Dehydroepiandrosterone increases β-cell mass and improves the glucose-induced insulin secretion by pancreatic islets from aged rats

被引:25
|
作者
Medina, MC
Souza, LC
Caperuto, LC
Anhêh, GF
Amanso, AM
Teixeira, VPA
Bordin, S
Carpinelli, AR
Britto, LRG
Barbieri, RL
Borella, MI
Carvalho, CRO [1 ]
机构
[1] Univ Sao Paulo, ICB, Dept Physiol & Biophys, BR-05389970 Sao Paulo, Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Dev & Cell Biol, Sao Paulo, Brazil
[3] Coll Med Triangulo Mineiro, Dept Gen Pathol, Uberaba, MG, Brazil
基金
巴西圣保罗研究基金会;
关键词
DHEA; insulin secretion; aged rats; Akt; IRS proteins; pancreatic islet;
D O I
10.1016/j.febslet.2005.12.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effect of dehydroepiandrosterone (DHEA) on pancreatic islet function of aged rats, an animal model with impaired glucose-induced insulin secretion, was investigated. The following parameters were examined: morphological analysis of endocrine pancreata by immunohistochemistry; protein levels of insulin receptor, IRS-1, IRS-2, PI 3-kinase, Akt-1, and Akt-2; and static insulin secretion in isolated pancreatic islets. Pancreatic islets from DHEA-treated rats showed an increased beta-cell mass accompanied by increased Akt-1 protein level but reduced IR, IRS-1, and IRS-2 protein levels and enhanced glucose-stimulated insulin secretion. The present results suggest that DHEA may be a promising drug to prevent diabetes during aging. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:285 / 290
页数:6
相关论文
共 50 条
  • [21] Prolonged exposure of pancreatic B-cells to free fatty acids in vivo increases glucose-induced insulin secretion and B-cell mass in rats
    Magnan, C
    Berthault, MF
    Laury, MC
    Leveteau, J
    Penicaud, L
    Ktorza, A
    AssimacopoulosJeannet, F
    DIABETOLOGIA, 1997, 40 : 96 - 96
  • [22] SIGMOID DOSE-RESPONSE RELATION FOR GLUCOSE-INDUCED INSULIN-SECRETION FROM PANCREATIC-ISLETS
    DESIMONE, JA
    PRICE, S
    BIOPHYSICAL JOURNAL, 1978, 21 (03) : A133 - A133
  • [23] Tranilast inhibits glucose-induced insulin secretion from pancreatic β-cells
    Taguchi, S.
    Ozaki, N.
    Umeda, H.
    Mizutani, N.
    Yamada, T.
    Oiso, Y.
    HORMONE AND METABOLIC RESEARCH, 2008, 40 (08) : 518 - 523
  • [24] Reduced glucose-induced insulin secretion in low-protein-fed rats is associated with altered pancreatic islets redox status
    Cappelli, Ana Paula G.
    Zoppi, Claudio C.
    Silveira, Leonardo R.
    Batista, Thiago M.
    Paula, Flavia M.
    da Silva, Priscilla M. R.
    Rafacho, Alex
    Barbosa-Sampaio, Helena C.
    Boschero, Antonio C.
    Carneiro, Everardo M.
    JOURNAL OF CELLULAR PHYSIOLOGY, 2018, 233 (01) : 486 - 496
  • [25] PANCREATIC BETA-CELL HETEROGENEITY IN GLUCOSE-INDUCED INSULIN-SECRETION
    VANSCHRAVENDIJK, CFH
    KIEKENS, R
    PIPELEERS, DG
    JOURNAL OF BIOLOGICAL CHEMISTRY, 1992, 267 (30) : 21344 - 21348
  • [26] EFFECT OF STREPTOZOTOCIN ON GLUCOSE-INDUCED INSULIN SECRETION BY ISOLATED ISLETS OF LANGERHANS
    GOLDEN, P
    BAIRD, L
    MALAISSE, WJ
    MALAISSE.F
    WALKER, MM
    DIABETES, 1971, 20 (08) : 513 - &
  • [27] Leptin inhibits glucose-induced insulin secretion from isolated rat islets of Langerhans
    Poitout, V
    Rouault, C
    GuerreMillo, M
    Briaud, I
    Reach, G
    DIABETES, 1997, 46 : 13 - 13
  • [28] Autocrine action of PACAP in islets augments glucose-induced insulin secretion
    Yada, T
    Sakurada, M
    Nakata, M
    Shioda, S
    VIP, PACAP, AND RELATED PEPTIDES: THIRD INTERNATIONAL SYMPOSIUM, 1998, 865 : 451 - 457
  • [29] Endogenous nitric oxide inhibits glucose-induced insulin secretion by suppression of phosphofructokinase activity in pancreatic islets
    Tsuura, Y
    Ishida, H
    Shinomura, T
    Nishimura, M
    Seino, Y
    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 252 (01) : 34 - 38
  • [30] Biotin enhances ATP synthesis in pancreatic islets of the rat, resulting in reinforcement of glucose-induced insulin secretion
    Sone, H
    Sasaki, Y
    Komai, M
    Toyomizu, M
    Kagawa, Y
    Furukawa, Y
    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 314 (03) : 824 - 829