title: Low-dose diet supplement of a natural flavonoid, luteolin, ameliorates diet-induced obesity and insulin resistance in mice.
abstract: METHODS
  Mast cells play important roles in diet-induced obesity and diabetes, and some synthetic mast cell stabilizers can improve related metabolic disturbances in mice. Luteolin (LU) is a potent natural mast cell stabilizer. However, a direct correlation between LU and these common metabolic diseases is not established.
  
  
  RESULTS
  Male C57BL/6 mice were fed low-fat diet, high-fat diet (HFD), HFD with 0.002 and 0.01% LU for 12 wk, respectively. Dietary LU suppressed HFD-induced body weight gain, fat deposition, and adipocyte hypertrophy. Meanwhile, glucose intolerance and insulin sensitivity was also improved. Interestingly, dietary LU ameliorated angiogenesis and associated cell apoptosis and cathepsin activity in epididymis adipose tissues, which is a critical mechanism that mast cells are involved in diet-induced obesity and diabetes. Further, we showed dietary LU reduced mast cell and macrophage infiltrations and inflammatory cytokine levels in epididymis adipose tissues. Finally, LU inhibited mast cell-derived IL-6 expression, which is a key cytokine that contributes to mast cell-associated metabolic derangements, and protein kinase C activator phorbol myristoyl acetate reversed the inhibitory effects.
  
  
  CONCLUSIONS
  As a natural flavonoid, low-dose diet supplement of LU ameliorates diet-induced obesity and insulin resistance in mice, suggesting a new therapeutic and interventional approach for these diseases.
authors.affiliation: School of Biotechnology & Food Engineering, Hefei University of Technology, Hefei, P. R. China; School of Life Science, University of Anhui Science & Technology, Fengyang, P. R. China.
authors.forename: Na
authors.initials: N
authors.lastname: Xu
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Jing
authors.initials: J
authors.lastname: Dong
authors.forename: Xian
authors.initials: X
authors.lastname: Zhang
authors.forename: Yan-Guang
authors.initials: YG
authors.lastname: Chen
authors.forename: Bin
authors.initials: B
authors.lastname: Bao
authors.forename: Jian
authors.initials: J
authors.lastname: Liu
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001854:Bone Marrow Cells / Q000187:drug effects / Q000378:metabolism; D002403:Cathepsins / Q000187:drug effects / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects*; D019587:Dietary Supplements; D015536:Down-Regulation; D007249:Inflammation / Q000188:drug therapy; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D047311:Luteolin / Q000494:pharmacology*; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000188:drug therapy* / Q000209:etiology; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D015430:Weight Gain
chemical_list: D015850:Interleukin-6; D047495:PPAR gamma; D014409:Tumor Necrosis Factor-alpha; D002403:Cathepsins; D047311:Luteolin
keywords: Angiogenesis; Insulin resistance; Luteolin; Mast cells; Obesity