Figure 7. Niacin suppresses colonic inflammation and carcinogenesis in absence of gut microbiota and dietary fibers via Gpr109a.
(A) Experimental paradigm for antibiotic treatment (gentamicin sulfate, ciprofloxacin, streptomycin and bacitracin in drinking water) and niacin administration to mice in the (AOM+DSS)-induced colon cancer model.
(B) Weight loss in WT and Niacr1−/− mice treated with antibiotics in the presence or absence of antibiotics and subjected to AOM+DSS as in A.
(C) Tumor burden in WT and Niacr1−/− mice under various treatment conditions. Error bars represent standard deviation of mean (n≥4).
(D) Representative photographs of dissected colons of WT and Niacr1−/− mice subjected to various treatments as described in A.
(E) Niacr1−/− mice were treated as in Figure 4A. Some mice also received rIL-10 or rIL-18 intraperitoneally (50 ng/mouse/injection) starting day 2 and every alternate day till day 60. Shown are the weight loss and diarrhea during first cycle of DSS.
(F) Tumor burden on day 70 in Niacr1−/− mice treated as described in (E) (n=4).
(G) Two-month-old, ApcMin/+ and Niacr1−/−ApcMin/+ mice were fed with dietary fiber containing normal chow (FC) or fiber-free (FF) chow. Some mice in FF diet group also received niacin in drinking water ad libitum. Five weeks later, mice were sacrificed and colonic polyps were counted (n=2–5). * p<0.007
(H) A representative photographs of dissected colon from mice subjected to experimental protocol described in G.
Values represent mean ± SD or representative of at least 2 independent experiments.