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New findings What is the central question of this study? Exercise can stimulate BAT with subsequent increase in UCP1 expression and mitochondrial biogenesis. In that case, does BAT-specific Hox gene(s) modify BAT functioning and cause UCP expression changes due to exercise? What is the main finding and its importance? Exercise enhanced brown adipocyte markers, with significant upregulation of HoxA5 and downregulation of HoxC10 mRNA expression in rat BAT. HoxA5 and HoxC10 are thus likely to play distinct roles in exercise-induced changes in BAT markers during the early postnatal period. These findings provide new insight into the mechanisms underlying exercise-induced changes in BAT function. Abstract Brown adipose tissue (BAT) recruitment is involved in increased energy expenditure associated with cold exposure and exercise training. We explored whether exercise training induced changes in expression levels of brown adipocyte-selective factors and Homeobox (Hox) genes during the post-weaning growth period of male Wistar rats. Relative to total body weight, BAT weights alone were lower in exercise-trained (EX) rats compared to sedentary control (SED) rats. mRNA expression of HoxA5 was higher and that of HoxC10 was lower in EX rats than in SED rats, accompanied by both higher citrate synthase activity and protein expression levels for uncoupling protein 1 (UCP1), peroxisome proliferator-activated receptor (PPAR) α, and PPARγ-coactivator (PGC)-1α. HoxA5 knockdown with siRNA reduced the expression of PR-domain containing 16 (Prdm16), cell death-inducing DNA fragmentation factor-α-like effector A (Cidea) gene, type 2 deiodinase mRNA, and PRDM16 protein. Comparatively, HoxC10 knockdown with siRNA enhanced mRNA expression of Prdm16, Pparα, and Pgc1α and protein expression of UCP1, PPARα, and PGC1α in brown adipocytes. The stimulation of brown adipocytes with isoproterenol, a β-adrenoceptor agonist, caused a phenomenon similar to the effect of exercise training on the genes tested: upregulation of HoxA5 mRNA, downregulation of HoxC10 mRNA, and increased protein expression for UCP1 and PGC1α. Collectively, HoxA5 and HoxC10 may have unique functions that contribute to modulating the expression of BAT-selective markers in BAT of juvenile rats during exercise training. The study findings regarding activation and recruitment of BAT during exercise training have implications for anti-obesity management. This article is protected by copyright. All rights reserved.

Aims Obesity suppresses brain‐derived neurotrophic factor (BDNF) expression and increases the expression of pro‐inflammatory cytokines. Herein, we assessed whether exercise training (ET), melatonin administration (MT), or their combination can affect the expressions of BDNF and cytokines in the cerebellum of high‐fat diet (HFD)‐fed rats. Methods Wistar rats (4 weeks old) were divided into five groups: normal diet (ND)‐fed control (ND‐SED), HFD‐fed control (HFD‐SED), HFD‐fed ET (HFD‐ET), HFD‐fed MT (HFD‐MT), and HFD‐fed MT plus ET (HFD‐ETMT) group. The rats were fed ND or HFD for 17 weeks. Rats were subjected to ET (running on a treadmill) and/or MT (melatonin 5 mg/kg body weight, i.p.) for 9 weeks, 8 weeks after beginning the diet intervention. Changes in BDNF and cytokine expression levels were determined using immunoblotting and cytokine arrays, respectively, 36 hours following the last bout of ET. Results Neither HFD‐ET nor HFD‐MT rats exhibited enhanced BDNF expression in the cerebellum, but HFD‐ETMT rats had higher level of BDNF expression compared with the others. The expression of TrkB, a BDNF receptor, was higher in HFD‐ETMT rats than in HFD‐ET and HFD‐MT rats. HFD enhanced the expression of interleukin (IL)‐1, IL‐2, and interferon‐γ but reduced the expression of IL‐4, IL‐6, and IL13. ET and ET plus MT counteracted these HFD‐induced changes in cytokine expressions. Conclusion Exercise in combination with melatonin confers the potential benefits of increasing BDNF and improving HFD‐induced dysregulations of cytokines in the cerebellum., High‐fat diet feeding enhanced the expressions of pro‐inflammatory cytokines but reduced those of anti‐inflammatory cytokines in the rat cerebellum. Interestingly, exercise training and exercise in combination with melatonin administration had a reversal effect on high‐fat diet feeding‐induced changes in cytokine expressions.

Controlling the differentiation potential of adipose-derived stem cells (ADSCs) is attracting attention as a new strategy for the prevention and treatment of obesity. Here, we aimed to observe the effect of exercise training (TR) and high-fat diet (HFD) on the metabolic profiles of ADSCs-derived adipocytes. The rats were divided into four groups: normal diet (ND)-fed control (ND-SED), ND-fed TR (ND-TR), HFD-fed control (HFD-SED), and HFD-fed TR (HFD-TR). After 9 weeks of intervention, ADSCs of epididymal and inguinal adipose tissues were differentiated into adipocytes. In the metabolome analysis of adipocytes after isoproterenol stimulation, 116 metabolites were detected. The principal component analysis demonstrated that ADSCs-derived adipocytes segregated into four clusters in each fat pad. Amino acid accumulation was greater in epididymal ADSCs-derived adipocytes of ND-TR and HFD-TR, but lower in inguinal ADSCs-derived adipocytes of ND-TR, than in the respective controls. HFD accumulated several metabolites including amino acids in inguinal ADSCs-derived adipocytes and more other metabolites in epididymal ones. Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that TR mainly affected the pathways related to amino acid metabolism, except in inguinal ADSCs-derived adipocytes of HFD-TR rats. These findings provide a new way to understand the mechanisms underlying possible changes in the differentiation of ADSCs due to TR or HFD.