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  • Title: Inflammation markers are modulated by responses to diets differing in postprandial insulin responses in individuals with the metabolic syndrome.
    Author: Kallio P, Kolehmainen M, Laaksonen DE, Pulkkinen L, Atalay M, Mykkänen H, Uusitupa M, Poutanen K, Niskanen L.
    Journal: Am J Clin Nutr; 2008 May; 87(5):1497-503. PubMed ID: 18469276.
    Abstract:
    BACKGROUND: Inflammation may be a mechanism by which high postprandial insulin and glucose responses increase the risk of type 2 diabetes mellitus. OBJECTIVE: We hypothesized that dietary carbohydrates characterized by different postprandial insulin responses may differentially modify cytokine concentrations in plasma and gene expression in subcutaneous adipose tissue. DESIGN: Individuals (n = 47) with the metabolic syndrome were randomly assigned to a 12-wk diet with oat and wheat bread and potato (high postprandial insulin response) or rye bread and pasta (low postprandial insulin response). Postprandial glucose and insulin responses to the oat and wheat bread meal and to the rye bread meal were determined in 19 individuals before intervention. RESULTS: During the 12-wk diet, the change in the gene expression of interleukin (IL)-10 receptor alpha and tumor necrosis factor-alpha in subcutaneous adipose tissue differed between the groups (P = 0.002 and P = 0.083, respectively). Moreover, the change in fasting plasma concentrations of IL-1beta and IL-6 differed between the groups (P = 0.020 and P = 0.055, respectively). In the postprandial challenge, the insulin response to the rye bread meal was lower than that to the oat and wheat bread meal (P < 0.001), whereas there were no differences in the mean blood glucose response. In contrast, plasma glucose concentrations decreased more below fasting concentrations 2.5-3 h after the oat and wheat bread meal than after the rye bread meal. A late postprandial rebound of free fatty acids was detected after the oat and wheat bread meal (P = 0.048). CONCLUSIONS: Long-term intake of cereal foods with differing postprandial insulin responses may be a factor that modulates the inflammatory status in individuals with the metabolic syndrome.
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