The effects of dietary-induced obesity on the biomechanical properties of femora in male rats

Brahmabhatt, V; Rho, Jae-Young; Bernardis, Lee L.; Gillespie, Roberta A.; Ziv, Israel

doi:10.1038/sj.ijo.0800668

Cited by 22 publications

(22 citation statements)

References 17 publications

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“…In addition to previous studies of the skeletal effects of obesity, the current study specifically examined the effects of increased intakes of calcium and vitamin D -key dietary components essential for bone health -on bone status and its regulation in DIO. The results obtained show that the weight of long bones (tibia and femur) was increased, although not significantly, in DIO mice, which is consistent with other studies evaluating bone status in obesity [42][43][44]. More significantly, the relative bone weight and the bone calcium and phosphorus content were dramatically decreased in the DIO group.…”

Section: Discussionsupporting

confidence: 90%

High vitamin D and calcium intakes increase bone mineral (Ca and P) content in high-fat diet-induced obese mice

Song

Сергеев

2015

Nutrition Research

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Section: Discussionsupporting

confidence: 90%

High vitamin D and calcium intakes increase bone mineral (Ca and P) content in high-fat diet-induced obese mice

Song

Сергеев

2015

Nutrition Research

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“…A study of bone biomechanics in adult rats with diet-induced obesity showed significantly greater bone strength in the obese rats than in the controls. The cross-sectional geometry and ultimate fracture load of the femur were higher in the obese rats than in the controls [8]. In our study, however, there were no significant differences in trabecular and cortical bone mass between the leptin-deficient obese mice and the leptin-deficient control mice.…”

Section: Discussioncontrasting

confidence: 75%

No Adaptations in Bone of Leptin-Deficient ob/ob Mice in Response to Loading

Heep¹,

Wedemeyer²,

Xu³

et al. 2008

BIOmaterialien

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Leptin is a peptide hormone produced predominantly by white fat cells [1,47]. The mature protein, encoded by the obesity (ob) gene localized in human and mouse 7 and 6 chromosomes, respectively, is a 16 kDa non-glycosylated protein. Leptin levels in the blood are proportional to adipose tissue mass. Initially discovered as a central regulator of appetite and energy expenditure, leptin levels can be considered as a signal to the body regarding its energy reserves. Although elevated leptin levels are present in obesity, it is likely that the physiological importance of leptin is that low levels indicate a state of starvation [2]. Recent data suggest that leptin may regulate a variety of other physiological processes, such as insulin action [7], hemopoiesis [5], immune function [28], reproduction [40], angiogenesis [26], and bone development and remodeling [19]. However, it is not clear whether leptin is a stimulator or an inhibitor of bone growth in humans. Some investigators noted a positive relationship between serum leptin levels and bone mineral density (BMD). Iwamoto et al. described a weakly correlation of serum leptin level with bone mineral density of pelvis and left leg in the premenopausal women and Odebasi et al. found that there was no correlation between plasma leptin concentrations and BMD values in healthy postmenopausal woman but a weak correlation was observed in postmenopausal woman with osteoporosis [23,35]. Whereas others observed a negative relationship. Blum et al. suggest that for a given body weight, a higher proportion of fat and a higher serum leptin concentration have negative associations with bone mass in premenopausal women [6]. Sato et al. suggest that an increase in serum leptin reduces bone formation and decreases BMD in adult men [42]. Furthermore, no associations between serum leptin levels and BMD have been reported, which further confounds the interpretation of leptin's effect on bone mass. Martini et al. conclude that serum leptin have no direct effect on bone mass and bone turnover in healthy postmenopausal women [32] and Rauch et al. appear that leptin has less influence on the mature than on the growing skeleton [41]. Only a few studies in humans have examined the direct effect of leptin administration on BMD. Ogueh et al. [36] Leptin was found to be involved in regulation of bone development and remodeling. This study was performed to evaluate the effects of biomechanical loading due to body weight in leptin-defient ob/ob mice at the same pubertal stage. No significant difference was found between the two groups for all the parameters (p>0.05) suggesting that the presence of leptin may be an important pre-condition for positive correlation between loading and bone mass. Furthermore, concordance of bone formation was found among appendicular regions, but was not found between the axial and appendicular regions.

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“…Surprisingly, only a few studies have addressed this question using animal models. Rat studies have found reductions in yield and maximum stresses, energy absorption, structural rigidity and failure loads, despite larger bone sizes as a result of high-fat and high-sugar diet-induced obesity [17,18,19]. Conclusions have not always been consistent; however, in general, a significant decrease in mechanical performance (reduced bone quality) concurrent with an increase in bone size (increased bone quantity) has been reported.…”

Section: Introductionmentioning

confidence: 99%

Reduced size-independent mechanical properties of cortical bone in high-fat diet-induced obesity

Ionova-Martin

Barth

et al. 2010

Bone

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Overweight and obesity is a rapidly expanding health problem in children and adolescents. Obesity is associated with greater bone mineral content that might be expected to protect against fracture, which has been observed in adults. Paradoxically however, the incidence of bone fractures has been found to increase in overweight and obese children and adolescents. Prior studies have shown some reduced mechanical properties as a result of high-fat diet (HFD) but do not fully address size-independent measures of mechanical properties, which are important to understand material behavior. To clarify the effects of HFD on the mechanical properties and microstructure of bone, femora from C57BL/6 mice fed either a HFD or standard laboratory chow (Chow) were evaluated for structural changes and tested for bending strength, bending stiffness and fracture toughness. Here we find that in young obese high fat fed mice all geometric parameters of the femoral bone, except length, are increased but strength, bending stiffness and fracture toughness all are reduced. This increased bone size and reduced size-independent mechanical properties suggests that obesity leads to a general reduction in bone quality despite an increase in bone quantity; yield and maximum loads, however, remained unchanged, suggesting compensatory mechanisms. We conclude that diet-induced obesity increases bone size and reduces size-independent mechanical properties of cortical bone in mice. This study indicates that bone quantity and bone quality play important compensatory roles in determining fracture risk.

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The effects of dietary-induced obesity on the biomechanical properties of femora in male rats

Cited by 22 publications

References 17 publications

High vitamin D and calcium intakes increase bone mineral (Ca and P) content in high-fat diet-induced obese mice

High vitamin D and calcium intakes increase bone mineral (Ca and P) content in high-fat diet-induced obese mice

No Adaptations in Bone of Leptin-Deficient ob/ob Mice in Response to Loading

Reduced size-independent mechanical properties of cortical bone in high-fat diet-induced obesity

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