Influence of Apelin-13 on osteoporosis in Type-2 diabetes mellitus: A clinical study

Liu, Supin; Wang, Wenlong; Yin, Linlin; Zhu, Yitang

doi:10.12669/pjms.341.14135

Cited by 11 publications

(12 citation statements)

References 15 publications

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“…As a common complication in T2DM patients, osteoporosis is characterised by a degeneration of bone morphological structure and decreased BMD [ 26 ]. At present, exercise is a green and healthy intervention method that can promote bone formation and inhibit bone resorption, thereby improving bone metabolism [ 4 , 12 , 16 ].…”

Section: Discussionmentioning

confidence: 99%

Exercise improves bone formation by upregulating the Wnt3a/β-catenin signalling pathway in type 2 diabetic mice

Chen

Kang

Sun

et al. 2021

Diabetol Metab Syndr

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Background The bone formation ability of type 2 diabetes is inhibited, and exercise can effectively improve the bone formation of T2DM. However, whether exercise can mediate the Wnt3a/β-catenin pathway to improve the mechanism of bone formation and metabolism still needs further research. Methods A T2DM mouse model was established by a high-fat diet and STZ injection, and the mice were trained with swimming and downhill running exercise. Alizarin red staining is used to observe the changes of the left femoral trabecular bone; micro-CT is used to analyze the trabecular and cortical BMD, BV/TV, BS/BV, BS/TV, Tb.Th, Tb.Sp; the ALP staining of skull was used to observe the changes in ALP activity of bone tissues at the skull herringbone sutures; ALP staining was performed to observe the changes in the number of OBs and ALP activity produced by differentiation; Quantitative PCR was used to detect mRNA expression; Western blot was used to detect protein expression levels. Results When the Wnt3a/β-catenin pathway in the bones of T2DM mice was inhibited, the bone formation ability of the mice was significantly reduced, resulting in the degradation of the bone tissue morphology and structure. Swimming caused the significant increase in body weight and Runx2 mRNA expression, while downhill running could significantly decrease the body weight of the mice, while the tibia length, wet weight, and the trabecular morphological structure of the distal femur and the indexes of bone histomorphology were significantly improved by activating the Wnt3a/β-catenin pathway. Conclusions Bone formation is inhibited in T2DM mice, leading to osteoporosis. Downhill running activates the Wnt3a/β-catenin pathway in the bones of T2DM mice, promotes OB differentiation and osteogenic capacity, enhances bone formation metabolism, and improves the bone morphological structure.

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Section: Discussionmentioning

confidence: 99%

Exercise improves bone formation by upregulating the Wnt3a/β-catenin signalling pathway in type 2 diabetic mice

Chen

Kang

Sun

et al. 2021

Diabetol Metab Syndr

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“…Apelin, a group of peptides initially isolated from the bovine stomach, is an endogenous ligand of the G protein-coupled APJ receptor [ 19 – 21 ]. Only by binding to the APJ receptor could apelin exert their biologic function [ 19 , 22 , 23 ]; while apelin and the APJ receptor are widely distributed in different organs and tissues [ 22 , 23 ], the apelin/APJ signal axis may play a role in diseases of different organs including pulmonary fibrosis, kidney inflammation [ 24 ], acute lung injury (ALI) [ 25 ], ischemic heart failure [ 26 ], and even osteoporosis [ 27 , 28 ]. What we are interested in is that the apelin/APJ signal axis is especially related to vascular pathophysiology [ 24 , 29 , 30 ].…”

Section: Introductionmentioning

confidence: 99%

Apelin/APJ‐Manipulated CaMKK/AMPK/GSK3β Signaling Works as an Endogenous Counterinjury Mechanism in Promoting the Vitality of Random‐Pattern Skin Flaps

Lou

Zhang

et al. 2021

Oxidative Medicine and Cellular Longevity

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A random-pattern skin flap plays an important role in the field of wound repair; the mechanisms that influence the survival of random-pattern skin flaps have been extensively studied but little attention has been paid to endogenous counterinjury substances and mechanism. Previous reports reveal that the apelin-APJ axis is an endogenous counterinjury mechanism that has considerable function in protecting against infection, inflammation, oxidative stress, necrosis, and apoptosis in various organs. As an in vivo study, our study proved that the apelin/APJ axis protected the skin flap by alleviating vascular oxidative stress and the apelin/APJ axis works as an antioxidant stress factor dependent on CaMKK/AMPK/GSK3β signaling. In addition, the apelin/APJ-manipulated CaMKK/AMPK/GSK3β-dependent mechanism improves HUVECs’ resistance to oxygen and glucose deprivation/reperfusion (OGD/R), reduces ROS production and accumulation, maintained the normal mitochondrial membrane potential, and suppresses oxidative stress in vitro. Besides, activation of the apelin/APJ axis promotes vascular migration and angiogenesis under relative hypoxia condition through CaMKK/AMPK/GSK3β signaling. In a word, we provide new evidence that the apelin/APJ axis is an effective antioxidant and can significantly improve the vitality of random flaps, so it has potential be a promising clinical treatment.

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“…Osteoporosis is a common complication in T2DM patients, which is characterized by a degeneration of bone morphological structure and decreased BMD (Liu et al, 2018). At present, exercise as a green and healthy intervention method, could promote bone formation and inhibit bone resorption, which improves bone metabolism (Gardinier et al, 2018;Friedman et al, 2016;Banu et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Exercise Improves Bone Formation by Upregulating the Wnt3a/β-catenin Signalling Pathway in Type 2 Diabetic Mice

Chen

Yang

Sun

et al. 2021

Preprint

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Bone formation in type 2 diabetes mellitus (T2DM) is inhibited by decreased bone formation capacity. Exercise can significantly improve bone metabolism; however, the effect and mechanism of exercise on bone formation in T2DM is not known. In this study, we used the method of a high-fat diet and injecting STZ to build a T2DM mouse model, and the mice were treated with swimming and downhill running for 8 weeks. Their body weights were obtained using an electronic scale. Their bone length and wet weights were measured by Vernier callipers and an electronic balance. The bone microstructure of the distal femur was analysed by Alizarin red staining of paraffin sections and micro-CT. An ALP dye was used to detect the changes in ALP activity in the mouse skull and osteoblasts. Alizarin red staining was applied to stain the osteoblasts produced by BMSCs. The mRNA expression of related factors were detected by RT-PCR. Our results showed that the body weights of T2DM mice were significantly increased by exercise. When the Wnt3a/β-catenin pathway in the bones of T2DM mice is inhibited, their bone formation ability is significantly reduced, resulting in the degradation of the bone tissue morphology and structure. Except for the significant increase in body weight and Runx2 mRNA expression, swimming had no significant effect on bone formation-related indicators in T2DM mice. However, downhill running could significantly increase their body weight, while the tibia length, wet weight, and the trabecular morphological structure of the distal femur and the indexes of bone histomorphology were significantly improved by activating the Wnt3a/β-catenin pathway. Compared with swimming, downhill running can activate the Wnt pathway to improve bone formation ability, thereby improving bone histomorphology. These findings suggest that exercise promotes OB differentiation, osteogenic capacity and enhances bone formation metabolism by regulating Wnt3a/β-catenin signalling in T2DM mice.

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Influence of Apelin-13 on osteoporosis in Type-2 diabetes mellitus: A clinical study

Cited by 11 publications

References 15 publications

Exercise improves bone formation by upregulating the Wnt3a/β-catenin signalling pathway in type 2 diabetic mice

Exercise improves bone formation by upregulating the Wnt3a/β-catenin signalling pathway in type 2 diabetic mice

Apelin/APJ‐Manipulated CaMKK/AMPK/GSK3β Signaling Works as an Endogenous Counterinjury Mechanism in Promoting the Vitality of Random‐Pattern Skin Flaps

Exercise Improves Bone Formation by Upregulating the Wnt3a/β-catenin Signalling Pathway in Type 2 Diabetic Mice

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