Exercise training prevents obesity/diabetes‐induced activation of inflammatory signaling in rat brown adipose tissue

Abstract

Brown adipose tissue (BAT) plays a crucial role in energy expenditure and is recognized as a therapeutic target in metabolic diseases. Chronic inflammation is a common etiology of obesity and type 2 diabetes. A previous study reported increased inflammation in BAT from obese animals. Regular exercise is an effective tool for improving obesity; however, it remains unclear whether exercise training affects the inflammation in BAT from obese animals.PurposeTo examine the effects of exercise training on the activation of inflammation‐related signaling in BAT from obese/diabetic rats.MethodsMale Otsuka Long‐Evans Tokushima Fatty (OLETF) rats, a rodent model for obesity/diabetes, were randomly assigned to either sedentary (n = 11) or exercise training (n = 8) groups. Long‐Evans Tokushima Otsuka (LETO; n = 9) rats were used as the non‐diabetic sedentary control. Exercise training on the treadmill was conducted 4 days/week for 20 weeks from 5 weeks of age. An intraperitoneal glucose tolerance test was performed and interscapular BAT was dissected, and phosphorylation levels of inflammatory‐related proteins, as well as the expression levels of mitochondrial proteins, were determined by western blot analysis.ResultsThe phosphorylation levels of p65 (a subunit of NF‐κB) and mitogen‐activated protein kinases (MAPK; p38, ERK1/2, and SAPK/JNK) in the BAT were significantly higher in the sedentary OLETF rats when compared to those in the LETO rats. Exercise training attenuated the increase in the phosphorylation levels of NF‐κB and MAPKs in the BAT from the OLETF rats. Moreover, the expression levels of UCP‐1 and ‐3 and oxidative phosphorylation‐related proteins (NDUFB8, SDHB, UQCRC2, MTCO1 and ATP5A) in the BAT were significantly lower in the sedentary OLETF rats than the LETO rats, but exercise training did not alter this.ConclusionExercise training prevents obesity‐induced activation of NF‐κB and MAPK signaling in BAT from obese/diabetic rats.Support or Funding InformationThis work was supported by grants from the MEXT‐Supported Program for the Strategic Research Foundation at Private Universities (S1101008) and a Grant‐in‐Aid for JSPS Fellows (13J10819).