High fat diet promotes achievement of peak bone mass in young rats

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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Probiotics Reduce the Inflammatory Response Induced by a High-Fat Diet in the Liver of Young Rats

Journal of Nutrition ◽

10.3945/jn.108.101808 ◽

2009 ◽

Vol 139 (5) ◽

pp. 905-911 ◽

Cited By ~ 138

Author(s):

Emanuela Esposito ◽

Anna Iacono ◽

Giuseppe Bianco ◽

Giuseppina Autore ◽

Salvatore Cuzzocrea ◽

...

Keyword(s):

Inflammatory Response ◽

High Fat Diet ◽

High Fat ◽

Young Rats

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Increasing Dietary Fish Oil Reduces Adiposity and Mitigates Bone Deterioration in Growing C57BL/6 Mice Fed a High-Fat Diet

Journal of Nutrition ◽

10.1093/jn/nxz215 ◽

2019 ◽

Vol 150 (1) ◽

pp. 99-107 ◽

Cited By ~ 4

Author(s):

Jay J Cao ◽

Brian R Gregoire ◽

Kim G Michelsen ◽

Matthew J Picklo

Keyword(s):

Adipose Tissue ◽

Bone Mass ◽

Fish Oil ◽

High Fat Diet ◽

Bone Structure ◽

Tartrate Resistant Acid Phosphatase ◽

Serum Concentrations ◽

Obese Mice ◽

High Fat ◽

Long Chain

ABSTRACT Background Intake of total fat is linked to obesity and inversely associated with bone density in humans. Epidemiologic and animal studies show that long-chain n–3 (ω-3) PUFAs supplied as fish oil (FO) are beneficial to skeletal health. Objective This study tested the hypothesis that increasing dietary FO would decrease adiposity and improve bone-related outcomes in growing obese mice. Methods Male C57BL/6 mice at 6 wk old were assigned to 6 treatment groups and fed either a normal-fat diet (3.85 kcal/g and 10% energy as fat) or a high-fat diet (HF; 4.73 kcal/g and 45% energy as fat) containing either 0%, 3%, or 9% energy as FO (0FO, 3FO, and 9FO, respectively) ad libitum for 6 mo. Bone structure, body composition, and serum bone-related cytokines were measured. Results The HF diet increased the expression of the adipose tissue tumor necrosis factor α (Tnfa) and serum concentrations of leptin and tartrate-resistant acid phosphatase (TRAP), and decreased serum concentrations of osteocalcin and bone-specific alkaline phosphatase (P < 0.05). FO decreased fat mass (P < 0.05), serum TRAP (P < 0.05), and adipose tissue Tnfa expression (P < 0.01). Bone content of long-chain n–3 PUFAs was increased and n–6 PUFAs were decreased with the elevation in dietary FO content (P < 0.01). Compared with mice fed 9FO, animals fed 3FO had higher femoral bone volume/total volume (25%), trabecular number (23%), connectivity density (82%), and bone mass of second lumbar vertebrae (12%) and lower femoral trabecular separation (−19%). Mice fed the 3FO HF diet had 42% higher bone mass than those fed the 0FO HF diet. Conclusions These data indicate increasing dietary FO ≤3% energy can decrease adiposity and mitigate HF diet–induced bone deterioration in growing C57BL/6 mice possibly by reducing inflammation and bone resorption. FO at 9% diet energy had no further beneficial effects on bone of obese mice.

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Does the perigestational exposure to chlorpyrifos and/or high-fat diet affect respiratory parameters and diaphragmatic muscle contractility in young rats?

Food and Chemical Toxicology ◽

10.1016/j.fct.2020.111322 ◽

2020 ◽

Vol 140 ◽

pp. 111322

Author(s):

Hiba El Khayat El Sabbouri ◽

Jérôme Gay-Quéheillard ◽

Wissam H. Joumaa ◽

Stephane Delanaud ◽

Marion Guibourdenche ◽

...

Keyword(s):

High Fat Diet ◽

High Fat ◽

Muscle Contractility ◽

Young Rats ◽

Diaphragmatic Muscle ◽

Respiratory Parameters

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Exposure Duration Is a Determinant of the Effect of Sinusoidal Electromagnetic Fields on Peak Bone Mass of Young Rats

Calcified Tissue International ◽

10.1007/s00223-018-0396-2 ◽

2018 ◽

Vol 103 (1) ◽

pp. 95-106 ◽

Cited By ~ 2

Author(s):

B. Y. Zhu ◽

Z. D. Yang ◽

X. R. Chen ◽

J. Zhou ◽

Y. H. Gao ◽

...

Keyword(s):

Bone Mass ◽

Electromagnetic Fields ◽

Exposure Duration ◽

Peak Bone Mass ◽

Young Rats

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

British Journal Of Nutrition ◽

10.1017/s0007114514000051 ◽

2014 ◽

Vol 111 (10) ◽

pp. 1811-1821 ◽

Cited By ~ 35

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.

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Deficiency of PPAR Gamma in Bone Marrow Stromal Cells Does Not Prevent High-Fat Diet-Induced Bone Deterioration in Mice

Current Developments in Nutrition ◽

10.1093/cdn/nzab055_010 ◽

2021 ◽

Vol 5 (Supplement_2) ◽

pp. 1200-1200

Author(s):

Jay Cao ◽

Brian Gregoire ◽

Kim Michelsen ◽

Xingming Shi

Keyword(s):

Bone Marrow ◽

Bone Mass ◽

Stromal Cells ◽

High Fat Diet ◽

Bone Marrow Stromal Cells ◽

Bone Structure ◽

Lumbar Vertebrae ◽

Ppar Gamma ◽

Marrow Stromal Cells ◽

High Fat

Abstract Objectives Obesity is detrimental to bone health in humans and in high-fat diet-induced obese animals. Bone marrow osteoblasts and adipocytes are derived from a common mesenchymal stem cell and have a reciprocal relationship. Peroxisome proliferator-activated receptor gamma (PPAR gamma), a regulator for adipocyte differentiation, may be a potential target for reducing obesity and increasing bone mass. This study tested the hypothesis that bone-specific PPAR gamma conditional knockout (cKO), via deletion of PPAR gamma gene from bone marrow stromal cells (BMSC) using Osterix 1 (Osx1)-Cre, would prevent high-fat diet-induced bone deterioration in mice. Methods PPAR gamma cKO (PPAR gammafl/fl: Osx1–Cre) and floxed littermate control (PPAR gammafl/fl Osx1-P-Cre-) mice at 6-wk-old were randomly assigned to 4 groups (n = 12/group, 6 male and 6 female) and fed ad libitum either a normal-fat purified diet (NF, 3.85 kcal/g, 10% energy as fat) or a high-fat diet (HF, 4.73 kcal/g) for 6 mo. Bone structure, body composition, and serum bone-related cytokines were measured. Results Compared to the NF diet, the HF diet increased body mass and fat mass (P < 0.05) but not lean mass. The HF diet also decreased tibial and lumbar vertebrae trabecular volume/total volume (BV/TV) and bone mineral density (BMD) in both control and PPAR gamma cKO mice. PPAR gamma cKO mice had lower body fat mass and lean mass than control mice. PPAR gamma cKO mice had greater tibial trabecular BV/TV, trabecular number, connectivity density, and BMD and lower structure model index, compared to control mice. None of trabecular bone parameters at 2nd lumbar vertebrae was affected by genotype. PPAR gamma cKO mice had lower cortical medullary area, compared to control mice. PPAR gamma cKO mice had lower (P < 0.01) serum concentration of leptin and higher (P < 0.05) concentration of osteocalcin, compared with control mice. Conclusions These data indicate that PPAR gamma has site-specific impact on bone structure in mice and that knockout PPAR gamma in BMSC increased bone mass in tibia likely through increased osteoblastogenesis. However, PPAR gamma disruption in BMSC did not prevent high-fat diet-induced bone deterioration in mice. Funding Sources USDA-ARS #3062-51,000-053-00D.

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