title: Anti-inflammatory effects of sucrose-derived oligosaccharides produced by a constitutive mutant L. mesenteroides B-512FMCM dextransucrase in high fat diet-fed mice.
abstract: Oligosaccharide (OS) is used as a sugar replacement as well as an ingredient in functional foods because of its beneficial effects, mainly on reducing calorie content and promoting intestinal health. By contrast, the effects of OS on inflammation are less well investigated. The purpose of this study was to investigate the effects of sucrose-derived OS on glucose control and inflammation in high fat (HF) diet-fed mice. Male C57BL6 mice were randomly assigned to six treatment groups (n = 10-14 mice per group): 1) lean control (CON), 2) HF control, 3) HF-low sucrose (LS, 100 mg/kg/day), 4) HF-high sucrose (HS, 1000 mg/kg/day), 5) HF-low OS (LOS, 100 mg/kg/day), and 6) HF-high OS (HOS, 1000 mg/kg/day). PBS (vehicle), sucrose, and OS were administered by stomach gavage. Body weight, food intake, and markers of liver function (activities of aspartate aminotransferase and alanine aminotransferase) were not affected by the treatments. HOS treatment decreased levels of serum glucose, insulin, and homeostasis model assessment-insulin resistance compared with sucrose treatment. However, serum adiponectin levels of the HOS group were higher than those of the sucrose groups. Serum levels of the pro-inflammatory cytokines interleukin-6 (IL-6) and fetuin-A were lower in the HOS group than in the sucrose groups. Hepatic gene expression levels of pro-inflammatory cytokines and related factors (fetuin-A, NF-κB, TLR4, TNF-alpha, and IL-6) were decreased and the levels of insulin signaling-related molecules (sirtuin 1, insulin receptor, and Akt) were increased in HOS-treated mice as compared with sucrose-treated mice. These results demonstrate that OS treatment is effective in improving glucose control and inflammation in high fat diet-fed mice.
authors.affiliation: Division of Food and Nutrition, Chonnam National University, Gwangju, 61186, Republic of Korea.
authors.forename: Min-Gyung
authors.initials: MG
authors.lastname: Kang
authors.affiliation: Department of Food and Nutrition, Seoul Women's University, Seoul, 01797, Republic of Korea.
authors.forename: Hee Jae
authors.initials: HJ
authors.lastname: Lee
authors.affiliation: Graduate School of International Agricultural Technology and Institute of Food Industrialization, Institutes of Green Bio Science & Technology, Seoul National University, Gangwon-do, 25354, Republic of Korea.
authors.forename: Jae-Young
authors.initials: JY
authors.lastname: Cho
authors.affiliation: Division of Food and Nutrition, Chonnam National University, Gwangju, 61186, Republic of Korea.
authors.forename: Kanghwa
authors.initials: K
authors.lastname: Kim
authors.affiliation: Department of Food and Nutrition, Seoul Women's University, Seoul, 01797, Republic of Korea. Electronic address: sjyang89@swu.ac.kr.
authors.forename: Soo Jin
authors.initials: SJ
authors.lastname: Yang
authors.affiliation: Graduate School of International Agricultural Technology and Institute of Food Industrialization, Institutes of Green Bio Science & Technology, Seoul National University, Gangwon-do, 25354, Republic of Korea. Electronic address: kimdm@snu.ac.kr.
authors.forename: Doman
authors.initials: D
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D059305:Diet, High-Fat; D005964:Glucosyltransferases / Q000235:genetics / Q000378:metabolism*; D000070007:Leuconostoc mesenteroides / Q000201:enzymology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D009844:Oligosaccharides / Q000494:pharmacology*; D009929:Organ Size / Q000187:drug effects; D013395:Sucrose / Q000737:chemistry*
chemical_list: D000893:Anti-Inflammatory Agents; D001786:Blood Glucose; D009844:Oligosaccharides; D013395:Sucrose; D005964:Glucosyltransferases; C020025:dextransucrase
keywords: Inflammation; Insulin resistance; Sirtuin; Sucrose-derived oligosaccharide