Isoflavone Consumption Does Not Increase the Bone Mass in Osteopenic Obese Female Zucker Rats

Picherit, Christel; Horcajada, Marie‐Noëlle; Mathey, Jacinthe; Chanteranne, Brigitte; Puel, Caroline; Lebecque, Patrice; Davicco, Marie-Jeanne; Coxam, Véronique; Barlet, J.P.

doi:10.1159/000069274

Cited by 17 publications

(14 citation statements)

References 39 publications

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“…In addition, the ZDF rats excreted urinary calcium at high levels compared to lean rats. More recently, Picherit et al (2003) reported that, at 24 weeks of age, the total, diaphyseal, and metaphyseal femoral bone densities of ZDF rats were significantly lower than those of littermate lean rats while in 12-week old animals, these parameters were no different in the two groups. Similarly, serum osteocalcin levels were lower in the ZDF rats than in lean controls at both 12 and 24 weeks of age, but the difference was statistically significant only in 24-week-old animals.…”

Section: Discussionmentioning

confidence: 96%

“…All male ZDF rats develop obesity, hyperleptinemia, hyperglycemia, hyperinsulinemia, and insulin resistance when fed a rodent diet of Purina 5008. Recent studies have shown that many diabetic complications are found in ZDF rats, including periodontal disease (Ryan et al 1999) and diabetic osteopenia (Shibata et al 2000, Picherit et al 2003.…”

Section: Discussionmentioning

confidence: 99%

“…This is characterized by hyperglycemia, hyperinsulinemia, insulin resistance, and obesity in all males (Shibata et al 2000). Recent studies have shown that many diabetic complications are found in the ZDF rats, including periodontal disease (Ryan et al 1999) and diabetic osteopenia (Shibata et al 2000, Picherit et al 2003. Decreased serum osteocalcin has been found in ZDF rats with diabetic osteopenia, which suggests that reduced bone density in ZDF rats may be associated with depressed osteoblast activities that would result in a decline in bone formation.…”

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confidence: 99%

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A novel rat model for the study of deficits in bone formation in type-2 diabetes

et al. 2007

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Background There is evidence to suggest that impairment in bone formation and/or turnover is associated with the metabolic abnormalities characteristic of type-2 diabetes mellitus. However, bone regeneration/repair in type-2 diabetes has not been modeled. Using Zucker Diabetic Fatty (ZDF) rats (a model of type-2 diabetes) for tibial distraction osteogenesis (DO), we hypothesized that bone formation within the distraction gap would be impaired.Animals and methods Rats were examined for body weight, glycosuria, and glycosemia to confirm the diabetic condition during the study. The rats received placement of the external fixators and osteotomies on the left tibia. Distraction was initiated the following day at 0.2 mm twice a day and continued for 14 days. The lengthened tibiae were harvested and distraction gaps were examined radiographically and histologically.Results We found significant reduction in new bone formation in the distraction gaps of the ZDF rats, both radiographically and histologically, compared to lean rats. We found a decrease in a marker of cellular proliferation in the distraction gaps and increased adipose volume in adjacent bone marrow of the ZDF rats.Interpretation Our findings suggest that this model might be used to study the contributions of leptin resistance, insulin resistance and/or hyperglycemia to impaired osteoblastogenesis in vivo.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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A novel rat model for the study of deficits in bone formation in type-2 diabetes

et al. 2007

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“…In contrast to studies on mice, obese fa/fa rats, which have a mutated leptin receptor, are reported to have a decreased bone mass (Foldes et al 1992, Picherit et al 2003. Models in which leptin has been administered centrally via an i.c.v route have shown a reduced bone mass (Ducy et al 2000, Takeda et al 2002, Elefteriou et al 2004.…”

Section: Discussionmentioning

confidence: 98%

Skeletal bone morphology is resistant to the high amplitude seasonal leptin cycle in the Siberian hamster

Rousseau

Atcha²,

Denton³

et al. 2005

Journal of Endocrinology

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Recent studies have suggested that the adipocyte-derived hormone, leptin, plays a role in the regulation of metabolism. Here, we tested this hypothesis in the seasonally breeding Siberian hamster, as this species exhibits profound seasonal changes in adiposity and circulating leptin concentrations driven by the annual photoperiodic cycle. Male hamsters were kept in either long (LD) or short (SD) photoperiods. Following exposure to short photoperiods for 8 weeks animals exhibited a significant weight-loss and a 16-fold reduction of serum leptin concentrations. At Week 9, animals in both photoperiods were infused with leptin or PBS via osmotic mini-pump for 14 days. Chronic leptin infusion mimicked LD-like concentrations in SDhoused animals and caused a further decline in body weight and adipose tissue. In LD-housed animals, leptin infusion resulted in a significant elevation of serum concentrations above natural LD-like levels, but had no discernable effect on body weight or overall adiposity. Both bending and compression characteristics and histomorphometric measurements of trabecular bone mass were unaltered by leptin treatment or photoperiod. Our data therefore show that despite a high natural amplitude cycle of leptin, this hormone has no apparent role in the regulation of bone metabolism, and therefore do not support recent propositions that this hormone is an important component in the metabolism of bone tissue.

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“…Lower femoral BMD and osteocalcin (a marker of bone formation) serum were described in fa/fa rats, as well as decreased trabecular bone volume, trabecular thickness and trabecular number, as measured both by micro-CT and histomorphometry. Picherit et al have compared femoral bone density and biochemical markers of bone metabolism in male and female fatty (leptin-resistant) Zucker rats and their lean homozygous controls at 3 and 6 months of age [39]. Tamasi et al used female leptin receptor-deficient Zucker (fa/fa) rats and their homozygous (Fa/Fa) and heterozygous (Fa/fa) lean controls at 9 and 15 weeks of age.…”

Section: Arbeiten Originalmentioning

confidence: 99%

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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Isoflavone Consumption Does Not Increase the Bone Mass in Osteopenic Obese Female Zucker Rats

Cited by 17 publications

References 39 publications

A novel rat model for the study of deficits in bone formation in type-2 diabetes

A novel rat model for the study of deficits in bone formation in type-2 diabetes

Skeletal bone morphology is resistant to the high amplitude seasonal leptin cycle in the Siberian hamster

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

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