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Abstract
The beneficial effects of exercise are partly mediated via local or systemic functions of the insulin-like growth factor-1 (IGF-1) system. As IGF-1 increases local brain hemoglobin beta (Hbb) transcripts, we hypothesized that exercise could have similar effects. Mice were single-housed with free access to running wheels for seven days. After sacrifice and saline perfusion, the expression of 13 genes was quantified using real-time quantitative polymerase chain reaction (RT-qPCR) in three brain regions: the prefrontal cortex, motor cortex, and hippocampus. In addition, plasma insulin, glucose, homeostatic model assessment of IR (HOMA-IR), C-peptide, and IGF-1 were investigated. We show that hemoglobin-related transcripts (Hbb and 5’-aminolevulinate synthase 2 [Alas2]) increased 46–63% in the running group, while IGF-1-related genes [Igf1 / growth hormone receptor (Ghr)] decreased slightly (7%). There were also moderate to large correlations between Hbb- and IGF-1-related genes in the running group but not in the sedentary group. HOMA-IR, plasma glucose, and insulin changed marginally and non-significantly, but there was a trend toward an increase in plasma-IGF-1 in the running group. In conclusion, seven days of running increased Hbb-related transcripts in three brain regions. Hbb-related transcripts correlated with components of the brain IGF-1 system only in the running group.
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1 University of Gothenburg, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, Gothenburg, Sweden (GRID:grid.8761.8) (ISNI:0000 0000 9919 9582); Sahlgrenska University Hospital, Laboratory of Experimental Endocrinology, Bruna Stråket 16, 413 45 , Region Västra Götaland, Department of Clinical Chemistry, Gothenburg, Sweden (GRID:grid.1649.a) (ISNI:0000 0000 9445 082X)
2 Stanford University, Department of Neurology and Neurological Sciences, Stanford, USA (GRID:grid.168010.e) (ISNI:0000 0004 1936 8956); The Sahlgrenska Academy at University of Gothenburg, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Gothenburg, Sweden (GRID:grid.8761.8) (ISNI:0000 0000 9919 9582)
3 The Sahlgrenska Academy at University of Gothenburg, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Gothenburg, Sweden (GRID:grid.8761.8) (ISNI:0000 0000 9919 9582)
4 University of Gothenburg, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, Gothenburg, Sweden (GRID:grid.8761.8) (ISNI:0000 0000 9919 9582); Sahlgrenska University Hospital, Region Västra Götaland, Department of Specialist Medicine, Gothenburg, Sweden (GRID:grid.1649.a) (ISNI:0000 0000 9445 082X)
5 The Sahlgrenska Academy at University of Gothenburg, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Gothenburg, Sweden (GRID:grid.8761.8) (ISNI:0000 0000 9919 9582); Institute for Public Health, Charité – Universitätsmedizin Berlin, Berlin, Germany (GRID:grid.6363.0) (ISNI:0000 0001 2218 4662)
6 University of Gothenburg, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, Gothenburg, Sweden (GRID:grid.8761.8) (ISNI:0000 0000 9919 9582); Sahlgrenska University Hospital, Region Västra Götaland, Department of Acute Medicine and Geriatrics, Gothenburg, Sweden (GRID:grid.1649.a) (ISNI:0000 0000 9445 082X)