Osteopetrosis in obese female rats is site‐specifically inhibited by physical training

Abstract

New Findings r What is the central question of this study?Clinical studies suggest that obesity 'protects' against osteoporosis. However, these studies used only bone densitometry and assessed only one bone site, which is insufficient to enable conclusions to be drawn about the response of the whole skeleton. Furthermore, the effects of exercise on bone responses in obesity have not been explored previously. r What is the main finding and what is its importance?We show that obesity causes osteopetrosis. Therefore, the classical perspective of 'protective effects of obesity' needs to be reviewed, and exercise is an important tool to avoid these alterations and to maintain the homeostasis of bone.A sedentary lifestyle and obesity induce systemic inflammatory responses. Although the effects of physical inactivity on osseous tissue have been well established, the effects of obesity on bone tissue remain controversial. Furthermore, the effects of physical training on bone tissue responses in the presence of diet-induced obesity are unknown. Our aim was to investigate the effects of obesity and physical training at multiple bone sites in rats. Female Wistar rats were divided into the following four groups: (i) control diet, non-trained (C-NT); (ii) high-refined carbohydrate-containing diet, non-trained (HC-NT); (iii) control diet, trained (C-T); and (iv) high-refined carbohydrate-containing diet, trained (HC-T). At 5 months of age, the rats were submitted to daily exercise for 30 min day −1 . After 13 weeks, blood samples, adipose and skeletal tissues were harvested. Two-way ANOVA was applied to detect differences (significance accepted when P ࣘ 0.05). The HC-NT group exhibited increased body mass, adiposity, serum leptin, serum insulin, insulin resistance index and concentrations of tumour necrosis factor-α and interleukin-6. Obese rats (HC-NT) exhibited thickening of nasal bones, trabecular bones in the lumbar vertebrae and long bones in a site-dependent manner. The HC-T group exhibited similar adiposity and inflammatory results. Morphological analysis of the lumbar vertebrae in rats fed the HC diet revealed characteristics of osteopetrosis that were inhibited by exercise. In conclusion, the HC diet induced obesity and inflammatory/hormonal alterations and increased the trabecular bone in a site-dependent manner. However, obesity caused osteopetrosis in the lumbar vertebrae, which could be inhibited by physical training. Although exercise inhibited the

Inhibiting myostatin signaling prevents femoral trabecular bone loss and microarchitecture deterioration in diet-induced obese rats

“…1 New insights view obesity as an important risk factor for osteoporosis. [2][3][4] Lean mass and fat mass are important components of body weight. Especially in men, body mass index (BMI) as a protective indicator of bone mineral density (BMD) was strongly associated with elevated muscle mass, but not fat mass.…”

Aerobic training reduces immune cell recruitment and cytokine levels in adipose tissue in obese mice

“…Following the induction of obesity, the mice were gradually introduced to exercise on the treadmill over 5 consecutive days (Soares et al 2007;Lacerda et al 2015). The familiarization protocol was performed to habituate the mice to the treadmill environment.…”

“…Each daily familiarization session consisted of resting on the treadmill turned off for 5 min. Immediately after, mice ran at speeds of 3-6 m/min for 5 min (Soares et al 2007;Lacerda et al 2015).…”

“…Briefly, this test consisted of running on a treadmill (incline set at 5%), starting at a speed of 3 m/min with increases of 3 m/min every 3 min, until volitional fatigue. Fatigue was determined as the point at which mice were unable to keep running even when being stimulated by light electrical shocks on the grid at the end of the treadmill for 10 s (Ferreira et al 2007;Lacerda et al 2015).…”

“…The consumption of high-refined carbohydrate (HC) diets, particularly those containing high amounts of sucrose, induces obesity, fatty liver deposition and adipose tissue inflammation (Oliveira et al 2013;Menezes-Garcia et al 2014;Lacerda et al 2015;Oliveira et al 2015;Martins et al 2017). Moreover, the HC diet-induced rapid fat tissue expansion is associated with leukocyte influx into adipose tissue vessels and increased levels of proinflammatory cytokines (Nishimura et al 2008;Oliveira et al 2013).…”