Abstract

OBJECTIVE:The purpose of this study was to investigate the effects of resistance training on angiogenesis markers of visceral adipose tissue in ovariectomized rats.METHOD:Adult Sprague-Dawley female rats were divided into four groups (n=6 per group): sham-sedentary, ovariectomized sedentary, sham-resistance training and ovariectomized resistance training. The rats were allowed to climb a 1.1-m vertical ladder with weights attached to their tails and the weights were progressively increased. Sessions were performed three times per week for 10 weeks. Visceral adipose tissue angiogenesis and morphology were analyzed by histology. VEGF-A mRNA and protein levels were analyzed by real-time PCR and ELISA, respectively.RESULTS:Ovariectomy resulted in higher body mass (p=0.0003), adipocyte hypertrophy (p=0.0003), decreased VEGF-A mRNA (p=0.0004) and protein levels (p=0.0009), and decreased micro-vascular density (p=0.0181) in the visceral adipose tissue of the rats. Resistance training for 10 weeks was not able to attenuate the reduced angiogenesis in the visceral adipose tissue of the ovariectomized rats.CONCLUSION:Our findings indicate that the resistance training program used in this study could not ameliorate low angiogenesis in the visceral adipose tissue of ovariectomized rats.

Highlights

  • The decline in estrogen levels that occurs in postmenopausal women is closely related to obesity, mainly due to the redistribution of subcutaneous fat to the visceral compartment [1]

  • Microvascular density in visceral adipose tissue (VAT) was reduced in the Ovx rats (p=0.0181) compared to the Sham-Sed rats (Figure 4A and B); there was no difference between the Sham-Sed and Sham-resistance training (Rt) groups or between the Ovx-Sed and Ovx-Rt groups

  • Evidence from rodent models has demonstrated that ovariectomy promotes obesity and its metabolic complications, in particular insulin resistance [26,27]

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Summary

Introduction

The decline in estrogen levels that occurs in postmenopausal women is closely related to obesity, mainly due to the redistribution of subcutaneous fat to the visceral compartment (intra-abdominal) [1]. Studies have demonstrated that postmenopausal women have enlarged adipocytes and that the lipolytic activity in these adipocytes is high, which may explain why postmenopausal. Stubbins et al [5] showed that ovariectomized (Ovx) female mice have hypertrophied adipocytes, creating hypoxia that can worsen the inflammatory environment. It is evident that one of the ways that estrogen modulates adiposity is by altering adipocyte size

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