title: Mangiferin protects against adverse skeletal muscle changes and enhances muscle oxidative capacity in obese rats.
abstract: Obesity-related skeletal muscle changes include muscle atrophy, slow-to-fast fiber-type transformation, and impaired mitochondrial oxidative capacity. These changes relate with increased risk of insulin resistance. Mangiferin, the major component of the plant Mangifera indica, is a well-known anti-inflammatory, anti-diabetic, and antihyperlipidemic agent. This study tested the hypothesis that mangiferin treatment counteracts obesity-induced fiber atrophy and slow-to-fast fiber transition, and favors an oxidative phenotype in skeletal muscle of obese rats. Obese Zucker rats were fed gelatin pellets with (15 mg/kg BW/day) or without (placebo group) mangiferin for 8 weeks. Lean Zucker rats received the same gelatin pellets without mangiferin and served as non-obese and non-diabetic controls. Lesser diameter, fiber composition, and histochemical succinic dehydrogenase activity (an oxidative marker) of myosin-based fiber-types were assessed in soleus and tibialis cranialis muscles. A multivariate discriminant analysis encompassing all fiber-type features indicated that obese rats treated with mangiferin displayed skeletal muscle phenotypes significantly different compared with both lean and obese control rats. Mangiferin significantly decreased inflammatory cytokines, preserved skeletal muscle mass, fiber cross-sectional size, and fiber-type composition, and enhanced muscle fiber oxidative capacity. These data demonstrate that mangiferin attenuated adverse skeletal muscle changes in obese rats.
authors.affiliation: Laboratory of Muscular Biopathology, Department of Comparative Anatomy and Pathological Anatomy, University of Cordoba, Cordoba, Spain.
authors.forename: Luz M
authors.initials: LM
authors.lastname: Acevedo
authors.affiliation: Department of Animal Medicine and Surgery, University of Cordoba, Cordoba, Spain.|Instituto Maimonides de Investigacion Biomedica de Cordoba (IMIBIC), Hospital Universitario Reina Sofia, University of Cordoba, Cordoba, Spain.
authors.forename: Ana I
authors.initials: AI
authors.lastname: Raya
authors.affiliation: Instituto Maimonides de Investigacion Biomedica de Cordoba (IMIBIC), Hospital Universitario Reina Sofia, University of Cordoba, Cordoba, Spain.
authors.forename: Julio M
authors.initials: JM
authors.lastname: Martínez-Moreno
authors.affiliation: Department of Animal Medicine and Surgery, University of Cordoba, Cordoba, Spain.|Instituto Maimonides de Investigacion Biomedica de Cordoba (IMIBIC), Hospital Universitario Reina Sofia, University of Cordoba, Cordoba, Spain.
authors.forename: Escolástico
authors.initials: E
authors.lastname: Aguilera-Tejero
authors.affiliation: Laboratory of Muscular Biopathology, Department of Comparative Anatomy and Pathological Anatomy, University of Cordoba, Cordoba, Spain.
authors.forename: José-Luis L
authors.identifier: http://orcid.org/0000-0001-7706-609X
authors.initials: JL
authors.lastname: Rivero
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D005346:Fibroblast Growth Factors / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D009765:Obesity / Q000378:metabolism*; D010084:Oxidation-Reduction; D051381:Rats; D011924:Rats, Zucker; D015430:Weight Gain / Q000187:drug effects; D044004:Xanthones / Q000494:pharmacology*
chemical_list: D001786:Blood Glucose; D044004:Xanthones; C414620:fibroblast growth factor 21; C013592:mangiferin; D005346:Fibroblast Growth Factors; D002784:Cholesterol