Rice bran prevents high-fat diet-induced inflammation and macrophage content in adipose tissue.
BACKGROUND
The inflammatory process associated with obesity mainly arises from white adipose tissue (WAT) alterations. In the last few years, nutritional-based strategies have been positioned as promising alternatives to pharmacological approaches against these pathologies. Our aim was to determine the potential of a rice bran enzymatic extract (RBEE)-supplemented diet in the prevention of metabolic, biochemical and functional adipose tissue and macrophage changes associated with a diet-induced obesity (DIO) in mice.


METHODS
C57BL/6J mice were fed high-fat diet (HF), 1 and 5 % RBEE-supplemented high-fat diet (HF1 % and HF5 %, respectively) and standard diet as control. Serum cardiometabolic parameters, adipocytes size and mRNA expression of pro-inflammatory biomarkers and macrophage polarization-related genes from WAT and liver were evaluated.


RESULTS
RBEE administration significantly decreased insulin resistance in obese mice. Serum triglycerides, total cholesterol, glucose, insulin, adiponectin and nitrites from treated mice were partially restored, mainly by 1 % RBEE-enriched diet. The incremented adipocytes size observed in HF group was reduced by RBEE treatment, being 1 % more effective than 5 % RBEE. Pro-inflammatory biomarkers in WAT such as IL-6 and IL-1β were significantly decreased in RBEE-treated mice. Adiponectin, PPARγ, TNF-α, Emr1 or M1/M2 levels were significantly restored in WAT from HF1 % compared to HF mice.


CONCLUSIONS
RBEE-supplemented diet attenuated insulin resistance, dyslipidemia and morphological and functional alterations of adipose tissue in DIO mice. These benefits were accompanied by a modulating effect in adipocytes secretion and some biomarkers associated with macrophage polarization. Therefore, RBEE may be considered an alternative nutritional complement over metabolic syndrome and its complications.
Department of Pharmacology, School of Pharmacy, University of Seville, C/Profesor Garcia-Gonzalez 2, 41012, Seville, Spain.
Maria Luisa
ML
Justo
Department of Pharmacology, School of Pharmacy, University of Seville, C/Profesor Garcia-Gonzalez 2, 41012, Seville, Spain.
Carmen
C
Claro
Christian Doppler Laboratory for Cardio-Metabolic Immunotherapy and Clinical Division for Endocrinology and Metabolism, Department of Medicine III, Medical University Vienna, 1090, Vienna, Austria.
Maximilian
M
Zeyda
Christian Doppler Laboratory for Cardio-Metabolic Immunotherapy and Clinical Division for Endocrinology and Metabolism, Department of Medicine III, Medical University Vienna, 1090, Vienna, Austria.
Thomas M
TM
Stulnig
Department of Pharmacology, School of Pharmacy, University of Seville, C/Profesor Garcia-Gonzalez 2, 41012, Seville, Spain.
María Dolores
MD
Herrera
Department of Pharmacology, School of Pharmacy, University of Seville, C/Profesor Garcia-Gonzalez 2, 41012, Seville, Spain. rodriguezr@us.es.|Department of Health Sciences, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya (UiC), Sant Cugat del Vallés, Spain. rodriguezr@us.es.|Basic Sciences Department, Faculty of Medicine and Health Sciences, Universitat Internacional de Catalunya (UiC), Josep Trueta s/n, 08195, Sant Cugat del Vallés, Barcelona, Spain. rodriguezr@us.es.
Rosalía
R
Rodríguez-Rodríguez
D017667:Adipocytes; D052242:Adiponectin / Q000378:metabolism; D052436:Adipose Tissue, White / Q000378:metabolism*; D000818:Animals; D015415:Biomarkers / Q000097:blood; D002135:Calcium-Binding Proteins; D002784:Cholesterol / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects*; D004043:Dietary Fiber / Q000008:administration & dosage*; D050171:Dyslipidemias / Q000178:diet therapy / Q000209:etiology; D007249:Inflammation / Q000178:diet therapy* / Q000209:etiology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000178:diet therapy / Q000209:etiology; D012275:Oryza / Q000737:chemistry*; D047495:PPAR gamma / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
C000634132:Adgre1 protein, mouse; D052242:Adiponectin; D015415:Biomarkers; D002135:Calcium-Binding Proteins; D004043:Dietary Fiber; D007328:Insulin; D053583:Interleukin-1beta; D015850:Interleukin-6; D047495:PPAR gamma; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D002784:Cholesterol
Adipose tissue; DIO mice; Inflammation; Macrophage polarization; Obesity; Rice bran; γ-Oryzanol