PloS one, 2017-06, Vol.12 (6), p.e0179204-e0179204
2017
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- Autor(en) / Beteiligte
- Titel
- α-Mangostin ameliorates hepatic steatosis and insulin resistance by inhibition C-C chemokine receptor 2
- Ist Teil von
- PloS one, 2017-06, Vol.12 (6), p.e0179204-e0179204
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2017
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Obesity induces various metabolic diseases such as dyslipidemia, nonalcoholic fatty liver disease (NAFLD), and type 2 diabetes. Fat expansion in adipose tissue induces adipose tissue dysfunction and inflammation, insulin resistance, and other metabolic syndromes. α-Mangostin (α-MG) has been previously studied for its anti-cancer, anti-inflammatory, and antioxidant activities. In this study, we investigated the effects of α-MG on adipose tissue inflammation and hepatic steatosis. We categorized study animals into four groups: regular diet control mice, RD mice treated with α-MG, high fat diet-induced obese mice, and HFD mice treated with α-MG. α-MG treatment significantly reduced not only the body, liver, and fat weights, but also plasma glucose, insulin, and triglyceride levels in HFD mice. Additionally, adiponectin levels of α-MG-treated mice were significantly higher than those of control HFD mice. Immunohistochemistry of liver and adipose tissue showed that CD11c expression was reduced in α-MG fed obese mice. α-MG treatment of HFD mice down-regulated the adipose-associated inflammatory cytokines and CCR2 in both liver and adipose tissue. Moreover, glucose tolerance and insulin sensitivity were significantly improved in α-MG fed obese mice. α-Mangostin ameliorates adipose inflammation and hepatic steatosis in HFD-induced obese mice.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0179204Titel-ID: cdi_plos_journals_1907782293
- Format
- –
- Schlagworte
- Adiponectin, Adipose tissue, Adipose Tissue - drug effects, Adipose Tissue - metabolism, Animals, Anticancer properties, Biology and Life Sciences, Body Weight - drug effects, Bone Marrow Cells - cytology, Bone Marrow Cells - immunology, Bone Marrow Cells - metabolism, Cancer, CC chemokine receptors, CCR2 protein, CD11c antigen, Cell Line, Chemokines, Cytokines, Cytokines - metabolism, Diabetes mellitus, Diet, High-Fat, Disease Models, Animal, Diseases, Disorders, Dyslipidemia, Expansion, Fatty Acids - biosynthesis, Fatty liver, Glucose, Glucose tolerance, Glucose Tolerance Test, High fat diet, Immunohistochemistry, Inflammation, Inflammation Mediators - metabolism, Inhibition, Insulin, Insulin Resistance, Liver, Liver - drug effects, Liver - metabolism, Liver diseases, Macrophages - drug effects, Macrophages - immunology, Macrophages - metabolism, Medical research, Medicine and Health Sciences, Metabolic disorders, Metabolic syndrome, Mice, Monocyte chemoattractant protein 1, Non-alcoholic Fatty Liver Disease - drug therapy, Non-alcoholic Fatty Liver Disease - etiology, Non-alcoholic Fatty Liver Disease - metabolism, Obesity, Obesity - drug therapy, Obesity - etiology, Obesity - metabolism, Protein Kinase Inhibitors - pharmacology, Receptors, CCR2 - antagonists & inhibitors, Receptors, CCR2 - metabolism, Sensitivity, Steatosis, Xanthones - pharmacology