Leucrose, a Sucrose Isomer, Suppresses Hepatic Fat Accumulation by Regulating Hepatic Lipogenesis and Fat Oxidation in High-fat Diet-induced Obese Mice

被引:11
作者
Lee, Jihye [1 ]
Kim, Eunju [1 ]
Kim, Yuri [1 ]
Yoo, Sang-Ho [2 ,3 ]
机构
[1] Ewha Womans Univ, Dept Nutr Sci & Food Management, 52 Ewhayeodae Gil, Seoul 03760, South Korea
[2] Sejong Univ, Dept Food Sci & Biotechnol, 209 Neungdong Ro, Seoul 05006, South Korea
[3] Sejong Univ, Carbohydrate Bioprod Res Ctr, 209 Neungdong Ro, Seoul 05006, South Korea
基金
新加坡国家研究基金会;
关键词
Leucrose; High fat diet; Lipogenesis; Liver;
D O I
10.15430/JCP.2018.23.2.99
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Obesity is currently one of the most serious public health problems and it can lead to numerous metabolic diseases. Leucrose, D-glucopyranosyl-alpha-(1-5)-D-fructopyranose, is an isoform of sucrose and it is naturally found in pollen and honey. The aim of this study was to investigate the effect of leucrose on metabolic changes induced by a high-fat diet (HFD) that lead to obesity. C57BL/6 mice were fed a 60% HFD or a HFD with 25% (L25) or 50% (L50) of its total sucrose content replaced with leucrose for 12 weeks. Leucrose supplementation improved fasting blood glucose levels and hepatic triglyceride content. In addition, leucrose supplementation reduced mRNA levels of lipogenesis-related genes, including peroxisome proliferator-activated receptor gamma, sterol regulatory element binding protein 1C, and fatty acid synthase in HFD mice. Conversely, mRNA levels of beta oxidation-related genes, such as carnitine palmitoyltransferase 1A and acyl CoA oxidase, returned to control levels with leucrose supplementation. Taken together, these results demonstrated the therapeutic potential of leucrose to prevent metabolic abnormalities by mediating regulation of plasma glucose level and hepatic triglyceride accumulation.
引用
收藏
页码:99 / 106
页数:8
相关论文
共 30 条
  • [1] FORMATION OF LEUCROSE IN DEXTRAN-PRODUCING CULTURES OF STREPTOCOCCUS-BOVIS
    BAILEY, RW
    BOURNE, EJ
    [J]. NATURE, 1959, 184 (4690) : 904 - 905
  • [2] WY14,643, a peroxisome proliferator-activated receptor α (PPARα) agonist, improves hepatic and muscle steatosis and reverses insulin resistance in lipoatrophic A-ZIP/F-1 mice
    Chou, CJ
    Haluzik, M
    Gregory, C
    Dietz, KR
    Vinson, C
    Gavrilova, O
    Reitman, ML
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (27) : 24484 - 24489
  • [3] Chung JY, 2017, J CANCER PREV, V22, P195, DOI 10.15430/JCP.2017.22.3.195
  • [4] Elias PS, 1996, J AM COLL TOXICOL, V15, P205, DOI 10.3109/10915819609008714
  • [5] PPARs and the complex journey to obesity
    Evans, RM
    Barish, GD
    Wang, YX
    [J]. NATURE MEDICINE, 2004, 10 (04) : 355 - 361
  • [6] Obesity and Nonalcoholic Fatty Liver Disease: Biochemical, Metabolic, and Clinical Implications
    Fabbrini, Elisa
    Sullivan, Shelby
    Klein, Samuel
    [J]. HEPATOLOGY, 2010, 51 (02) : 679 - 689
  • [7] Etiopathogenesis of Nonalcoholic Steatohepatitis: Role of Obesity, Insulin Resistance and Mechanisms of Hepatotoxicity
    Guturu, Praveen
    Duchini, Andrea
    [J]. INTERNATIONAL JOURNAL OF HEPATOLOGY, 2012, 2012
  • [8] Increased expression of PPARγ in high fat diet-induced liver steatosis in mice
    Inoue, M
    Ohtake, T
    Motomura, W
    Takahashi, N
    Hosoki, Y
    Miyoshi, S
    Suzuki, Y
    Saito, H
    Kohgo, Y
    Okumura, T
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2005, 336 (01) : 215 - 222
  • [9] 13-week oral toxicity study with isomaltulose (Palatinose®) in rats
    Jonker, D
    Lina, BAR
    Kozianowski, G
    [J]. FOOD AND CHEMICAL TOXICOLOGY, 2002, 40 (10) : 1383 - 1389
  • [10] Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease
    Kawano, Yuki
    Cohen, David E.
    [J]. JOURNAL OF GASTROENTEROLOGY, 2013, 48 (04) : 434 - 441