scholarly journals Micro-architectural changes in cancellous bone differ in female and male C57BL/6 mice with high-fat diet-induced low bone mineral density

2014 ◽  
Vol 111 (10) ◽  
pp. 1811-1821 ◽  
Author(s):  
Jyoti Gautam ◽  
Dharmendra Choudhary ◽  
Vikram Khedgikar ◽  
Priyanka Kushwaha ◽  
Ravi Shankar Singh ◽  
...  
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Cancellous Bone ◽  
High Fat Diet ◽  
Female Rats ◽  
Male Mice ◽  
High Fat ◽  
Mineral Density ◽  
Collagen Crosslinks ◽  
Males And Females

The relationship between fat and bone mass at distinct trabecular and cortical skeletal compartments in a high-fat diet (HFD) model was studied. For this, C57BL/6 mice were assigned to four groups of eight animals each. Two groups, each of males and females, received a standard chow diet while the remaining other two groups received the HFD for a period of 10 weeks. Male mice on the HFD were heavier and gained more weight (15·8 %; P<  0·05) v. those on the control diet or when compared with the female rats fed the HFD. We observed an increased lipid profile in both males and females, with significantly higher lipid levels (about 20–25 %; P< 0·01) in males. However, glucose intolerance was more pronounced in females than males on the HFD (about 30 %; P< 0·05). The micro-architectural assessment of bones showed that compared with female mice on the HFD, male mice on the HFD showed more deterioration at the trabecular region. This was corroborated by plasma osteocalcin and carboxy-terminal collagen crosslinks (CTx) levels confirming greater loss in males (about 20 %; P< 0·01). In both sexes cortical bone parameters and strength remained unchanged after 10 weeks of HFD treatment. The direct effect of the HFD on bone at the messenger RNA level in progenitor cells isolated from femoral bone marrow was a significantly increased expression of adipogenic marker genes v. osteogenic genes. Overall, the present data indicate that obesity induced by a HFD aggravates bone loss in the cancellous bone compartment, with a greater loss in males than females, although 10 weeks of HFD treatment did not alter cortical bone mass and strength in both males and females.

High-fat diet decreases cancellous bone mass but has no effect on cortical bone mass in the tibia in mice

Bone ◽  
2009 ◽  
Vol 44 (6) ◽  
pp. 1097-1104 ◽  
Author(s):  
Jay J. Cao ◽  
Brian R. Gregoire ◽  
Hongwei Gao
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Cancellous Bone ◽  
High Fat Diet ◽  
High Fat ◽  
Cortical Bone Mass

scholarly journals Osteopontin Deficiency Induces Parathyroid Hormone Enhancement of Cortical Bone Formation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2132-2140 ◽  
Author(s):  
Keiichiro Kitahara ◽  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Cancellous Bone ◽  
Wild Type ◽  
Mineral Density ◽  
Cortical Bone Mass ◽  
Intermittent Pth

Intermittent PTH treatment increases cancellous bone mass in osteoporosis patients; however, it reveals diverse effects on cortical bone mass. Underlying molecular mechanisms for anabolic PTH actions are largely unknown. Because PTH regulates expression of osteopontin (OPN) in osteoblasts, OPN could be one of the targets of PTH in bone. Therefore, we examined the role of OPN in the PTH actions in bone. Intermittent PTH treatment neither altered whole long-bone bone mineral density nor changed cortical bone mass in wild-type 129 mice, although it enhanced cancellous bone volume as reported previously. In contrast, OPN deficiency induced PTH enhancement of whole-bone bone mineral density as well as cortical bone mass. Strikingly, although PTH suppressed periosteal bone formation rate (BFR) and mineral apposition rate (MAR) in cortical bone in wild type, OPN deficiency induced PTH activation of periosteal BFR and MAR. In cancellous bone, OPN deficiency further enhanced PTH increase in BFR and MAR. Analysis on the cellular bases for these phenomena indicated that OPN deficiency augmented PTH enhancement in the increase in mineralized nodule formation in vitro. OPN deficiency did not alter the levels of PTH enhancement of the excretion of deoxypyridinoline in urine, the osteoclast number in vivo, and tartrate-resistant acid phosphatase-positive cell development in vitro. These observations indicated that OPN deficiency specifically induces PTH activation of periosteal bone formation in the cortical bone envelope.

scholarly journals Cortical bone adaptation to a moderate level of mechanical loading in male Sost deficient mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Haisheng Yang ◽  
Alexander Büttner ◽  
Laia Albiol ◽  
Catherine Julien ◽  
Tobias Thiele ◽  
...  
Keyword(s):  
Physical Activity ◽  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Bone Adaptation ◽  
Moderate Level ◽  
Skeletal Maturation ◽  
Male Mice ◽  
Males And Females

AbstractLoss-of-function mutations in the Sost gene lead to high bone mass phenotypes. Pharmacological inhibition of Sost/sclerostin provides a new drug strategy for treating osteoporosis. Questions remain as to how physical activity may affect bone mass under sclerostin inhibition and if that effect differs between males and females. We previously observed in female Sost knockout (KO) mice an enhanced cortical bone formation response to a moderate level of applied loading (900 με at the tibial midshaft). The purpose of the present study was to examine cortical bone adaptation to the same strain level applied to male Sost KO mice. Strain-matched in vivo compressive loading was applied to the tibiae of 10-, 26- and 52-week-old male Sost KO and littermate control (LC) mice. The effect of tibial loading on bone (re)modeling was measured by microCT, 3D time-lapse in vivo morphometry, 2D histomorphometry and gene expression analyses. As expected, Sost deficiency led to high cortical bone mass in 10- and 26-week-old male mice as a result of increased bone formation. However, the enhanced bone formation associated with Sost deficiency did not appear to diminish with skeletal maturation. An increase in bone resorption was observed with skeletal maturation in male LC and Sost KO mice. Two weeks of in vivo loading (900 με at the tibial midshaft) induced only a mild anabolic response in 10- and 26-week-old male mice, independent of Sost deficiency. A decrease in the Wnt inhibitor Dkk1 expression was observed 3 h after loading in 52-week-old Sost KO and LC mice, and an increase in Lef1 expression was observed 8 h after loading in 10-week-old Sost KO mice. The current results suggest that long-term inhibition of sclerostin in male mice does not influence the adaptive response of cortical bone to moderate levels of loading. In contrast with our previous strain-matched study in females showing enhanced bone responses with Sost ablation, these results in males indicate that the influence of Sost deficiency on the cortical bone formation response to a moderate level of loading differs between males and females. Clinical studies examining antibodies to inhibit sclerostin may need to consider that the efficacy of additional physical activity regimens may be sex dependent.

scholarly journals Astragalus Extract Mixture HT042 Improves Bone Growth, Mass, and Microarchitecture in Prepubertal Female Rats: A Microcomputed Tomographic Study

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Jungbin Song ◽  
Sung Hyun Lee ◽  
Donghun Lee ◽  
Hocheol Kim
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Bone Growth ◽  
Volume Fraction ◽  
Control Diet ◽  
Female Rats ◽  
Volumetric Bone Mineral Density ◽  
Mineral Density ◽  
Longitudinal Bone Growth ◽  
Tibial Length

Astragalus extract mixture HT042 is a standardized multiherbal mixture comprising Astragalus membranaceus, Eleutherococcus senticosus, and Phlomis umbrosa, which has proven to promote children’s height growth. The aim of this study was to investigate the effects of HT042 on longitudinal bone growth, bone mass, and bone microstructure in growing rats using a high-resolution microcomputed tomography system. Four-week-old female rats were fed an HT042-containing diet for 2 weeks. Tibial length was measured at baseline and weekly in vivo. At the end of the study, volumetric bone mineral density (vBMD) and microarchitectural parameters were estimated in the trabecular and cortical bone of the tibia. Tibial length gain was significantly increased by HT042 compared to that reported with the control diet. In the proximal tibial metaphysis, HT042-treated rats had significantly higher trabecular vBMD, bone volume fraction, and trabecular number and lower trabecular separation, trabecular pattern factor, and structure model index values than control rats did. Total cross-sectional area and bone area of the cortical bone in the tibial diaphysis also increased. These findings suggest that HT042 increases longitudinal bone growth rate, improves trabecular bone mass, and enhances the microarchitecture of trabecular and cortical bone during growth.

Hindlimb unloading has a greater effect on cortical compared with cancellous bone in mature female rats

2003 ◽  
Vol 94 (2) ◽  
pp. 642-650 ◽  
Author(s):  
Matthew R. Allen ◽  
Susan A. Bloomfield
Keyword(s):  
Cortical Bone ◽  
Bone Mineral ◽  
Cancellous Bone ◽  
Proximal Tibia ◽  
Mature Female ◽  
Hindlimb Unloading ◽  
Female Rats ◽  
Female Rat ◽  
Mineral Density ◽  
Tibia Bone

This study was designed to determine the effects of 28 days of hindlimb unloading (HU) on the mature female rat skeleton. In vivo proximal tibia bone mineral density and geometry of HU and cage control (CC) rats were measured with peripheral quantitative computed tomography (pQCT) on days 0and 28. Postmortem pQCT, histomorphometry, and mechanical testing were performed on tibiae and femora. After 28 days, HU animals had significantly higher daily food consumption (+39%) and lower serum estradiol levels (−49%, P = 0.079) compared with CC. Proximal tibia bone mineral content and cortical bone area significantly declined over 28 days in HU animals (−4.0 and 4.8%, respectively), whereas total and cancellous bone mineral densities were unchanged. HU animals had lower cortical bone formation rates and mineralizing surface at tibial midshaft, whereas differences in similar properties were not detected in cancellous bone of the distal femur. These results suggest that cortical bone, rather than cancellous bone, is more prominently affected by unloading in skeletally mature retired breeder female rats.

scholarly journals Negative Influence of a Long-Term High-Fat Diet on Murine Bone Architecture

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Hinrich Fehrendt ◽  
Thomas Linn ◽  
Sonja Hartmann ◽  
Gabor Szalay ◽  
Christian Heiss ◽  
...  
Keyword(s):  
Body Weight ◽  
Bone Mass ◽  
High Fat Diet ◽  
Bone Microstructure ◽  
Negative Influence ◽  
Bone Architecture ◽  
High Fat ◽  
Mineral Density ◽  
Cell Contacts ◽  
Underlying Mechanisms

A correlation between obesity and bone metabolism is strongly assumed because adipocytes and osteoblasts originate from the same precursor cells and their differentiation is conversely regulated by the same factors. It is controversially discussed if obesity protects bone or leads to loss of bone mass. Thus, the aim of the present study was to investigate the influence of diet-induced mild obesity (11% increased body weight compared to control) on bone microstructure in mice. Four-week-old male C57BL/6J mice received a high-fat diet (HFD, 60% kcal from fat) and were analyzed by means of dual X-ray absorptiometry, histological methods, real-time RT-PCR, and transmission electron microscopy in comparison to control animals (10% kcal from fat). The cancellous bone mass, collagen 1α1 expression, amount of osteoid, and cohesion of cells via cell-to-cell contacts decreased in HFD mice whereas the bone mineral density and the amount of osteoblasts and osteoclasts were not modified. The amount of apoptotic osteocytes was increased in HFD mice in comparison to controls. We conclude that moderately increased body weight does not protect bone architecture from age-dependent degeneration. By contrast, bone microstructure is negatively affected and reduced maintenance of cell-cell contacts may be one of the underlying mechanisms.

scholarly journals A High Fat Diet Increases Bone Marrow Adipose Tissue (MAT) But Does Not Alter Trabecular or Cortical Bone Mass in C57BL/6J Mice

2015 ◽  
Vol 230 (9) ◽  
pp. 2032-2037 ◽  
Author(s):  
Casey R. Doucette ◽  
Mark C. Horowitz ◽  
Ryan Berry ◽  
Ormond A. MacDougald ◽  
Rea Anunciado-Koza ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Adipose Tissue ◽  
Bone Mass ◽  
Cortical Bone ◽  
High Fat Diet ◽  
High Fat ◽  
Bone Marrow Adipose Tissue ◽  
Marrow Adipose Tissue ◽  
Cortical Bone Mass

scholarly journals Blueberry and blackcurrant consumption increases bone mineral density and content in high fat diet‐induced obese male mice

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Sang Gil Lee ◽  
Terrence Vance ◽  
Do Yu Soung ◽  
Bohkyung Kim ◽  
Jiyoung Lee ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Mineral ◽  
High Fat Diet ◽  
Male Mice ◽  
High Fat ◽  
Mineral Density ◽  
Obese Male

scholarly journals Flaxseed oil ameliorated high-fat-diet-induced bone loss in rats by promoting osteoblastic function in rat primary osteoblasts

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Fulian Chen ◽  
Yan Wang ◽  
Hongwei Wang ◽  
Zhenhua Dong ◽  
Yan Wang ◽  
...  
Keyword(s):  
Cortical Bone ◽  
High Fat Diet ◽  
Bone Markers ◽  
Maximum Load ◽  
Biomechanical Properties ◽  
Flaxseed Oil ◽  
Fracture Load ◽  
Bone Volume ◽  
High Fat ◽  
Mineral Density

Abstract Background α-Linolenic acid (ALA) is a plant-derived omega-3 unsaturated fatty acid that is rich in flaxseed oil (FO). The effect of FO on bone health is controversial. This study aims to evaluate the effect of FO on bone damage induced by a high-fat diet (HFD) and to explore the possible mechanism. Methods Male Sprague-Dawley rats were fed a normal control diet (NC, 10% fat), FO diet (NY, 10% fat), HFD (60% fat), or HFD containing 10% FO (HY, 60% fat) for 22 weeks. Micro CT and three-point bending tests were conducted to evaluate bone microstructure and biomechanics. Serum was collected for the detection of ALP, P1NP, and CTX-1. Rat primary osteoblasts (OBs) were treated with different concentrations of ALA with or without palmitic acid (PA) treatment. The ALP activity, osteogenic-related gene and protein expression were measured. Results Rats in the HFD group displayed decreased biomechanical properties, such as maximum load, maximum fracture load, ultimate tensile strength, stiffness, energy absorption, and elastic modulus, compared with the NC group (p < 0.05). However, HY attenuated the HFD-induced decreases in bone biomechanical properties, including maximum load, maximum fracture load, and ultimate tensile strength (p < 0.05). Trabecular bone markers such as trabecular volume bone mineral density (Tb. vBMD), trabecular bone volume/total volume (Tb. BV/TV), trabecular number (Tb. N), trabecular thickness (Tb. Th) were decreased, trabecular separation (Tb. Sp) and the structure model index (SMI) were increased in the HFD group compared with the NC group, and all parameters were remarkably improved in the HY group compared to the HFD group (p < 0.05). However, cortical bone markers such as cortical volume bone mineral density (Ct. vBMD), cortical bone volume/total volume (Ct. BV/TV) and cortical bone thickness (Ct. Th) were not significantly different among all groups. Moreover, the serum bone formation markers ALP and P1NP were higher and the bone resorption marker CTX-1 was lower in the HY group compared with levels in the HFD group. Compared with the NC group, the NY group had no difference in the above indicators. In rat primary OBs, PA treatment significantly decreased ALP activity and osteogenic gene and protein (β-catenin, RUNX2, and osterix) expression, and ALA dose-dependently restored the inhibition induced by PA. Conclusions FO might be a potential therapeutic agent for HFD-induced bone loss, most likely by promoting osteogenesis.

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