Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort.

BACKGROUND: Type 2 diabetes (DM), metabolic syndrome (MetS), and inflammation are linked to reduced magnesium and fiber intakes; these associations are attenuated by adjustment for each of these nutrients. OBJECTIVE: We investigated the association among magnesium and fiber intakes, metabolic variables, and high-sensitivity C-reactive protein (hs-CRP) values. DESIGN: Cross-sectional analyses were performed in a representative cohort of 1653 adults and in a subgroup with normal body mass index without dysmetabolisms (n = 205). A validated semiquantitative food-frequency questionnaire was used; magnesium intake was computed by multiplying its content in each food by the frequency of food consumption. RESULTS: The prevalence of DM, MetS, and hs-CRP >/= 3 mg/L significantly decreased from the lowest to the highest tertile of magnesium and fiber intakes. Subjects within the lowest tertiles of magnesium and fiber intakes were 3-4 times as likely to have DM, MetS, and hs-CRP >/= 3 mg/L, after multiple adjustments. After the analysis was additionally controlled for fiber intake, associations with hs-CRP >/= 3 mg/L proved to be significant (odds ratio: 2.05; 95% CI: 1.30, 3.25), whereas reduced magnesium intake and DM and MetS were no longer significant. The lowest tertile of fiber intake remained associated with DM, hs-CRP >/= 3 mg/L, and MetS after adjustments for multiple confounders and magnesium intake. In the lean, healthy subject subgroup, hs-CRP values were inversely associated with magnesium and fiber intakes in a multivariate model (P < 0.001). CONCLUSIONS: Reduced fiber intake was significantly associated with metabolic abnormalities; the magnesium effect might be confounded by fiber being in foods that also provided magnesium. Lower magnesium and fiber intakes were linked to hs-CRP >/= 3 mg/L in both the entire cohort and healthy persons.

4-Hydroxynonenal is markedly higher in patients on a standard long-term home parenteral nutrition.

Parenteral nutrition, a commonly used procedure in patients with gastrointestinal disorders, may lead with time to liver steatosis and fibrosis, whose pathogenesis has yet to be elucidated. Oxidative stress and particularly lipid peroxidation likely contribute to the expression of such hepatobiliary complications, by means of their recognized proinflammatory and profibrogenic effects. To evaluate the adequacy against oxidative insult of a standard micronutrient supplementation in patients under long term parenteral nutrition, a comprehensive patterns of redox indices has been determined on peripheral blood samples from forty one adults in comparison to fifty eight blood donors taken as controls. A sustained oxidative stress in peripheral blood of home parenteral patients was observed. Of the two lipid peroxidation markers found to be markedly increased, namely fluorescent plasma protein adducts with malondialdehyde and 4-hydroxynonenal, respectively, only the second was statistically correlated with all the antioxidant-related changes consistently detected in the patients, namely decreased plasma alpha-tocopherol and selenium intake and higher erythrocyte oxidized glutathione. Plasma level of 4-hydroxynonenal-protein adducts appears to be a reliable and easily measurable marker of oxidative status, particularly indicated to monitor the adequacy of dietary regimen during parenteral nutrition.

Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis.

The relations of dietary habits to insulin sensitivity and postprandial triglyceride metabolism were evaluated in 25 patients with nonalcoholic steatohepatitis (NASH) and 25 age-, body mass index (BMI)-, and gender-matched healthy controls. After a 7-day alimentary record, they underwent a standard oral glucose tolerance test (OGTT), and the insulin sensitivity index (ISI) was calculated from the OGTT; an oral fat load test was also performed in 15 patients and 15 controls. The dietary intake of NASH patients was richer in saturated fat (13.7% +/- 3.1% vs. 10.0% +/- 2.1% total kcal, respectively, P =.0001) and in cholesterol (506 +/- 108 vs. 405 +/- 111 mg/d, respectively, P =.002) and was poorer in polyunsaturated fat (10.0% +/- 3.5% vs. 14.5% +/- 4.0% total fat, respectively, P =.0001), fiber (12.9 +/- 4.1 vs. 23.2 +/- 7.8 g/d, respectively, P =.000), and antioxidant vitamins C (84.3 +/- 43.1 vs. 144.2 +/- 63.1 mg/d, respectively, P =.0001) and E (5.4 +/- 1.9 vs. 8.7 +/- 2.9 mg/d, respectively, P =.0001). The ISI was significantly lower in NASH patients than in controls. Postprandial total and very low density lipoproteins triglyceride at +4 hours and +6 hours, triglyceride area under the curve, and incremental triglyceride area under the curve were higher in NASH compared with controls. Saturated fat intake correlated with ISI, with the different features of the metabolic syndrome, and with the postprandial rise of triglyceride. Postprandial apolipoprotein (Apo) B48 and ApoB100 responses in NASH were flat and strikingly dissociated from the triglyceride response, suggesting a defect in ApoB secretion. In conclusion, dietary habits may promote steatohepatitis directly by modulating hepatic triglyceride accumulation and antioxidant activity as well as indirectly by affecting insulin sensitivity and postprandial triglyceride metabolism. Our findings provide further rationale for more specific alimentary interventions, particularly in nonobese, nondiabetic normolipidemic NASH patients.