
Abstract

AIM

To evaluate whether insulin intervention could affect the metabolic and endocrine functions of adipose tissue.

METHODS

C57BL/6 mice were fed on a high-fat-diet for 12-16 weeks to induce insulin resistance. Insulin intervention was administered in the high-fat-diet mice for 4 weeks at 12 weeks (early insulin treatment) or 16 weeks (late insulin treatment). Intraperitoneal glucose tolerance tests were performed before and after insulin treatment. Expression levels of factors involved in the triglyceride synthesis and endocrine functions of adipose tissue including phosphoenolpyruvate carboxykinase (PEPCK-C), fatty acid synthase (FAS), aquaporin 7 (AQP7), adiponectin, visfatin, and interleukin-6 (IL-6) were determined by Western blot.

RESULTS

In the obese mice, glucose tolerance was impaired; triglyceride content was increased in the liver tissue; protein expression of FAS and adiponectin was decreased; expression of visfatin was increased in adipose tissue. After 4-week insulin treatment, glucose tolerance was improved; triglyceride content was decreased in the liver and skeletal muscle; expression of PEPCK-C, FAS, and adiponectin was increased in the adipose tissue; IL-6 and AQP7 expression was reduced in the fat. Early insulin treatment had better effect in increasing the expression of FAS and PEPCK-C and decreasing the expression of IL-6.

CONCLUSION

These results indicate that insulin can target adipocytes for improvement of insulin sensitivity through stimulating triglyceride synthesis and partly improving endocrine functions.

摘要

目的

评估胰岛素干预是否能影响脂肪组织的代谢和内分泌功能。

方法

用高脂肪饮食喂养 C57BL/6 小鼠 12-16 周,诱导胰岛素抵抗。在 12 周(早期胰岛素治疗)或 16 周(晚期胰岛素治疗)时,对高脂肪饮食小鼠进行 4 周的胰岛素干预。在胰岛素治疗前后进行腹腔内葡萄糖耐量试验。通过 Western blot 测定参与甘油三酯合成和脂肪组织内分泌功能的因子的表达水平,包括磷酸烯醇丙酮酸羧激酶(PEPCK-C)、脂肪酸合酶(FAS)、水通道蛋白 7(AQP7)、脂联素、内脂素和白细胞介素-6(IL-6)。

结果

在肥胖小鼠中,葡萄糖耐量受损;肝组织甘油三酯含量增加;FAS 和脂联素的蛋白表达减少;脂肪组织中内脂素的表达增加。经过 4 周胰岛素治疗,葡萄糖耐量改善;肝和骨骼肌中的甘油三酯含量降低;脂肪组织中 PEPCK-C、FAS 和脂联素的表达增加;脂肪中的 IL-6 和 AQP7 表达减少。早期胰岛素治疗在增加 FAS 和 PEPCK-C 的表达和减少 IL-6 的表达方面效果更好。

结论

这些结果表明,胰岛素可以通过刺激甘油三酯合成和部分改善内分泌功能,针对脂肪细胞来提高胰岛素敏感性。