Long-term dietary intake influences the structure and activity of the trillions of microorganisms residing in the human gut, but it remains unclear how rapidly and reproducibly the human gut microbiome responds to short-term macronutrient change. Here we show that the short-term consumption of diets composed entirely of animal or plant products alters microbial community structure and overwhelms inter-individual differences in microbial gene expression. The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale and Ruminococcus bromii). Microbial activity mirrored differences between herbivorous and carnivorous mammals, reflecting trade-offs between carbohydrate and protein fermentation. Foodborne microbes from both diets transiently colonized the gut, including bacteria, fungi and even viruses. Finally, increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids and the outgrowth of microorganisms capable of triggering inflammatory bowel disease. In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles.

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Diet rapidly and reproducibly alters the human gut microbiome

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(00)04046-0.pdf

Inflammation and cancer: back to Virchow?

The importance of the ratio of omega-6/omega-3 essential fatty acids.

http://envismadrasuniv.org/Physiology/pdf/Gut%20flora%20in%20health%20and%20disease.pdf

Gut flora in health and disease

Organismal life encounters reactive oxidants from internal metabolism and environmental toxicant exposure. Reactive oxygen and nitrogen species cause oxidative stress and are traditionally viewed as being harmful. On the other hand, controlled production of oxidants in normal cells serves useful purposes to regulate signaling pathways. Reactive oxidants are counterbalanced by complex antioxidant defense systems regulated by a web of pathways to ensure that the response to oxidants is adequate for the body's needs. A recurrent theme in oxidant signaling and antioxidant defense is reactive cysteine thiol–based redox signaling. The nuclear factor erythroid 2–related factor 2 (Nrf2) is an emerging regulator of cellular resistance to oxidants. Nrf2 controls the basal and induced expression of an array of antioxidant response element–dependent genes to regulate the physiological and pathophysiological outcomes of oxidant exposure. This review discusses the impact of Nrf2 on oxidative stress and toxicity and how...

/pdf/role-of-nrf2-in-oxidative-stress-and-toxicity-2utmvoa3ko.pdf

Role of nrf2 in oxidative stress and toxicity.

1-Nitro[U-4,5,9,10-14C]pyrene in trioctanoin was administered by gavage to male germfree F344 rats. Extracts of the 120 h feces and urine were analyzed by h.p.l.c., with or without acetylation. 4,5-Dihydro-4,5-dihydroxy-1-nitropyrene, 1-nitro-3-hydroxypyrene, 1-nitro-6-hydroxypyrene and 1-nitro-8-hydroxypyrene but not 1-aminopyrene, 1-amino-6-hydroxypyrene or 1-amino-8-hydroxypyrene were identified by co-chromatography with standards. These results are in contrast to those obtained in the conventional F344 rat in which 1-aminopyrene, 1-amino-6-hydroxypyrene, and 1-amino-8-hydroxypyrene were fecal and urinary metabolites, indicating that intestinal microflora are involved in their formation.

Identification of ring oxidized metabolites of 1-nitropyrene in the feces and urine of germfree F344 rats.

The effect of dietary p-methoxybenzeneselenol, a new organoselenium compound, on azoxymethane (AOM)-induced hepatocarcinogenesis was examined in female F344 rats. Semipurified diets containing 0 and 5 ppm p-methoxybenzeneselenol were fed to the rats, starting at 5 weeks of age until one week after the carcinogen treatment. At 7 weeks of age, all animals except the vehicle-treated controls were given weekly sc injections of AOM (15 mg/kg body weight, 3 times). At 34 weeks after the last AOM treatment, the liver neoplasm incidence and liver tumor multiplicity as well as the incidence of altered liver cell foci were significantly lower in AOM-treated rats fed the diet containing 50 ppm p-methoxybenzeneselenol (tumor incidence 19%, tumor multiplicity 0.45/rat, foci incidence 3.47/cm2) than in AOM-treated animals fed the diet without p-methoxybenzeneselenol (tumor incidence 66%, tumor multiplicity 2.24/rat, foci incidence 12.08/cm2). These results indicate that dietary p-methoxybenzeneselenol at a dose of 50 ppm inhibits AOM-induced hepatic tumorigenesis.

Inhibition by dietary organoselenium, p-methoxybenzene-selenol, of hepatocarcinogenesis induced by azoxymethane in rats.

The nutrient intake, fecal neutral sterol concentration, and bile acid concentration of populations with a varied risk for colon cancer development were investigated. High‐risk populations in the metropolitan New York area and Malmo, Sweden, were compared with an intermediate‐risk population in Umea, Sweden. The mean daily intake of protein and fat was comparable in all groups, but the total daily fiber intake was higher in Umea, as was the total daily stool output. There was no difference in the total fiber intake and stool output between Malmo and metropolitan New York. The fecal secondary bile acid concentration was lower in Umea than in the other two areas; no difference was observed between Malmo and metropolitan New York. These results suggest that high fiber intake may be considered protective against colon cancer even in a population with a high fat intake. A high dietary fiber intake may limit colon cancer risk by increasing stool bulk, and thus diluting and/or binding tumor promoters.

Metabolie epidemiology of colon cancer: Dietary pattern and fecal sterol concentrations of three populations

Studies in laboratory animals have demonstrated that dietary supplements of organoselenium, 1,4-phenylenebis(methylene)selenocyanate (p-XSC) inhibit colon carcinogenesis. Diverse chemopreventive agents and clinically used anticancer drugs have been shown to induce apoptosis in colonic tumors. Inducing apoptosis is a key mechanism for the effectiveness of some chemopreventive agents; however, failure of apoptosis is now believed to contribute to the development of human cancer. In this study, we determined the number of apoptotic bodies in the colon tumors of rats fed a low-fat (LF) or a high-fat (HF) diet with or without p-XSC treatment. At 5 weeks of age, male F344 rats were divided into four groups, which were then maintained on one of the following diets: LF, 5% corn oil; HF, 23.5% corn oil; and LF and HF supplemented with 20 ppm p-XSC. In addition, the LF or HF diet with p-XSC supplements was administered either during the initiation stage or postinitiation. At 7 weeks of age, all rats except those intended for vehicle (normal saline) treatment were given 15 mg/kg of body weight of azoxymethane once weekly for 2 weeks. The animals were sacrificed 38 weeks after carcinogen treatment, and their colonic tumors were examined for appearance of apoptosis. The LF diet significantly increased the percentage of apoptosis as compared to the HF diet; the percentage of apoptosis in LF and HF diets were 12.4 and 2.9. The colon tumors that were present in the groups fed p-XSC together with a LF or a HF diet after carcinogen administration (postinitiation period) had a higher number of apoptotic bodies than those that were present in the animals fed p-XSC before carcinogen treatment (initiation period). The extent of apoptosis was weak when p-XSC was given with a HF diet (4.4%) during the initiation phase, but it was high significant when p-XSC was administered with LF diet (25.2%). Taken together, our data suggest that administration of LF diet supplemented with p-XSC increases apoptosis as compared to a HF diet alone.

/pdf/the-role-of-apoptosis-in-the-modulation-of-colon-57oix8m82i.pdf

The role of apoptosis in the modulation of colon carcinogenesis by dietary fat and by the organoselenium compound 1,4-phenylenebis(methylene)selenocyanate.

The effect of dietary sodium ascorbate (SA) on colon carcinogenesis evoked by 1,2-dimethylhydrazine (DMH) or N-methyl-N-nitrosourea (MNU) was studied in female F344 rats. Animals were fed diets containing 0, 0.25 and 1% of SA and given s.c. a single dose of 150 mg DMH/kg body wt., 10 weekly s.c. injections of 20 mg DMH/kg body wt. or intra-rectal administration of 2 mg MNU, twice a week for 2 weeks. The incidence of colon and kidney tumors was lower in rats fed the 0.25 or 1% SA and treated with a single dose of DMH than in the animals fed the diet without SA; however, the tumour incidences did not differ between the SA- and control diet-fed animals and treated with multiple doses of DMH or MNU.

Bandaru S. Reddy

Papers

Identification of ring oxidized metabolites of 1-nitropyrene in the feces and urine of germfree F344 rats.

Inhibition by dietary organoselenium, p-methoxybenzene-selenol, of hepatocarcinogenesis induced by azoxymethane in rats.

Metabolie epidemiology of colon cancer: Dietary pattern and fecal sterol concentrations of three populations

The role of apoptosis in the modulation of colon carcinogenesis by dietary fat and by the organoselenium compound 1,4-phenylenebis(methylene)selenocyanate.

Effect of dietary sodium ascorbate on 1,2-dimethylhydrazine- or methylnitrosourea-induced colon carcinogenesis in rats.