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 (k25-54%) are seen with increased fibre consumption (X3.3 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 antiinflammatory effect and long-term cardiovascular reduction.

The activities of 13 liver and 6 brain enzymes were studied in 7-12 week old CD2F1 male mice that had been fed ad libitum and standardized either to 12 hours of light (0600-1800) alternating with 12 hours of darkness (1800-0600) (LD12:12); or to a reversed light-dark cycle (darkness 0600-1800; light 1800-0600) (DL12:12). Three separate studies were performed on two different days; in each experiment, subgroups of 14 animals were sacrificed at 3-hour intervals. Livers were assayed for: isocitrate dehydrogenase, glutamate dehydrogenase, lactate dehydrogenase, alcohol dehydrogenase, glutathione reductase, glyoxylate reductase, L-alanine aminotransferase, glutamate oxalacetate transaminase, pyruvate decarboxylase, fructose-1-phosphate aldolase, fructose diphosphate aldolase, fructose 1,6-diphosphatase, and fatty acid synthetase. Brains were assayed for phosphoglucose isomerase, adenosine triphosphatase, creatine phosphokinase, pyruvate kinase, adenylate kinase, and malate dehydrogenase. All 19 enzymes demonstrated a prominent circadian rhythm in at least one experiment. Moreover, each rhythmic variable showed a statistically significant fit to a 24-hour cosine (sine) curve by the method of least squares. In general, peak activities of the liver enzymes analyzed were associated with the beginning of the dark cycle and initiation of the animal's activity, while the group of brain enzymes had peak activities which occurred at the beginning of the animals' rest span and were near the beginning of the light cycle. The phasing of each of the rhythms could be reversed within a two-week span after reversing the environmental light-dark cycle 180 degrees.