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

J Nutr Biochem. 2007 Feb;18(2):120-6. doi: 10.1016/j.jnutbio.2006.03.008. Epub 2006 May 18.

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.

MeSH terms

  • Animals
  • Blood Glucose / analysis
  • Body Weight
  • Caloric Restriction*
  • Cytokines / blood*
  • Diabetes Mellitus, Experimental / blood*
  • Haptoglobins / analysis*
  • Inflammation / blood*
  • Interleukin-10 / blood
  • Interleukin-1beta / blood
  • Interleukin-4 / blood
  • Interleukin-6 / blood
  • Male
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Blood Glucose
  • Cytokines
  • Haptoglobins
  • Interleukin-1beta
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Interleukin-4