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Muscle adaptation in obese rats exposed to chronic hypoxia (1167.3)
Author(s) -
Gamboa Jorge,
Macarlupu Jose,
Anza Cecilia,
Rojas Percy,
Villafuerte Francisco
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1167.3
Subject(s) - medicine , endocrinology , skeletal muscle , hypoxia (environmental) , insulin resistance , carbohydrate metabolism , insulin , metabolism , biology , western blot , chemistry , biochemistry , organic chemistry , oxygen , gene
Chronic hypoxia decreases fasting glucose and increases glucose utilization in lean and obese rats. Hypoxia increases insulin sensitivity in obese rats, but insulin resistance remains higher compared to lean rats exposed to hypoxia (figure). Skeletal muscle plays an important role in glucose metabolism; thus changes in insulin pathway and mitochondrial metabolism may impact skeletal muscle glucose uptake. We evaluated the adaptation of skeletal muscle to chronic hypoxia in lean and obese rats. We hypothesized that obese rats have less mitochondrial protein content and decreased activation of the ERK/MAPK pathway, one of the components of the insulin‐signaling cascade. For this purpose, Sprague‐Dawley rats were fed with normal chow diet or high‐fat diet (45% Kcal from fat) for 24 weeks in a normoxic environment. Rats were then exposed to hypobaric hypoxia (simulated altitude of 4500m) for 3 weeks. Triceps surae muscles were removed at the end of the hypoxia exposure and processed for western blot analysis. Mitochondrial protein content was evaluated using a monoclonal antibody against the subunit α of complex V. Contrary to our hypothesis, obese rats have a higher mitochondrial protein content than lean rats (35% higher, p=0.025). There was no difference in the activation of the ERK/MAPK pathway between the groups. Further studies are required to elucidate how chronic hypoxia affects glucose metabolism in obese rats. $graphic_082DEB25‐E5FC‐41C5‐820C‐9A23528E6536$ Grant Funding Source : Supported by FINCyT (No 046‐FINCyT‐PITEI‐2010) and NIH (K23DK100533)