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J Nutr Biochem. 2007 Feb;18(2):120-6. Epub 2006 May 18.

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

Author information

1
Department of Chemistry, Florida A&M University, Tallahassee, FL 32307, USA. ngozi.ugochukwu@famu.edu

Abstract

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)-1beta, 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.

PMID:
16713232
DOI:
10.1016/j.jnutbio.2006.03.008
[Indexed for MEDLINE]

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