title: Pectin and high-amylose maize starch increase caecal hydrogen production and relieve hepatic ischaemia-reperfusion injury in rats.
abstract: We investigated whether the feeding of high H2-generating dietary fibre and resistant starch (RS) could suppress hepatic ischaemia-reperfusion (IR) injury, which results from oxidative stress, in rats fed a pectin (Pec) or high-amylose maize starch (HAS) diet. Male Sprague-Dawley rats were fed a control (C) diet, with or without Pec (0-5 % Pec) or HAS (0-30 % HAS) supplementation for 7 d. Portal H2 concentration showed a significant dose-dependent increase with the amount of Pec or HAS supplementation. Plasma alanine and aspartate aminotransferase activities remarkably increased in the C rats (5 % cellulose) due to IR treatment, while it decreased significantly or showed tendencies to decrease in 5 % Pec and 20 % HAS diet-fed rats. The hepatic oxidised glutathione (GSSG):total glutathione ratio increased significantly in IR rats maintained on the C diet compared with sham-operated rats. On the other hand, reduced glutathione (GSH):total glutathione and GSH:GSSG ratios decreased significantly. The GSSG:total glutathione ratio that increased due to IR treatment decreased significantly on HAS and Pec intake, while GSH:total glutathione and GSH:GSSG ratios increased significantly. Hepatic sinusoids of IR rats fed the C diet were occluded, but those of IR rats fed the Pec diet were similar to those in the sham-operated rats. In conclusion, we found that Pec or HAS, which enhance H2 generation in the large intestine, alleviated hepatic IR injury. The present study demonstrates another physiological significance of dietary fibre and RS.
authors.affiliation: Department of Nutritional Sciences, Faculty of Health and Welfare Science, Nayoro City University, Kita 8-1, Nishi 4, Nayoro, Hokkaido, Japan. nishimura@nayoro.ac.jp
authors.forename: Naomichi
authors.initials: N
authors.lastname: Nishimura
authors.forename: Hiroki
authors.initials: H
authors.lastname: Tanabe
authors.forename: Yumi
authors.initials: Y
authors.lastname: Sasaki
authors.forename: Yui
authors.initials: Y
authors.lastname: Makita
authors.forename: Misako
authors.initials: M
authors.lastname: Ohata
authors.forename: Saori
authors.initials: S
authors.lastname: Yokoyama
authors.forename: Mami
authors.initials: M
authors.lastname: Asano
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Shuhachi
authors.initials: S
authors.lastname: Kiriyama
mesh_terms: D000688:Amylose / Q000008:administration & dosage / Q000032:analysis / Q000627:therapeutic use; D000818:Animals; D002432:Cecum / Q000382:microbiology; D005285:Fermentation; D005978:Glutathione; D006504:Hepatic Veno-Occlusive Disease / Q000209:etiology / Q000503:physiopathology; D006859:Hydrogen / Q000097:blood* / Q000378:metabolism; D007511:Ischemia / Q000503:physiopathology*; D008099:Liver / Q000098:blood supply / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010368:Pectins / Q000008:administration & dosage / Q000627:therapeutic use*; D056692:Prebiotics / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000178:diet therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D012639:Seeds / Q000737:chemistry; D013213:Starch / Q000008:administration & dosage / Q000737:chemistry / Q000378:metabolism / Q000627:therapeutic use*; D003313:Zea mays / Q000737:chemistry
chemical_list: D056692:Prebiotics; D006859:Hydrogen; D010368:Pectins; D013213:Starch; D000688:Amylose; D005978:Glutathione