Caloric restriction inhibits up-regulation of inflammatory cytokines and TNF-α, and activates IL-10 and haptoglobin in the plasma of streptozotocin-induced diabetic rats

被引:47
作者
Ugochukwu, Ngozi H. [1 ]
Figgers, Cynthia L. [1 ]
机构
[1] Florida A&M Univ, Dept Chem, Tallahassee, FL 32307 USA
关键词
inflammation; diabetes; caloric restriction; interleukins; TNF-alpha; haptoglobin;
D O I
10.1016/j.jnutbio.2006.03.008
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
Diabetes mellitus is a significant risk factor for cardiovascular diseases, and low-grade systemic inflammation, mediated by oxidative stress, may play a central role. Caloric restriction (CR) has been reported to be effective in reducing oxidative stress during diabetes and moderating the expression of some markers of inflammation that are up-regulated during aging. Forty male Wistar rats were randomly divided into four groups: nondiabetic feeding ad libitum and under CR, and diabetic feeding ad libitum and under CR. The animals were subjected to 30% CR and ad libitum feeding for 9 weeks before the induction of diabetes by intraperitoneal injection with 35 mg/kg body weight streptozotocin. The inflammatory cytokines [interleukin (IL)-1 beta, IL-4 and IL-6] and tumor necrosis factor alpha up-regulated in diabetes were found to be significantly depressed by CR, whereas the antiinflammatory mediators, haptoglobin and IL-10 levels, were increased. These results indicated that CR could prevent diabetic complications through suppression of inflammatory responses. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:120 / 126
页数:7
相关论文
共 50 条
[1]   Tumor necrosis factor-α exerts interleukin-6-dependent and -independent effects on cultured skeletal muscle cells [J].
Alvarez, B ;
Quinn, LS ;
Busquets, S ;
Quiles, MT ;
López-Soriano, FJ ;
Argilés, JM .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2002, 1542 (1-3) :66-72
[2]  
Amrani Y, 2001, MOL PHARMACOL, V60, P646
[3]  
[Anonymous], DRUG DISCOV TODAY DI
[4]   Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake [J].
Anson, RM ;
Guo, ZH ;
de Cabo, R ;
Iyun, T ;
Rios, M ;
Hagepanos, A ;
Ingram, DK ;
Lane, MA ;
Mattson, MP .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (10) :6216-6220
[5]   Interleukin-10 in cutaneous disorders:: implications for its pathophysiological importance and therapeutic use [J].
Asadullah, K ;
Sabat, R ;
Wiese, A ;
Döcke, WD ;
Volk, HD ;
Sterry, W .
ARCHIVES OF DERMATOLOGICAL RESEARCH, 1999, 291 (12) :628-636
[6]   Mechanisms of endothelial dysfunction in obesity [J].
Avogaro, A ;
de Kreutzenberg, SV .
CLINICA CHIMICA ACTA, 2005, 360 (1-2) :9-26
[7]   Haptoglobin polymorphism in breast cancer patients form Jordan [J].
Awadallah, SM ;
Atoum, MF .
CLINICA CHIMICA ACTA, 2004, 341 (1-2) :17-21
[8]   Cytokines and the aging brain - what we don't know might help us [J].
Bodles, AM ;
Barger, SW .
TRENDS IN NEUROSCIENCES, 2004, 27 (10) :621-626
[9]   TNF-α is involved in activating DNA fragmentation in skeletal muscle [J].
Carbó, N ;
Busquets, S ;
van Royen, M ;
Alvarez, B ;
López-Soriano, FJ ;
Argilés, JM .
BRITISH JOURNAL OF CANCER, 2002, 86 (06) :1012-1016
[10]   Calorie restriction attenuates inflammatory responses to myocardial ischemia-reperfusion injury [J].
Chandrasekar, B ;
Nelson, JF ;
Colston, JT ;
Freeman, GL .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2001, 280 (05) :H2094-H2102