title: Gut carbohydrate metabolism instead of fat metabolism regulated by gut microbes mediates high-fat diet-induced obesity.
abstract: The aim of this study was to investigate the mechanisms underlying the involvement of gut microbes in body weight gain of high-fat diet-fed obesity-prone (obese) and obesity-resistant (lean) mice. C57BL/6 mice were grouped into an obese group, a lean group and a normal control group. Both obese and lean mice were fed a high-fat diet while normal control mice were fed a normal diet; they were observed for six weeks. The results showed that lean mice had lower serum lipid levels, body fat and weight gain than obese mice. The ATPase, succinate dehydrogenase and malate dehydrogenase activities in liver as well as oxygen expenditure and rectal temperature of lean mice were significantly lower than in obese mice. As compared with obese mice, the absorption of intestinal carbohydrates but not of fats or proteins was significantly attenuated in lean mice. Furthermore, 16S rRNA abundances of faecal Firmicutes and Bacteroidetes were significantly reduced in lean mice. In addition, faecal β-D-galactosidase activity and short chain fatty acid levels were significantly decreased in lean mice. Expressions of peroxisome proliferator-activated receptor gamma 2 and CCAAT/enhancer binding protein-β in visceral adipose tissues were significantly downregulated in lean mice as compared with obese mice. Resistance to dyslipidaemia and high-fat diet-induced obesity was mediated by ineffective absorption of intestinal carbohydrates but not of fats or proteins, probably through reducing gut Bacteroidetes and Firmicutes contents and lowering of gut carbohydrate metabolism. The regulation of intestinal carbohydrates instead of fat absorption by gut microbes might be a potential treatment strategy for high-fat diet-induced obesity.
authors.affiliation: School of Life Sciences, Tsinghua University, Beijing, 100084, China P.R. Shenzhen Key Lab of Health Science and Technology, Division of Life Science & Health, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, China P.R.
authors.forename: M
authors.initials: M
authors.lastname: Li
authors.affiliation: Institute of Disease Control and Prevention, Shenzhen International Travel Health Care Center, Shenzhen Entry-Exit Inspection and Quarantine Bureau, 518045 Shenzhen, China P.R.
authors.forename: D
authors.initials: D
authors.lastname: Gu
authors.affiliation: Shenzhen Key Lab of Health Science and Technology, Division of Life Science & Health, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, China P.R.
authors.forename: N
authors.initials: N
authors.lastname: Xu
authors.affiliation: School of Life Sciences, Tsinghua University, Beijing, 100084, China P.R.
authors.forename: F
authors.initials: F
authors.lastname: Lei
authors.affiliation: School of Life Sciences, Tsinghua University, Beijing, 100084, China P.R.
authors.forename: L
authors.initials: L
authors.lastname: Du
authors.affiliation: Shenzhen Key Lab of Health Science and Technology, Division of Life Science & Health, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, China P.R.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Shenzhen Key Lab of Health Science and Technology, Division of Life Science & Health, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, China P.R.
authors.forename: W
authors.initials: W
authors.lastname: Xie
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism / Q000502:physiology; D000818:Animals; D041963:Bacteroidetes / Q000235:genetics; D001835:Body Weight; D022782:CCAAT-Enhancer-Binding Protein-beta / Q000096:biosynthesis; D050260:Carbohydrate Metabolism / Q000502:physiology*; D059305:Diet, High-Fat; D050171:Dyslipidemias; D005232:Fatty Acids, Volatile / Q000032:analysis; D005243:Feces / Q000382:microbiology; D005951:Glucose Tolerance Test; D006003:Glycogen / Q000032:analysis; D007333:Insulin Resistance; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000382:microbiology*; D050356:Lipid Metabolism / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D009765:Obesity / Q000382:microbiology*; D010101:Oxygen Consumption; D047495:PPAR gamma / Q000096:biosynthesis; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D011897:Random Allocation; D013385:Succinate Dehydrogenase / Q000378:metabolism; D015430:Weight Gain; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D022782:CCAAT-Enhancer-Binding Protein-beta; D005232:Fatty Acids, Volatile; D008055:Lipids; D047495:PPAR gamma; D012336:RNA, Ribosomal, 16S; D006003:Glycogen; D008291:Malate Dehydrogenase; D013385:Succinate Dehydrogenase; D001616:beta-Galactosidase; D000251:Adenosine Triphosphatases
keywords: 16S rRNA; fat mass reduction; host-microbe balance/interaction