AIM: To explore the change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis (NASH) in rats. METHODS: Thirty-two Sprague-Dawley (SD) rats were randomly divided into control group and model group. Rats in the control group were given normal diet, and rats in the model group were given fat-rich diet. Eight rats in each group were killed at end of the 8th and 12th wk, respectively. The levels of endotoxin, D-xylose, TG, TC, ALT and AST, intestinal tissue SOD and MDA as well as intestinal mucus secretory IgA (sIgA) were measured. The pathology of liver was observed by HE staining. RESULTS: At end of the 8th wk, there was no marked difference in the levels of endotoxin, D-xylose and sIgA between the two groups. At end of the 12th wk, rats in the model group developed steatohepatitis and had a higher serum level of endotoxin (P = 0.01) and D-xylose (P = 0.00) and a lower serum level of sIgA (P = 0.007). CONCLUSION: Intestinal mucosa barrier malfunction may exist in NASH rats and may be an important promoter of NASH in rats.
AIM: To explore the change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis (NASH) in rats. METHODS: Thirty-two Sprague-Dawley (SD) rats were randomly divided into control group and model group. Rats in the control group were given normal diet, and rats in the model group were given fat-rich diet. Eight rats in each group were killed at end of the 8th and 12th wk, respectively. The levels of endotoxin, D-xylose, TG, TC, ALT and AST, intestinal tissue SOD and MDA as well as intestinal mucus secretory IgA (sIgA) were measured. The pathology of liver was observed by HE staining. RESULTS: At end of the 8th wk, there was no marked difference in the levels of endotoxin, D-xylose and sIgA between the two groups. At end of the 12th wk, rats in the model group developed steatohepatitis and had a higher serum level of endotoxin (P = 0.01) and D-xylose (P = 0.00) and a lower serum level of sIgA (P = 0.007). CONCLUSION: Intestinal mucosa barrier malfunction may exist in NASH rats and may be an important promoter of NASH in rats.
Authors: K Tomita; G Tamiya; S Ando; K Ohsumi; T Chiyo; A Mizutani; N Kitamura; K Toda; T Kaneko; Y Horie; J-Y Han; S Kato; M Shimoda; Y Oike; M Tomizawa; S Makino; T Ohkura; H Saito; N Kumagai; H Nagata; H Ishii; T Hibi Journal: Gut Date: 2005-09-20 Impact factor: 23.059
Authors: Jaime Poniachik; Attila Csendes; Juan C Díaz; Jorge Rojas; Patricio Burdiles; Fernando Maluenda; Gladys Smok; Ramón Rodrigo; Luis A Videla Journal: Cytokine Date: 2006-03-27 Impact factor: 3.861
Authors: Richard Kirsch; Vivian Clarkson; Robert C Verdonk; Adrian D Marais; Enid G Shephard; Bernard Ryffel; Pauline de la M Hall Journal: J Gastroenterol Hepatol Date: 2006-01 Impact factor: 4.029
Authors: Danyelle M Liddle; Amber L Hutchinson; Hannah R Wellings; Krista A Power; Lindsay E Robinson; Jennifer M Monk Journal: Nutrients Date: 2017-11-27 Impact factor: 5.717
Authors: Richard Truse; Steven Grewe; Anna Herminghaus; Jan Schulz; Andreas P M Weber; Tabea Mettler-Altmann; Inge Bauer; Olaf Picker; Christian Vollmer Journal: Crit Care Date: 2019-11-12 Impact factor: 9.097