No abstract

No abstract

No abstract

No abstract

No abstract

No abstract

Metabolic diseases, such as obesity and type 2 diabetes, are world-wide health problems. The prevalence of metabolic diseases is associated with dynamic changes in dietary macronutrient intake during the past decades. Based on national statistics and from a public health viewpoint, traditional approaches, such as diet and physical activity, have been unsuccessful in decreasing the prevalence of metabolic diseases. Since the approaches strongly rely on individual’s behavior and motivation, novel science-based strategies should be considered for prevention and therapy for the diseases. Metabolism and immune system are linked. Both overnutrition and infection result in inflammation through nutrient and pathogen sensing systems which recognize compounds with structural similarities. Dietary macronutrients (fats and sugars) can induce inflammation through activation of an innate immune receptor, Toll-like receptor 4 (TLR4). Long-term intake of diets high in fats and meats appear to induce chronic systemic low-grade inflammation, endotoxicity, and metabolic diseases. Recent investigations support the idea of the involvement of intestinal bacteria in host metabolism and preventative and therapeutic potentials of probiotic and prebiotic interventions for metabolic diseases. Specific intestinal bacteria seem to serve as lipopolysaccharide (LPS) sources through LPS and/or bacterial translocation into the circulation due to a vulnerable microbial barrier and increased intestinal permeability and to play a role in systemic inflammation and progression of metabolic diseases. This review focuses on mechanistic links between metabolic diseases (mainly obesity and type 2 diabetes), chronic systemic low-grade inflammation, intestinal environment, and nutrition and prospective views of probiotic and prebiotic interventions for the diseases.

Biochemical indicators of ascorbic acid (AA) status were studied in eleven young adult males fed the same AA deficient diet for 14 wk in a live-in metabolic unit. Supplements of AA were added to the diet to give AA-intake periods of 65 mg/d (2 wk), 5 mg/d (4 wk), 605 mg/d (3 wk), 5 mg/d (4 wk), 605 mg/d (4 d), and 65 mg/d (3 d). Blood plasma, erythrocyte, and leukocyte AA levels all reflected AA intake, however, plasma AA showed less variability than red cell AA levels and was considerably easier to determine than leukocyte AA. Plasma AA values less than 0.40 mg/dL (23 mumol/L) reflected marginal AA status. The daily AA intake calculated to maintain plasma AA levels of at least 0.4 mg/dL (23 mumol/L) in healthy young men was 41 mg. The average AA intake estimated to maximize the total body pool was 138 mg/d. Urine and salivary AA levels were not useful indicators of AA status because urinary AA levels did not discriminate well between adequate and deficient AA intakes and salivary AA levels did not consistently reflect AA intake.