The impact of forced swimming on expression of RANKL and OPG in a type 2 diabetes mellitus rat model

Pezhman, Laleh; Hesari, Farzam Sheikhzadeh; Ghiasi, Rafighe; Alipour, Mohammad Reza

doi:10.1080/13813455.2018.1446178

Cited by 9 publications

(4 citation statements)

References 41 publications

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“… 34 In addition, Pezhman et al found that swim training could partially compensate for T2DM-associated changes of bone. 35 On the macro level, Aoi Ikedo et al found that a 6-week resistance training regimen effectively increased BMD and improved bone quality in T2DM model rats, which is also consistent with our study.…”

Section: Discussionsupporting

confidence: 92%

Bone Autophagy: A Potential Way of Exercise-Mediated Meg3/P62/Runx2 Pathway to Regulate Bone Formation in T2DM Mice

Chen¹,

Kang²,

Jin³

et al. 2021

DMSO

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Background Meg3 has been shown to attenuate T2DM bone autophagy by activating p62 to inhibit bone formation. However, whether exercise can reverse this process to promote T2DM bone formation and its mechanism remains unknown. Methods A T2DM mouse model was established by a high-fat diet and STZ injection, and the mice were trained with 8-week HIIT and downhill running exercise. Micro-CT was used to scan the bone microstructure. Bone morphology was observed by HE staining, and the osteoblast (OB) activity in bones was observed by AKP staining. Calcium ion and phosphorus concentration in serum was detected by ELISA; RT-PCR was used to detect the mRNA level, and Western blot was used to detect the protein level of related indexes in Meg3/p62/Runx2 pathway. Results The inhibition of bone autophagy, in the bones of T2DM mice, resulted in the degradation of the bone tissue morphology and structure, with the increase of the expressions of Meg3, PI3K, Akt, mTOR, p62 and NF-κB. However, 8-week HIIT and downhill running could reverse this process, especially downhill running, manifested with the up-regulation of miR-16 mRNA level, along with Beclin-1, LC3 II and Runx2 mRNA and protein level. Conclusion T2DM leads to pathology in model mice. Eight-week HIIT and downhill running exercise can inhibit Meg3, activate autophagy of osteoblasts and promote bone formation in T2DM mice.

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Section: Discussionsupporting

confidence: 92%

Bone Autophagy: A Potential Way of Exercise-Mediated Meg3/P62/Runx2 Pathway to Regulate Bone Formation in T2DM Mice

Chen¹,

Kang²,

Jin³

et al. 2021

DMSO

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“…Several animal experiments reported similar effects on other forms of exercise: reduced RANKL levels and increased OPG levels were observed in osteoblast experiments in acutely trained mice [39]. Diabetic model rats showed significant OPG in bone and serum and decreased mRNA and protein expression of RANKL after forced swimming training [40]. However, another study found that exercise may not change the level of RANKL and OPG and their expression: a 12-week joint exercise experiment for healthy female college students showed that the bone metabolic response of OPG/RANK/ RANKL signaling is not obvious.…”

Section: Exercise Affects the Postmenopausal Osteoporosismentioning

confidence: 66%

The Potential Mechanism of Exercise Combined with Natural Extracts to Prevent and Treat Postmenopausal Osteoporosis

Zhou

Gai

Gao

et al. 2021

Journal of Healthcare Engineering

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Postmenopausal osteoporosis (PMOP) is a systemic chronic bone metabolic disease caused by the imbalance between bone formation and bone resorption mediated by estrogen deficiency. Both exercise and natural extracts are safe and effective means to prevent and control PMOP. The additive effect of exercise synergy extract against PMOP may be no less than that of traditional medicine. However, the mechanism of action of this method has not been clarified in detail. A large number of studies have shown that the pathogenesis of PMOP mainly involves the OPG-RANKL-RANK system, inflammation, and oxidative stress. Based on the abovementioned approaches, the present study reviews the anti-PMOP effects and mechanisms of exercise and natural extracts. Finally, it aims to explore the possibility of the target of the two combined anti-PMOP through this approach, thereby providing a new perspective for joint intervention research and providing a new direction for the treatment strategy of PMOP.

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“…A 60 × 100 cm cylindrical tank was filled with 35 °C water up to 35-45 cm in height, and used for training. During the course of the training, exercise groups were allowed to swim for 60s once a day (for 60 min/5 days/ weekly for 12 weeks) [26,27].…”

Section: Swimming Trainingmentioning

confidence: 99%

Swimming training attenuates pancreatic apoptosis through miR-34a/Sirtu in1/P53 Axis in high-fat diet and Streptozotocin-induced Type-2 diabetic rats

Alipour

Naderi

Alihemmati

et al. 2020

J Diabetes Metab Disord

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Objective The present study sought to evaluate the miR-34a/Sirtuin1/p53 pro-apoptotic pathway, and reveal its modulation in diabetic rats undergoing swimming exercise. Methods Twenty-eight male Wistar rats were divided into four groups. They were inducted to develop diabetes by injection of streptozotocin. After 12 weeks of swimming, the pancreatic tissue of these rats were removed to be evaluated for the expression level of Sitruin1/P53/miR-34a through qPCR. Results Findings indicated a marked rise in the expression of miR-34 and P53 (P < 0.01) as well as a significant decrease in expression of Sitruin1 (P < 0.01) in the diabetic group. In contrast, swimming resulted in a significant decrease in miR-34a expression (P < 0.01), and a prominent rise in the level of Sitruin1 in the swimming-trained-diabetic group (P < 0.01). Additionally, high, moderate and low apoptosis rate were observed in the pancreatic tissue of the diabetic, swimming-trained diabetic, and control groups, respectively. Conclusion Our findings suggested a correlation between pancreatic tissue apoptosis rate and miR-34a/Sitruin1/p53 signaling, that was subject to modulation by training.

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The impact of forced swimming on expression of RANKL and OPG in a type 2 diabetes mellitus rat model

Abstract: Swim training could partially compensate T2DM associated changes of bone and serum OPG/RANKL in rats.

Cited by 9 publications

References 41 publications

Bone Autophagy: A Potential Way of Exercise-Mediated Meg3/P62/Runx2 Pathway to Regulate Bone Formation in T2DM Mice

Bone Autophagy: A Potential Way of Exercise-Mediated Meg3/P62/Runx2 Pathway to Regulate Bone Formation in T2DM Mice

The Potential Mechanism of Exercise Combined with Natural Extracts to Prevent and Treat Postmenopausal Osteoporosis

Swimming training attenuates pancreatic apoptosis through miR-34a/Sirtu in1/P53 Axis in high-fat diet and Streptozotocin-induced Type-2 diabetic rats

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