AIMS: To investigate the relations between the formation of pigment gallstone and the function of the intestinal mucosal barrier, as well as the underlying mechanism. METHODS: Eighty guinea pigs were randomly divided into three groups in which they were respectively given normal diet, gallstone-causing diet, and gallstone-formation diet with a supplementary intestinal mucosal protection compound known as glutamine. The model of pigment gallstone was established after 8 weeks of dietary administration. Indices about the function of the intestinal mucosal barrier and bacterial translocation were measured. Clinical cases were divided into three groups: control, cholesterol gallstone, and pigment gallstone, where the levels of plasma diamine oxidase (DAO), plasma endotoxin and the excretion rates of technetium 99m-diethylene triamine pentaacetic acid (99mTC-DTPA) in the urine of each group were measured. RESULTS: In the pigment gallstone group, the level of plasma DAO and endotoxin, the excretory ratio of lactulose and mannitol in urine, the bacterial translocation ratio in the celiac lymph nodes and the activities of beta-glucuronidase increased comparing to the control group. The gallstone-formation rate for the intestinal mucosal protection group (GLN) decreased, and other indices, except the activity of beta-glucuronidase, were all lower than that of gallstone-formation group. In the clinical experiment, the levels of plasma DAO and endotoxin, as well as the excretory rate of 99mTC-DTPA in urine were higher in the patients with gallstones than that in the control group. CONCLUSIONS: The formation of pigment gallstone was related to the abnormal function of the intestinal mucosal barrier. The abnormality in the function of the intestinal mucosal barrier probably induced the formation of gallstone by a bacterial translocation mechanism.
AIMS: To investigate the relations between the formation of pigment gallstone and the function of the intestinal mucosal barrier, as well as the underlying mechanism. METHODS: Eighty guinea pigs were randomly divided into three groups in which they were respectively given normal diet, gallstone-causing diet, and gallstone-formation diet with a supplementary intestinal mucosal protection compound known as glutamine. The model of pigment gallstone was established after 8 weeks of dietary administration. Indices about the function of the intestinal mucosal barrier and bacterial translocation were measured. Clinical cases were divided into three groups: control, cholesterol gallstone, and pigment gallstone, where the levels of plasma diamine oxidase (DAO), plasma endotoxin and the excretion rates of technetium 99m-diethylene triamine pentaacetic acid (99mTC-DTPA) in the urine of each group were measured. RESULTS: In the pigment gallstone group, the level of plasma DAO and endotoxin, the excretory ratio of lactulose and mannitol in urine, the bacterial translocation ratio in the celiac lymph nodes and the activities of beta-glucuronidase increased comparing to the control group. The gallstone-formation rate for the intestinal mucosal protection group (GLN) decreased, and other indices, except the activity of beta-glucuronidase, were all lower than that of gallstone-formation group. In the clinical experiment, the levels of plasma DAO and endotoxin, as well as the excretory rate of 99mTC-DTPA in urine were higher in the patients with gallstones than that in the control group. CONCLUSIONS: The formation of pigment gallstone was related to the abnormal function of the intestinal mucosal barrier. The abnormality in the function of the intestinal mucosal barrier probably induced the formation of gallstone by a bacterial translocation mechanism.
Authors: Stephanie E Woods; Monika R Leonard; Joshua A Hayden; Megan Brunjes Brophy; Kara R Bernert; Brigitte Lavoie; Sureshkumar Muthupalani; Mark T Whary; Gary M Mawe; Elizabeth M Nolan; Martin C Carey; James G Fox Journal: Am J Physiol Gastrointest Liver Physiol Date: 2014-12-04 Impact factor: 4.052
Authors: Marius Trøseid; Torunn K Nestvold; Knut Rudi; Hanne Thoresen; Erik W Nielsen; Knut T Lappegård Journal: Diabetes Care Date: 2013-07-08 Impact factor: 19.112