Ingestion of collagen peptides prevents bone loss and improves bone microarchitecture in chronologically aged mice

2019 ◽  
Vol 52 ◽  
pp. 1-7 ◽  
Author(s):  
Hongdong Song ◽  
Siqi Zhang ◽  
Ling Zhang ◽  
Bo Li
Keyword(s):  
Bone Loss ◽  
Bone Microarchitecture ◽  
Aged Mice ◽  
Collagen Peptides

scholarly journals Activation of 4-1BB signaling in bone marrow stromal cells triggers bone loss via the p-38 MAPK-DKK1 axis in aged mice

2021 ◽  
Author(s):  
Daqian Wan ◽  
Songtao Ai ◽  
Huoniu Ouyang ◽  
Liming Cheng
Keyword(s):  
Bone Marrow ◽  
Bone Loss ◽  
Osteogenic Differentiation ◽  
Stromal Cells ◽  
Bone Marrow Stromal Cells ◽  
Bone Marrow Microenvironment ◽  
Marrow Stromal Cells ◽  
Senile Osteoporosis ◽  
Aged Mice ◽  
Old Mice

AbstractSenile osteoporosis can cause bone fragility and increased fracture risks and has been one of the most prevalent and severe diseases affecting the elderly population. Bone formation depends on the proper osteogenic differentiation of bone marrow stromal cells (BMSCs) in the bone marrow microenvironment, which is generated by the functional relationship among different cell types in the bone marrow. With aging, bone marrow provides signals that repress osteogenesis. Finding the signals that oppose BMSC osteogenic differentiation from the bone marrow microenvironment and identifying the abnormal changes in BMSCs with aging are key to elucidating the mechanisms of senile osteoporosis. In a pilot experiment, we found that 4-1BBL and 4-1BB were more abundant in bone marrow from aged (18-month-old) mice than young (6-month-old) mice. Meanwhile, significant bone loss was observed in aged mice compared with young mice. However, very little data have been generated regarding whether high-level 4-1BB/4-1BBL in bone marrow was associated with bone loss in aged mice. In the current study, we found upregulation of 4-1BB in the BMSCs of aged mice, which resulted in the attenuation of the osteogenic differentiation potential of BMSCs from aged mice via the p38 MAPK-Dkk1 pathway. More importantly, bone loss of aged mice could be rescued through the blockade of 4-1BB signaling in vivo. Our study will benefit not only our understanding of the pathogenesis of age-related trabecular bone loss but also the search for new targets to treat senile osteoporosis.

scholarly journals Octanoic acid a major component of widely consumed medium-chain triglyceride ketogenic diet is detrimental to bone

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shreshta Jain ◽  
Reena Rai ◽  
Divya Singh ◽  
Divya Vohora
Keyword(s):  
Bone Loss ◽  
Ketogenic Diet ◽  
Octanoic Acid ◽  
Bone Microarchitecture ◽  
Medium Chain Triglyceride ◽  
Decanoic Acid ◽  
Clinical Findings ◽  
Micro Computed Tomography ◽  
Negative Effects ◽  
Treatment Groups

AbstractOctanoic acid is a medium-chained saturated fatty acid found abundantly in the ketogenic dietary supplements containing medium chained triglycerides (MCT) along with decanoic acid. The MCT ketogenic diet is commonly consumed for weight loss but has also showcased neuroprotective potential against neurodegenerative disorders. However, recent clinical findings have reported a critical disadvantage with the long-term consumption of ketogenic diet i.e. bone loss. The following study was employed to investigate whether the two major components of MCT diet also possess bone loss potential as observed with classical ketogenic diet. Swiss albino mice aged between 10 and 12 weeks, were divided into 3 treatment groups that were administered with oral suspensions of octanoic acid, decanoic acid and a combination of both for 4 weeks. Bone specific markers, microarchitectural parameters, using micro computed tomography, and biomechanical strength were analyzed. Remarkably deleterious alterations in the trabecular bone microarchitecture, and on bone markers were observed in the octanoic acid treated groups. Our results suggest significant negative effects on bone health by octanoic acid. These findings require further investigation and validation in order to provide significant clinically relevant data to possibly modify dietary composition of the MCT ketogenic diet.

scholarly journals Effect of Orally Administered Collagen Peptides from Bovine Bone on Skin Aging in Chronologically Aged Mice

Nutrients ◽  
2017 ◽  
Vol 9 (11) ◽  
pp. 1209 ◽  
Author(s):  
Hongdong Song ◽  
Siqi Zhang ◽  
Ling Zhang ◽  
Bo Li
Keyword(s):  
Skin Aging ◽  
Bovine Bone ◽  
Aged Mice ◽  
Collagen Peptides

scholarly journals Rehmannia glutinosa Libosch Extracts Prevent Bone Loss and Architectural Deterioration and Enhance Osteoblastic Bone Formation by Regulating the IGF-1/PI3K/mTOR Pathway in Streptozotocin-Induced Diabetic Rats

2019 ◽  
Vol 20 (16) ◽  
pp. 3964 ◽  
Author(s):  
Wan Gong ◽  
Naidan Zhang ◽  
Gang Cheng ◽  
Quanlong Zhang ◽  
Yuqiong He ◽  
...  
Keyword(s):  
Bone Loss ◽  
Bone Formation ◽  
Signaling Pathways ◽  
Bone Microarchitecture ◽  
Diabetic Rats ◽  
Mtor Pathway ◽  
Mtor Signaling ◽  
Rehmannia Glutinosa ◽  
Mineral Density ◽  
Rehmannia Glutinosa Libosch

Rehmanniae Radix Praeparata (RR, named as Shudihuang in traditional Chinese medicine), the steamed roots of Rehmannia glutinosa Libosch (Scrophulariaceae), has been demonstrated to have anti-diabetic and anti-osteoporotic activities. This study aimed to explore the protective effect and underlying mechanism of RR on diabetes-induced bone loss. It was found that RR regulated the alkaline phosphatase activity and osteocalcin level, enhanced bone mineral density, and improved the bone microarchitecture in diabetic rats. The catalpol (CAT), acteoside (ACT), and echinacoside (ECH) from RR increased the proliferation and differentiation of osteoblastic MC3T3-E1 cells injured by high glucose and promoted the production of IGF-1 and expression of related proteins in BMP and IGF-1/PI3K/mammalian target of rapamycin complex 1 (mTOR) signaling pathways. The verifying tests of inhibitors of BMP pathway (noggin) and IGF-1/PI3K/mTOR pathway (picropodophyllin) and molecular docking of IGF-1R further indicated that CAT, ACT, and ECH extracted from RR enhanced bone formation by regulating IGF-1/PI3K/mTOR signaling pathways. These findings suggest that RR may prove to be a promising candidate drug for the prevention and treatment of diabetes-induced osteoporosis.

scholarly journals Bone Metabolism in Adolescents Undergoing Bariatric Surgery

2020 ◽  
Author(s):  
Madhusmita Misra ◽  
Miriam A Bredella
Keyword(s):  
Bariatric Surgery ◽  
Sleeve Gastrectomy ◽  
Lumbar Spine ◽  
Bone Loss ◽  
Bone Microarchitecture ◽  
Quantitative Computed Tomography ◽  
Areal Bone Mineral Density ◽  
Mineral Density ◽  
Cross Sectional ◽  
Peripheral Skeleton

Abstract Purpose The prevalence of childhood obesity has increased over past decades with a concomitant increase in metabolic and bariatric surgery (MBS). While MBS in adults is associated with bone loss, only a few studies have examined the effect of MBS on the growing skeleton in adolescents. Methods This mini-review summarizes available data on the effects of the most commonly performed MBS (sleeve gastrectomy and gastric bypass) on bone in adolescents. A literature review was performed using PubMed for English-language articles. Results Dual-energy x-ray absorptiometry (DXA) measures of areal bone mineral density (aBMD) and BMD Z scores decreased following all MBS. Volumetric BMD (vBMD) by quantitative computed tomography (QCT) decreased at the lumbar spine while cortical vBMD of the distal radius and tibia increased over a year following sleeve gastrectomy (total vBMD did not change). Reductions in narrow neck and intertrochanteric cross-sectional area and cortical thickness were observed over this duration, and hip strength estimates were deleteriously impacted. Marrow adipose tissue (MAT) of the lumbar spine increased while MAT of the peripheral skeleton decreased a year following sleeve gastrectomy. The amount of weight loss and reductions in lean and fat mass correlated with bone loss at all sites, and with changes in bone microarchitecture at peripheral sites. Conclusion MBS in adolescents is associated with aBMD reductions, and increases in MAT of the axial skeleton, while sleeve gastrectomy is associated with an increase in cortical vBMD and decrease in MAT of the peripheral skeleton. No reductions have been reported in peripheral strength estimates.

scholarly journals Protective Effects of Curcumin and Broccoli Seed Extract Against Age-Related Bone Loss in Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 46-46
Author(s):  
Jing Li ◽  
Dong Zhang ◽  
Yiping Ren ◽  
Zhongdong Qiao ◽  
Doug Stevenson ◽  
...  
Keyword(s):  
Bone Loss ◽  
Seed Extract ◽  
Control Group ◽  
Protective Effects ◽  
Trabecular Thickness ◽  
Time Points ◽  
Aged Mice ◽  
Funding Sources ◽  
Age Related ◽  
Young Mice

Abstract Objectives Age-related bone loss occurs in both men and women, and is the leading cause of elderly disability. An age-related bone loss model was established in mice to investigate the protective effects of curcumin and broccoli seed extract. Methods 20 young (6-month-old) male C57BL/6 J mice after administration with vehicle once daily were sacrificed at four time points: day 0, 30, 60 and 90. 8 out of the 109 aged (18-month-old) male C57BL/6 J mice were sacrificed at the beginning and used as control. The rest of these aged mice were then randomly divided into four groups: one group served as control (vehicle), the other three groups were administrated with curcumin (CMN) and/or broccoli seed extract (BSE) by oral gavage. Mice in each group were sacrificed at four time points: day 0, 30, 60 and 90. L2 vertebrae of mice were fixed with paraformaldehyde and scanned with a Scanco Medical μCT40 scanner. Quantitative analyses of bone volume (BV), tissue volume (TV), trabecular number (Tb.N), trabecular thickness (Tb.Th) and trabecular spacing (Tb.Sp) were performed with the Scanco Medical's software. Results BV/TV of the young mice group were significantly higher compared to the aged mice group at all four time points. Similarly, Tb.N and Tb.Th were also higher in the young mice group compared to the aged mice group. In contrast, Tb.Sp was lower in the young mice group. When comparing different groups in the aged mice, we found that mice administered with CMN had a higher BV/TV value compared to the mice in the control group at all three time points. Such a difference is significant by day 30. The mice administered with combined CMN and BSE also showed significant increase in BV/TV on day 30. For Tb.N, both mice administered with either CMN or BSE had higher values at all three time points. But no obvious difference in Tb.N was found for mice administered with combined CMN and BSE. For Tb.Th, both mice administered with CMN and with combined CMN and BSE had higher values compared to the control. For Tb.Sp, both mice administered with either CMN or BSE had lower values compared to the control. Conclusions This study showed that curcumin could slow down bone loss in the mouse model. There is no obvious positive effect with broccoli seed extract or with curcumin and broccoli seed extract combined. The curcumin used in this study may shed light on the alleviation of bone loss in humans. Funding Sources Nu Skin Enterprises.

scholarly journals Age dependence of systemic bone loss and recovery following femur fracture in mice

2018 ◽  
Author(s):  
Armaun J. Emami ◽  
Chrisoula A. Toupadakis ◽  
Stephanie M. Telek ◽  
David P. Fyhrie ◽  
Clare E. Yellowley ◽  
...  
Keyword(s):  
Bone Loss ◽  
Fracture Risk ◽  
Trabecular Bone ◽  
Voluntary Movement ◽  
Whole Body ◽  
Middle Aged ◽  
Aged Mice ◽  
Future Fracture ◽  
Systemic Bone Loss ◽  
Young Mice

AbstractThe most reliable predictor of future fracture risk is a previous fracture of any kind. The etiology of this increased fracture risk is not fully known, but it is possible that fracture initiates systemic bone loss leading to greater fracture risk at all skeletal sites. In this study we investigated systemic bone loss and recovery following femoral fracture in young (3 month old) and middle-aged (12 month old) mice. Transverse femur fractures were created using a controlled impact, and whole-body bone mineral density (BMD), trabecular and cortical microstructure, bone mechanical properties, bone formation and resorption rates, mouse voluntary movement, and systemic inflammation were quantified at multiple time points post-fracture. We found that fracture led to decreased whole-body BMD in both young and middle-aged mice 2 weeks post-fracture; this bone loss was recovered by 6 weeks in young, but not middle-aged mice. Similarly, trabecular bone volume fraction (BV/TV) of the L5 vertebral body was significantly reduced in fractured mice relative to control mice 2 weeks post-fracture (−11% for young mice, −18% for middle-aged mice); this bone loss was fully recovered by 6 weeks post-fracture in young mice. At 3 days post-fracture we observed significant increases in serum levels of interleukin-6 and significant decreases in voluntary movement in fractured mice compared to control mice, with considerably greater changes in middle-aged mice than in young mice. At this time point we also observed increased osteoclast number on L5 vertebral body trabecular bone of fractured mice compared to control mice. These data show that systemic bone loss occurs after fracture in both young and middle-aged mice, and recovery from this bone loss may vary with age. This systemic response could contribute to increased future fracture risk following fracture, and these data may inform clinical treatment of fractures with respect to improving long-term skeletal health.

scholarly journals Sickle cell disease promotes sex-dependent pathological bone loss through enhanced cathepsin proteolytic activity

2021 ◽  
Author(s):  
Jada M Selma ◽  
Hannah Song ◽  
Christian Rivera ◽  
Simone Andrea Douglas ◽  
Abhiramgopal Akella ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Bone Loss ◽  
Sickle Cell ◽  
Sickle Cell Trait ◽  
Bone Microarchitecture ◽  
The United States ◽  
Cell Disease ◽  
Female Mice ◽  
Blood Disorder ◽  
The Impact

Sickle cell disease (SCD) is the most common hereditary blood disorder in the United States. SCD is frequently associated with osteonecrosis, osteoporosis and osteopenia and other bone related complications such as vaso-occlusive pain, ischemic damage, osteomyelitis, and bone marrow hyperplasia known as sickle bone disease (SBD)1,2. Previous SBD models have failed to distinguish the age- and sex-specific characteristics of bone morphometry. In this study, we use the Townes mouse model of SCD to study the pathophysiological complications of SBD in both SCD and sickle cell trait. Changes in bone microarchitecture and bone development were assessed by high-resolution quantitative micro-computed tomography (microCT) and the 3D reconstruction of femurs from male and female mice. Our results indicate that SCD causes bone loss and sex-dependent anatomical changes in bone. Particularly, SCD female mice are prone to trabecular bone loss while cortical bone degradation occurs in both sexes. Additionally, we describe the impact of genetic knockdown of cathepsin K and E-64 mediated cathepsin inhibition on SBD.

scholarly journals Vitamin D deficiency is associated with cortical bone loss and fractures in the elderly

2019 ◽  
Vol 181 (5) ◽  
pp. 509-517 ◽  
Author(s):  
F P Paranhos-Neto ◽  
L Vieira Neto ◽  
M Madeira ◽  
A B Moraes ◽  
L M C Mendonça ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Loss ◽  
Vitamin D Deficiency ◽  
Cortical Bone ◽  
Vertebral Fractures ◽  
Elderly Women ◽  
Bone Microarchitecture ◽  
Quantitative Computed Tomography ◽  
X Rays ◽  
Cortical Bone Loss

Introduction The role of vitamin D on bone microarchitecture and fragility is not clear. Objective To investigate whether vitamin D deficiency (25(OH)D <20 ng/mL) increases cortical bone loss and the severity of fractures. Design Cross-sectional study of 287 elderly women with at least one prevalent low-impact fracture. Methods Biochemistry, X-rays to identify vertebral fractures (VFs) and to confirm non-vertebral fractures (NonVFs), and high-resolution peripheral quantitative computed tomography (HR-pQCT) to evaluate bone microstructure. Results Serum 25(OH)D levels were associated with body mass index (BMI: r = −0.161, P = 0.006), PTH (r = −0.165; P = 0.005), CTX (r = −0.119; P = 0.043) and vBMD at cortical bone (Dcomp: r = 0.132; P = 0.033) and entire bone (D100: r = 0.162 P = 0.009) at the distal radius, but not at the tibia. Age and PTH levels were potential confounding variables, but in the multiple linear regressions only BMI (95% CI: 0.11–4.16; P < 0.01), 25(OH)D (95% CI: −0.007 to 1.70; P = 0.05) and CTX (95% CI: −149.04 to 21.80; P < 0.01) predicted Dcomp, while BMI (95% CI: 1.13–4.18; P < 0.01) and 25(OH)D (95% CI: 0.24–1.52; P < 0.01) predicted D100. NonVFs predominated in patients with 25(OH)D <20 ng/mL (P = 0.013). Logistic regression analysis showed a decrease in the likelihood of presenting grade 2–3 VFs/NonVFs for every increase in 25(OH)D (OR = 0.962, 95% CI: 0.940–0.984; P = 0.001), BMI (OR = 0.932, 95% CI: 0.885–0.981; P = 0.007) and D100 at radius (OR = 0.994, 95% CI: 0.990–0.998; P = 0.005). Conclusion In elderly patients with prevalent fractures, vitamin D deficiency was associated with cortical bone loss and severity of fractures.

Characterization of Skeletal Phenotype and Associated Mechanisms With Chronic Intestinal Inflammation in the Winnie Mouse Model of Spontaneous Chronic Colitis

2021 ◽  
Author(s):  
Ahmed Al Saedi ◽  
Shilpa Sharma ◽  
Ebrahim Bani Hassan ◽  
Lulu Chen ◽  
Ali Ghasem-Zadeh ◽  
...  
Keyword(s):  
Bone Loss ◽  
Mouse Model ◽  
Bone Formation ◽  
Intestinal Inflammation ◽  
Bone Microarchitecture ◽  
Mineral Apposition Rate ◽  
Serotonin Level ◽  
Chronic Colitis ◽  
Skeletal Phenotype ◽  
Chronic Intestinal Inflammation

Abstract Background Osteoporosis is a common extraintestinal manifestation of inflammatory bowel disease (IBD). However, studies have been scarce, mainly because of the lack of an appropriate animal model of colitis-associated bone loss. In this study, we aimed to decipher skeletal manifestations in the Winnie mouse model of spontaneous chronic colitis, which carries a MUC2 gene mutation and closely replicates ulcerative colitis. In our study, Winnie mice, prior to the colitis onset at 6 weeks old and progression at 14 and 24 weeks old, were compared with age-matched C57BL/6 controls. We studied several possible mechanisms involved in colitis-associated bone loss. Methods We assessed for bone quality (eg, microcomputed tomography [micro-CT], static and dynamic histomorphometry, 3-point bending, and ex vivo bone marrow analysis) and associated mechanisms (eg, electrochemical recordings for gut-derived serotonin levels, real-time polymerase chain reaction [qRT-PCR], double immunofluorescence microscopy, intestinal inflammation levels by lipocalin-2 assay, serum levels of calcium, phosphorus, and vitamin D) from Winnie (6–24 weeks) and age-matched C57BL6 mice. Results Deterioration in trabecular and cortical bone microarchitecture, reductions in bone formation, mineral apposition rate, bone volume/total volume, osteoid volume/bone surface, and bone strength were observed in Winnie mice compared with controls. Decreased osteoblast and increased osteoclast numbers were prominent in Winnie mice compared with controls. Upregulation of 5-HTR1B gene and increased association of FOXO1 with ATF4 complex were identified as associated mechanisms concomitant to overt inflammation and high levels of gut-derived serotonin in 14-week and 24-week Winnie mice. Conclusions Skeletal phenotype of the Winnie mouse model of spontaneous chronic colitis closely represents manifestations of IBD-associated osteoporosis/osteopenia. The onset and progression of intestinal inflammation are associated with increased gut-derived serotonin level, increased bone resorption, and decreased bone formation.

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