Comparison of visceral fat lipolysis adaptation to high-intensity interval training in obesity-prone and obesity-resistant rats

Abstract

Background/objectives: Visceral obesity is one of the key features of metabolic syndrome. High-intensity interval training (HIIT) could effectively reduce visceral fat, but its effects show strong heterogeneity in populations with different degrees of obesity. The mechanism may be related to the differential adaptation to training between obesity phenotypes, namely obesity prone (OP) and obesity resistant (OR). The aim of the present study was to compare adaptive changes of visceral adipose lipolysis adaptation to HIIT between OP and OR animals and further explore the upstream pathway.

Methods: OP and OR Sprague Dawley rats were established after feeding a high-fat diet for 6 weeks; they were then divided into HIIT (H-OP and H-OR) and control (C-OP and C-OR) groups. After 12 weeks of HIIT or a sedentary lifestyle, animals were fasted for 12 h and then sacrificed for histology as well as gene and protein analysis. Visceral adipocytes were isolated without fasting for catecholamine stimulation and β3-adrenergic receptor (β3-AR) blockade in vitro to evaluate the role of upstream pathways.

Results: After training, there were no differences in weight loss or food intake between OP and OR rats (P > 0.05). However, the visceral fat mass, adipocyte volume, serum triglycerides and liver lipids of OP rats decreased by more than those of OR rats (P < 0.05). Meanwhile, the cell lipolytic capacity and the increase in the expression of β3-AR were higher in the OP compared with OR groups (P < 0.05). Although training did not increase sympathetic nervous system activity (P > 0.05), the cell sensitivity to catecholamine increased significantly in the OP compared with OR groups (P < 0.05). Following blocking β3-AR, the increased sensitivity disappeared.

Conclusion: With HIIT, OP rats lost more visceral fat than OR rats, which was related to stronger adaptive changes in lipolysis. Increased β3-AR expression mediated this adaptation.

Keywords: Adrenergic receptors; HIIT; Obesity prone; Obesity resistance; Visceral adipose.

Fig. 1

Study design. C- the control groups; H- the groups subjected to high-intensity interval training; OP obesity prone; OR obesity resistant; 0.1, 1 and 10 μM the gradient of isoproterenol stimulation; SR SR59230a, a selective antagonist of β3-adrenergic receptors

Fig. 2

Body weight and food intake during the model establishment period. A Body weight changes during the 6-week model establishment period, analysed by repeated measures analysis of variance. B Body weight distribution after 6 weeks, with the fourth and first quartiles (n = 12 each) of rats selected as obesity prone (OP) and obesity resistant (OR) rats, respectively. C The total food intake during the 6-week model establishment period, analysed by t-test. *P < 0.05, **P < 0.01

Fig. 3

Body weight and food intake during and after 12 weeks of high-intensity interval training (HIIT). A Body weight changes during 12 weeks of HIIT, analysed by repeated measures analysis of variance (ANOVA); ^△time × OP/OR P < 0.05. B Body weight at week 12; ⁺⁺main effect of HIIT/sedentary P < 0.01, analysed by two-way ANOVA. C The total food intake during training; ^&&main effect of OP/OR P < 0.01, analysed by two-way ANOVA

Fig. 4

Fat Mass, VAT, TBX1 expression and mitochondrial histology. A Epididymal fat mass. B Visceral adipocyte area. C TBX1 mRNA expression. D Transmission electron micrographs showing mitochondria in adipocytes (denoted by red arrows). For A, B ^△HIIT/Sedentary × OP/OR P < 0.05. **H-group vs C-group P < 0.01; ^##C-OP vs C-OR P < 0.01, analysed by simple effect

Fig. 5

TC, TG, LDL-C, HDL-C and liver histology. A Serum total cholesterol. B Serum triglycerides. C LDL-C. D HDL-C. E Oil red O staining of liver. F Lipid deposition of liver (grey value of Oil red O). For A–D, F △, HIIT/Sedentary × OP/OR P < 0.05, ⁺⁺main effect of HIIT/sedentary P < 0.01, analysed by two-way ANOVA.; *H-group vs C-group P < 0.05, **P < 0.01; ^##C-OP vs C-OR P < 0.01, analysed by simple effect

Fig. 6

Expression of hormone-sensitive lipase (HSL) and phosphorylated HSL-ser660. A TH protein expression. B β3-AR protein expression. C HSL protein expression. D Phosphorylated HSL-ser660 protein expression. ^△HIIT/Sedentary × OP/OR P < 0.05, analysed by two-way analysis of variance. ^#C-OP vs C-OR P < 0.05; *H-OR vs C-OR P < 0.05; and **H-OP vs H-OR P < 0.01, analysed by simple effect; ⁺⁺main effect of HIIT/sedentary P < 0.01; ^&&main effect of OP/OR P < 0.01, analysed by two-way analysis of variance

Fig. 7

Glycerol release from adipocytes stimulated by isoproterenol (ISO) in vitro. A Overview of the glycerol release of all adipocyte groups. B Comparison between the control (C) groups. C Comparison between the exercise (H) groups; ^&main effect of OP/OR P < 0.05, analysed by two-way analysis of variance. D Changes in glycerol release with or without β3-adrenergic receptor blockade with SR59230a; *P < 0.05, analysed by t-test; ISO isoproterenol, SR SR59230a