Abstract
This study compares the effect of two types of exercise training, i.e., moderate-intensity continuous training (MICT) or high-intensity interval training (HIIT) on the browning of subcutaneous white adipose tissue (scWAT) in obese male rats. Effects on fat composition, metabolites, and molecular markers of differentiation and energy expenditure were examined. Forty male Wistar rats were assigned to lean (n = 8) or obese (n = 32) groups and fed either a standard chow or high-fat obesogenic diet for 10 weeks. Eight lean and obese rats were then blood and tissue sampled, and the remaining obese animals were randomly allocated into sedentary, MICT, or HIIT (running on a treadmill 5 days/week) groups that were maintained for 12 weeks. Obesity increased plasma glucose and insulin and decreased irisin and FGF-21. In scWAT, this was accompanied with raised protein abundance of markers of adipocyte differentiation, i.e., C/EBP-α, C/EBP-β, and PPAR-γ, whereas brown fat-related genes, i.e., PRDM-16, AMPK/SIRT1/PGC-1α, were reduced as was UCP1 and markers of fatty acid transport, i.e., CD36 and CPT1. Exercise training increased protein expression of brown fat-related markers, i.e., PRDM-16, AMPK/SIRT1/PGC-1α, and UCP1, together with gene expression of fatty acid transport, i.e., CD36 and CPT1, but decreased markers of adipocyte differentiation, i.e., C/EBP-α, C/EBP-β, and plasma glucose. The majority of these adaptations were greater with HIIT compared to MICT. Our findings indicate that prolonged exercise training promotes the browning of white adipocytes, possibly through suppression of adipogenesis together with white to beige trans-differentiation and is dependent on the intensity of exercise.
Highlights
Obesity is the result of an imbalance between energy intake and energy consumption, characterized by the accumulation of excess adipose tissue (AT) and adipocyte dysfunction [1]
Both high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) resulted in an increase in irisin and fibroblast growth factor-21 (FGF-21) compared with obese animals
Obesity had no effect on mitochondrial DNA (mtDNA), whereas exercise training resulted in an increase, an adaptation that was greater for HIIT compared with MICT
Summary
Obesity is the result of an imbalance between energy intake and energy consumption, characterized by the accumulation of excess adipose tissue (AT) and adipocyte dysfunction [1]. Beige adipocytes have been identified in WAT that are characterized as possessing more mitochondria than WAT, with enhanced gene expression for proteins involved in lipolysis and thermogenesis, such as UCP1 [8], together with a higher rate of fatty acid transport and oxidation [9]. There are numerous regulatory components and molecular mechanisms that control adipogenesis, of which peroxisome proliferator-activated receptor gamma (PPAR-γ) and CCAAT/enhancer-binding protein beta isoforms (C/EBPs) are the main transcription factors [10,11]. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is the main regulator of mitochondrial biogenesis and a primary activator of PPAR-γ [12,13], which is directly regulated by AMP-activated protein kinase (AMPK) and the SIRT1 pathway [14,15,16] and is upregulated by calorie restriction and exercise training [17,18]. Differentiation of brown and beige adipocytes is regulated by PR domain containing 16 (PRDM16) [19,20], and the browning of WAT is accompanied with an increase in the abundance of cluster of differentiation 36 (CD36)
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