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限制能量摄入对大鼠胰岛细胞衰老及胰岛素表达的影响

Effect of caloric restriction on cell senescence and insulin expression of pancreatic islets
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摘要 目的探讨限制能量摄入对大鼠胰岛细胞衰老及胰岛素表达的影响。方法18月龄SD大鼠经过限制能量摄入(给予正常饮食量的60%)6个月,建立限制能量摄入动物模型。取限制能量摄入组(实验组)及对照组胰腺,行β-半乳糖苷酶(SA-β-Gal)染色并检测胰岛内p16的表达,以了解胰岛细胞衰老状态;同时检测胰岛B细胞胰岛素的表达。结果实验组与对照组比较。胰岛内p16表达减少,分别为(0.19130±0.02852)个和(0.24526±0.03191)个,差异有统计学意义(P〈 0.01);胰岛内β-Gal染色阳性率分别为84%和100%(P〈0.01)、着色面积1.672和2.118(P〈 0.05)、着色程度1.725和2.412(P〈0.05);胰岛素表达增加(201.7±35.3和187.8±26.0),差异有统计学意义(P〈0.05)结论限制能量摄入可延缓胰岛B细胞衰老,改善胰岛的分泌功能。 Objective To investigate the effect of caloric restriction (CR) on pancreatic beta cell senescence and its insulin secretion. Methods Eighteen-month-old SD rats received calory restriction (60% of regular intake) for 6 months. Rats of calory-restricted group and control group were killed at the end of the study, and sections of pancreas were stained for senescence-associated β-galactosidase (SA-β-Gal) and stained immunohistochemically with anti-p16 antibody to identify cell senescence of pancreatic islets, and stained immunohistoehemically with anti-insulin antibody. Results SA-β-Gal stain (presence, frequency, extent) decreased in calory-restricted rats (presence: 84%, frequency: 1.672, extent.. 1.725) compared with control group (presence: 100%, frequency: 2. 118, extent: 2. 412)(all P〈0. 05). p16 expression was lower in calory-restricted rats compared with control group (0. 19130 ± 0. 02852 vs. 0. 24526±0. 03198, P〈0.01). Insulin expression was higher in CR group compared with control group ( 201.7 ± 35.3 vs. 187.8 ± 26. 0, P 〈0. 05 ). Conclusions Calory resiriction can slow down the pancreatic beta cell senescence and improve insulin secretion of pancreatic islets.
出处 《中华老年医学杂志》 CAS CSCD 北大核心 2007年第8期616-619,共4页 Chinese Journal of Geriatrics
基金 广东省自然科学基金资助(5008346)
关键词 胰岛 热量限制 β半乳糖苷酶类 胰岛素 Islet Caloric restriction Beta-galactosidase Insulin
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  • 1Koubova J, Guarente L. How does calorie restriction work? Genes & Dev, 2003, 17..313-321.
  • 2Kyrylenko S, Kyrylenko O, Suuronen T, et al. Differential regulation of the Sir2 histone deaeetylase gene family by inhibitors of class Ⅰ and Ⅱ histone deacetylases. Cell Mol Life Sci, 2003, 60:1990-1997.
  • 3Mikhail VB. Cell senescence and hypermitogenic arrest. EMBO Reports, 2003, 4: 358-362.
  • 4Halvorsen TL, Beattie GM, Lopez AD, et al. Accelerated telomere shortening and senescence in human pancreatic islet cells stimulated to divide in vitro. J Endocrinol, 2000, 166:103-109.
  • 55Melk A, Kittikowit W, Sandhu I, et al. Cell senescence in rat kidneys in vivo increases with growth and age despite lack of telomere shortening. Kidney Int, 2003, 63: 2134-2143.
  • 6Dimri GP, Lee X, Basile G, et al. A biomarker that identifies senescent human cells in culture and in aging skin in vivo. Proc Natl Acad Sci USA, 1995, 92: 9363 9367.
  • 7Ravussin E, Smith SR. Increased fat intake, impaired fat oxidation, and failure of fat cell proliferation result in ectopic fat storage, insulin resistance, and type 2 diabetes mellitus. Ann NY Acad Sci, 2002, 967:363-378.
  • 8Holzenberger M, Dupont J, Ducos B, et al. IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice. Nature, 2003, 421:182-187.
  • 9Weindruch R, Kayo T, Lee CK, et al. Gene expression profiling of aging using DNA microarrays. Mech Ageing Dev, 2002, 123:177-193.
  • 10Welle S, Brooks A, Thornton CA. Senescence-related changes in gene expression in muscle., similarities and differences between mice and men. Physiol Genomics, 2001, 5:67-73.

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