title: Spirulina improves non-alcoholic steatohepatitis, visceral fat macrophage aggregation, and serum leptin in a mouse model of metabolic syndrome.
abstract: BACKGROUND
  Nutritional approaches are sought to overcome the limits of pioglitazone in metabolic syndrome and non-alcoholic fatty liver disease. Spirulina, a filamentous unicellular alga, reduces serum lipids and blood pressure while exerting antioxidant effects.
  
  
  OBJECTIVE
  To determine whether Spirulina may impact macrophages infiltrating the visceral fat in obesity characterizing our metabolic syndrome mouse model induced by the subcutaneous injection treatment of monosodium glutamate.
  
  
  METHODS
  Mice were randomized to receive standard food added with 5% Spirulina, 0.02% pioglitazone, or neither. We tested multiple biochemistry and histology (both liver and visceral fat) readouts at 24 weeks of age.
  
  
  RESULTS
  Data demonstrate that both the Spirulina and the pioglitazone groups had significantly lower serum cholesterol and triglyceride levels and liver non-esterified fatty acid compared to untreated mice. Spirulina and pioglitazone were associated with significantly lower leptin and higher levels, respectively, compared to the control group. At liver histology, non-alcoholic fatty liver disease activity score and lipid peroxide were significantly lower in mice treated with Spirulina.
  
  
  CONCLUSIONS
  Spirulina reduces dyslipidaemia in our metabolic syndrome model while ameliorating visceral adipose tissue macrophages. Human studies are needed to determine whether this safe supplement could prove beneficial in patients with metabolic syndrome.
authors.affiliation: Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan. fsakura@med.u-toyama.ac.jp
authors.forename: Makoto
authors.initials: M
authors.lastname: Fujimoto
authors.forename: Koichi
authors.initials: K
authors.lastname: Tsuneyama
authors.forename: Takako
authors.initials: T
authors.lastname: Fujimoto
authors.forename: Carlo
authors.initials: C
authors.lastname: Selmi
authors.forename: M Eric
authors.initials: ME
authors.lastname: Gershwin
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Shimada
mesh_terms: D000818:Animals; D002449:Cell Aggregation; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005234:Fatty Liver / Q000473:pathology / Q000628:therapy*; D005526:Food, Formulated; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000097:blood; D015850:Interleukin-6 / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism* / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D051379:Mice; D000077205:Pioglitazone; D011897:Random Allocation; D012970:Sodium Glutamate; D053545:Spirulina; D045162:Thiazolidinediones / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D005230:Fatty Acids, Nonesterified; D007004:Hypoglycemic Agents; D007328:Insulin; D015850:Interleukin-6; D020738:Leptin; D008054:Lipid Peroxides; D045162:Thiazolidinediones; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol; D012970:Sodium Glutamate; D000077205:Pioglitazone