Drosophila melanogaster as a Model for Diabetes Type 2 Progression

被引:45
作者
Alvarez-Rendon, Jessica P. [1 ]
Salceda, Rocio [2 ]
Riesgo-Escovar, Juan R. [1 ]
机构
[1] Univ Nacl Autonoma Mexico, Inst Neurobiol, Campus UNAM Juriquilla,Blvd Juriquilla 3001, Queretaro 76226, Qro, Mexico
[2] Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Ave Univ 3000, Ciuded De Mexico 04510, Mexico
关键词
PROTEIN-KINASE-B; INSULIN-LIKE PEPTIDES; GLYCOGEN-SYNTHASE ACTIVATION; BETA-CELL DYSFUNCTION; HIGH-FAT-DIET; LIFE-SPAN; TRANSCRIPTION FACTOR; PHOSPHOINOSITIDE; 3-KINASE; MOLECULAR-MECHANISMS; LEW.1AR1/ZTM-IDDM RAT;
D O I
10.1155/2018/1417528
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Drosophila melanogaster has been used as a very versatile and potent model in the past few years for studies in metabolism and metabolic disorders, including diabetes types 1 and 2. Drosophila insulin signaling, despite having seven insulin-like peptides with partially redundant functions, is very similar to the human insulin pathway and has served to study many different aspects of diabetes and the diabetic state. Yet, very few studies have addressed the chronic nature of diabetes, key for understanding the full-blown disease, which most studies normally explore. One of the advantages of having Drosophila mutant viable combinations at different levels of the insulin pathway, with significantly reduced insulin pathway signaling, is that the abnormal metabolic state can be studied from the onset of the life cycle and followed throughout. In this review, we look at the chronic nature of impaired insulin signaling. We also compare these results to the results gleaned from vertebrate model studies.
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页数:16
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共 229 条
  • [1] FoxOs at the crossroads of cellular metabolism, differentiation, and transformation
    Accili, D
    Arden, KC
    [J]. CELL, 2004, 117 (04) : 421 - 426
  • [2] Goto-kakizaki Rats: Its Suitability as Non-obese Diabetic Animal Model for Spontaneous Type 2 Diabetes Mellitus
    Akash, Muhammad Sajid Hamid
    Rehman, Kanwal
    Chen, Shuqing
    [J]. CURRENT DIABETES REVIEWS, 2013, 9 (05) : 387 - 396
  • [3] Mechanism of activation of protein kinase B by insulin and IGF-1
    Alessi, DR
    Andjelkovic, M
    Caudwell, B
    Cron, P
    Morrice, N
    Cohen, P
    Hemmings, BA
    [J]. EMBO JOURNAL, 1996, 15 (23) : 6541 - 6551
  • [4] Using Drosophila to discover mechanisms underlying type 2 diabetes
    Alfa, Ronald W.
    Kim, Seung K.
    [J]. DISEASE MODELS & MECHANISMS, 2016, 9 (04) : 365 - 376
  • [5] The Lnk/SH2B adaptor provides a fail-safe mechanism to establish the Insulin receptor-Chico interaction
    Almudi, Isabel
    Poernbacher, Ingrid
    Hafen, Ernst
    Stocker, Hugo
    [J]. CELL COMMUNICATION AND SIGNALING, 2013, 11
  • [6] Network-level molecular evolutionary analysis of the insulin/TOR signal transduction pathway across 12 Drosophila genomes
    Alvarez-Ponce, David
    Aguade, Montserrat
    Rozas, Julio
    [J]. GENOME RESEARCH, 2009, 19 (02) : 234 - 242
  • [7] Genetic analysis of Drosophila sechellia specialization:: Oviposition behavior toward the major aliphatic acids of its host plant
    Amlou, M
    Moreteau, B
    David, JR
    [J]. BEHAVIOR GENETICS, 1998, 28 (06) : 455 - 464
  • [8] [Anonymous], 1977, NUTR REV, V35, P181
  • [9] A novel Dock8 gene mutation confers diabetogenic susceptibility in the LEW.1AR1/Ztm-iddm rat, an animal model of human type 1 diabetes
    Arndt, Tanja
    Wedekind, Dirk
    Joerns, Anne
    Tsiavaliaris, Georgios
    Cuppen, Edwin
    Hedrich, Hans-Juergen
    Lenzen, Sigurd
    [J]. DIABETOLOGIA, 2015, 58 (12) : 2800 - 2809
  • [10] Drosophila ALS regulates growth and metabolism through functional interaction with insulin-like peptides
    Arquier, Nathalie
    Geminard, Charles
    Bourouis, Marc
    Jarretou, Gisele
    Honegger, Basil
    Paix, Alexandre
    Leopold, Pierre
    [J]. CELL METABOLISM, 2008, 7 (04) : 333 - 338