The effects of dietary fibre on C-reactive protein, an inflammation marker predicting cardiovascular disease.

BACKGROUND: C-reactive protein (CRP), a sensitive marker of inflammation, is an independent predictor of future cardiovascular disease (CVD), which is a major cause of death worldwide. In epidemiological trials, high-fibre intakes have consistently been associated with reduction in CVD risk and CRP levels. OBJECTIVE: The objective of this study was to assess the influence of dietary fibre (DF) on CRP in clinical trials. DATA SOURCES: Databases were searched from the earliest record to April 2008 and supplemented by crosschecking reference lists of relevant publications. STUDY SELECTION: Human adult intervention trials, at least 2 weeks in duration, with an increased and measurable consumption of DF were included and rated for quality. DATA SYNTHESIS: Seven clinical trials were included, and six of these reported significantly lower CRP concentrations of 25-54% with increased DF consumption with dosages ranging between 3.3-7.8 g/MJ. The seventh trial with psyllium fibre supplementation failed to lower CRP levels significantly in overweight/obese individuals. Weight loss and altered fatty acid intakes were present in most of the studies. CONCLUSIONS: In the presence of weight loss and modified saturated, monounsaturated and polyunsaturated fat intakes, significantly lower CRP concentrations (downward arrow 25-54%) are seen with increased fibre consumption (> or =3.3 g/MJ). Mechanisms are inconclusive but may involve the effect of DF on weight loss, and/or changes in the secretion, turnover or metabolism of insulin, glucose, adiponectin, interleukin-6, free fatty acids and triglycerides. Clinical studies of high- and low-fibre diets are needed to explore the potential favourable effects as observed epidemiologically, and to understand individual susceptibility to its anti-inflammatory effect and long-term cardiovascular reduction.

Comparative studies on nafenopin-induced hepatic peroxisome proliferation in the rat, Syrian hamster, guinea pig, and marmoset.

Nafenopin was administered orally for 21 days to male Sprague-Dawley rats (0.5-50 mg/kg/day), Syrian hamsters (5-250 mg/kg/day), Dunkin-Hartley guinea pigs (50 and 250 mg/kg/day), and marmosets (Callithrix jacchus, 50 and 250 mg/kg/day). With the rat, and to a lesser extent in the hamster, nafenopin treatment produced dose-related increases in liver size and induction of peroxisomal (palmitoyl-CoA oxidation) and microsomal (lauric acid 12-hydroxylase) fatty acid oxidizing enzyme activities. In contrast, in the guinea pig and marmoset, there was no effect on liver size and only comparatively small changes were observed in these enzyme activities. Ultrastructural examination of liver sections from nafenopin-treated rats and hamsters revealed increased numbers of peroxisomes many of which lacked the characteristic crystalline nucleoid. While nafenopin had little effect on peroxisome numbers in either the guinea pig or marmoset, increases in microsomal cytochrome P450 content and mixed function oxidase activities were observed in these species. These results demonstrate marked species differences in nafenopin-induced hepatic peroxisome proliferation with the Syrian hamster being less responsive than the rat and the guinea pig and marmoset being only weakly responsive. As nafenopin is a known hepatocarcinogen in the rat, comparative long-term studies in poorly responsive species, such as the guinea pig and marmoset, may help clarify the role of organelle proliferation in the hepatocarcinogenicity of certain peroxisome proliferators.