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

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.

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

Journal of Cellular Physiology ◽

10.1002/jcp.24954 ◽

2015 ◽

Vol 230 (9) ◽

pp. 2032-2037 ◽

Cited By ~ 93

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

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Osteopontin Deficiency Induces Parathyroid Hormone Enhancement of Cortical Bone Formation

Endocrinology ◽

10.1210/en.2002-220996 ◽

2003 ◽

Vol 144 (5) ◽

pp. 2132-2140 ◽

Cited By ~ 36

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.

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Cold stress and high fat, high protein diet decreases trabecular and cortical bone mass in male C57BL/6J mice

The FASEB Journal ◽

10.1096/fasebj.2019.33.1_supplement.19.1 ◽

2019 ◽

Vol 33 (S1) ◽

Author(s):

Maureen Devlin ◽

Amy Robbins ◽

Christina Tom ◽

Rebecca Tutino ◽

Miranda N. Cosman ◽

...

Keyword(s):

Bone Mass ◽

Cold Stress ◽

Cortical Bone ◽

High Protein Diet ◽

High Protein ◽

Protein Diet ◽

High Fat ◽

Cortical Bone Mass

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Influence of Gastrectomy on Cortical and Cancellous Bones in Rats

Gastroenterology Research and Practice ◽

10.1155/2013/381616 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 6

Author(s):

Jun Iwamoto ◽

Yoshihiro Sato ◽

Hideo Matsumoto

Keyword(s):

Bone Formation ◽

Bone Mass ◽

Cortical Bone ◽

Cancellous Bone ◽

Femoral Diaphysis ◽

Control Group ◽

Sham Operation ◽

Sprague Dawley ◽

Osteoid Surface ◽

Cortical Bone Mass

The aim of the present study was to examine the influence of gastrectomy (GX) on cortical and cancellous bones in rats. Twenty male Sprague-Dawley rats were randomized into the two groups of 10 animals each: a sham operation (control) group and a GX group. Seven weeks after surgery, the bone mineral content and density (BMC and BMD, resp.) and the mechanical strength of the femur were determined, and bone histomorphometric analyses were performed on the tibia. GX induced decreases in the BMC, BMD, ultimate force, work to failure, and stiffness of the femoral distal metaphysis and the BMC, BMD, and ultimate force of the femoral diaphysis. GX induced a decrease in cancellous bone mass, characterized by an increased osteoid thickness, osteoid surface, osteoid volume, and bone formation. GX also induced a decrease in cortical bone mass, characterized by increased endocortical bone resorption. The GX induced reductions in the bone mass and strength parameters were greater in cancellous bone than in cortical bone. The present study showed that the response of bone formation, resorption, and osteoid parameters to GX and the degree of GX-induced osteopenia and the deterioration of bone strength appeared to differ between cortical and cancellous bones in rats.

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Mice lacking estrogen receptor [alpha] in hypothalamic POMC neurons display enhanced estrogenic response on cortical bone mass

Bone Abstracts ◽

10.1530/boneabs.5.ht2 ◽

2016 ◽

Author(s):

Helen Farman ◽

Sara Windahl ◽

Deborah Clegg ◽

Shang Kui Xie ◽

Lars Westberg ◽

...

Keyword(s):

Estrogen Receptor ◽

Bone Mass ◽

Cortical Bone ◽

Estrogen Receptor Alpha ◽

Receptor Alpha ◽

Cortical Bone Mass

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Effects of long-term sedentary behaviour on the cortical bone mass and distribution during growth: The HAPPY bone study

Bone Abstracts ◽

10.1530/boneabs.6.lb10 ◽

2017 ◽

Author(s):

Rachel L Duckham ◽

Timo Rantalainen ◽

Christine Rodda ◽

Anna Timperio ◽

Nicola Hawley ◽

...

Keyword(s):

Bone Mass ◽

Cortical Bone ◽

Sedentary Behaviour ◽

Cortical Bone Mass

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Tissue-specific expression of Sprouty1 in mice protects against high-fat diet-induced fat accumulation, bone loss and metabolic dysfunction

British Journal Of Nutrition ◽

10.1017/s0007114511006209 ◽

2011 ◽

Vol 108 (6) ◽

pp. 1025-1033 ◽

Cited By ~ 7

Author(s):

Sumithra Urs ◽

Terry Henderson ◽

Phuong Le ◽

Clifford J. Rosen ◽

Lucy Liaw

Keyword(s):

Adipose Tissue ◽

Bone Loss ◽

Bone Mass ◽

Body Fat ◽

High Fat Diet ◽

Conditional Knockout ◽

Whole Body ◽

High Fat ◽

Tissue Specific ◽

Diet Induced Obesity

We recently characterised Sprouty1 (Spry1), a growth factor signalling inhibitor as a regulator of marrow progenitor cells promoting osteoblast differentiation at the expense of adipocytes. Adipose tissue-specific Spry1 expression in mice resulted in increased bone mass and reduced body fat, while conditional knockout of Spry1 had the opposite effect with decreased bone mass and increased body fat. Because Spry1 suppresses normal fat development, we tested the hypothesis that Spry1 expression prevents high-fat diet-induced obesity, bone loss and associated lipid abnormalities, and demonstrate that Spry1 has a long-term protective effect on mice fed a high-energy diet. We studied diet-induced obesity in mice with fatty acid binding promoter-driven expression or conditional knockout of Spry1 in adipocytes. Phenotyping was performed by whole-body dual-energy X-ray absorptiometry, microCT, histology and blood analysis. In conditional Spry1-null mice, a high-fat diet increased body fat by 40 %, impaired glucose regulation and led to liver steatosis. However, overexpression of Spry1 led to 35 % (P < 0·05) lower body fat, reduced bone loss and normal metabolic function compared with single transgenics. This protective phenotype was associated with decreased circulating insulin (70 %) and leptin (54 %; P < 0·005) compared with controls on a high-fat diet. Additionally, Spry1 expression decreased adipose tissue inflammation by 45 %. We show that conditional Spry1 expression in adipose tissue protects against high-fat diet-induced obesity and associated bone loss.

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