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Bone marrow fat accumulation accelerated by high fat diet is suppressed by exercise.

ABSTRACT: Marrow adipose tissue (MAT), associated with skeletal fragility and hematologic insufficiency, remains poorly understood and difficult to quantify. We tested the response of MAT to high fat diet (HFD) and exercise using a novel volumetric analysis, and compared it to measures of bone quantity. We hypothesized that HFD would increase MAT and diminish bone quantity, while exercise would slow MAT acquisition and promote bone formation. Eight week-old female C57BL/6 mice were fed a regular (RD) or HFD, and exercise groups were provided voluntary access to running wheels (RD-E, HFD-E). Femoral MAT was assessed by ?CT (lipid binder osmium) using a semi-automated approach employing rigid co-alignment, regional bone masks and was normalized for total femoral volume (TV) of the bone compartment. MAT was 2.6-fold higher in HFD relative to RD mice. Exercise suppressed MAT in RD-E mice by more than half compared with RD. Running similarly inhibited MAT acquisition in HFD mice. Exercise significantly increased bone quantity in both diet groups. Thus, HFD caused significant accumulation of MAT; importantly running exercise limited MAT acquisition while promoting bone formation during both diets. That MAT is exquisitely responsive to diet and exercise, and its regulation by exercise appears to be inversely proportional to effects on exercise induced bone formation, is relevant for an aging and sedentary population.

SUBMITTER: Styner M

PROVIDER: S-EPMC4041820 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature

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Bone marrow fat accumulation accelerated by high fat diet is suppressed by exercise.

Styner Maya M Thompson William R WR Galior Kornelia K Uzer Gunes G Wu Xin X Kadari Sanjay S Case Natasha N Xie Zhihui Z Sen Buer B Romaine Andrew A Pagnotti Gabriel M GM Rubin Clinton T CT Styner Martin A MA Horowitz Mark C MC Rubin Janet J

Bone 20140405

Marrow adipose tissue (MAT), associated with skeletal fragility and hematologic insufficiency, remains poorly understood and difficult to quantify. We tested the response of MAT to high fat diet (HFD) and exercise using a novel volumetric analysis, and compared it to measures of bone quantity. We hypothesized that HFD would increase MAT and diminish bone quantity, while exercise would slow MAT acquisition and promote bone formation. Eight week-old female C57BL/6 mice were fed a regular (RD) or H ...[more]

PMID: 24709686

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Project description:BackgroundBone marrow osteoblasts and adipocytes are derived from a common mesenchymal stem cell and have a reciprocal relationship. Peroxisome proliferator-activated receptor gamma (PPARγ), a regulator for adipocyte differentiation, may be a potential target for reducing obesity and increasing bone mass.ObjectivesThis study tested the hypothesis that bone-specific Pparg conditional knockout (cKO), via deletion of Pparg from bone marrow stromal cells (BMSC) using Osterix 1 (Osx1)-Cre, would prevent high-fat (HF) diet-induced bone deterioration in mice.MethodsPPARγ cKO (PPARγfl/fl: Osx1-Cre) and floxed littermate control (PPARγfl/fl Osx1-Cre- ) mice that were 6 weeks old were randomly assigned to 4 groups (n = 12/group, 6 male and 6 female) and fed ad libitum with either a normal-fat (NF) purified diet (3.85 kcal/g; 10% energy as fat) or an HF diet (4.73 kcal/g; 45% energy as fat) for 6 mo. Bone structure, body composition, and serum bone-related cytokines were measured. Data were analyzed by 2-way ANOVA with Tukey post hoc comparison.ResultsThe HF diet decreased the tibial and lumbar vertebrae trabecular bone volume/total volume (BV/TV) by 28% and 18%, respectively, compared to the NF diet (P < 0.01). PPARγ cKO mice had 23% lower body fat mass and 9% lower lean mass than control mice. PPARγ cKO mice had 41% greater tibial trabecular BV/TV compared to control mice. None of trabecular bone parameters at the second lumbar vertebra were affected by genotype. PPARγ cKO mice had decreased cortical thickness compared to control mice. PPARγ cKO mice had a 14% lower (P < 0.01) serum concentration of leptin and a 35% higher (P < 0.05) concentration of osteocalcin compared with control mice.ConclusionsThese data indicate that PPARγ has site-specific impacts on bone structures in mice and that knockout PPARγ in BMSC increased bone mass (BV/TV) in the tibia but not the lumbar vertebrae. PPARγ disruption in BMSC did not prevent HF diet-induced bone deterioration in mice.

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Bone marrow fat accumulation accelerated by high fat diet is suppressed by exercise.

Publications

Bone marrow fat accumulation accelerated by high fat diet is suppressed by exercise.

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