Impact of energy and casein or whey protein intake on bone status in a rat model of age-related bone loss

Mardon, Julie; Zangarelli, Aude; Walrand, Stéphane; Davicco, Marie-Jeanne; Lebecque, Patrice; Demigné, Christian; Horcajada, Marie‐Noëlle; Boirie‌, Yves; Coxam, Véronique

doi:10.1017/s0007114507837469

Cited by 17 publications

(22 citation statements)

References 52 publications

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“…Indeed, in contrast with our previous findings in old rats (2,3), dietary restrictions did not induce body weight loss but only erased weight gain, suggesting a slowing down of the growth rate. The supplementation of dietary protein limited the bone loss due to energy deficiency, whereas it failed to improve bone status in old rats.…”

Section: Discussioncontrasting

confidence: 99%

“…At the diaphyseal site, femoral biomechanical properties were highly correlated with BMD values (r ϭ 0.618, p Ͻ 0.0001) and tended to be impaired by the two types of restriction. As previously reported, this observation might also be attributed to decreased diaphyseal cortical area, which contributes to bone fragility (3). Similarly, Talbott et al (18) observed decreased BMD and BMC, respectively, in rats after 9 and 16 wk of 40% energy restriction.…”

Section: Discussionmentioning

confidence: 61%

“…In particular, alterations in energy intake have been demonstrated to impair bone quality and strength in rodent models (1)(2)(3)(4)(5). Lamothe et al (1) and Mardon et al (2) reported that energy restriction adversely affected bone mineral content (BMC), bone mineral density (BMD), and mechanical properties in old rats, despite a micronutrient compensation.…”

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confidence: 99%

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Dietary Protein Supplementation Increases Peak Bone Mass Acquisition in Energy-Restricted Growing Rats

et al. 2009

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Peak bone mass is a major determinant of osteoporosis pathogenesis during aging. Respective influences of energy and protein supplies on skeletal growth remains unclear. We investigated the effect of a 5-mo dietary restriction on bone status in young rats randomized into six groups (n ϭ 10 per group). Control animals were fed a diet containing a normal (13%) (C-NP) or a high-protein content (26%) (C-HP). The other groups received a 40% protein energy-restricted diet (PER-NP and PER-HP) or a 40% energyrestricted diet (ER-NP and ER-HP). High-protein intake did not modulate bone acquisition, although a metabolic acidosis was induced and calcium retention impaired. PER and ER diets were associated with a decrease in femoral bone mineral density. The compensation for protein intake in energy-restricted conditions induced a bone sparing effect. Plasma osteocalcin (OC) and urinary deoxypyridinoline (DPD) assays revealed a decreased OC/DPD ratio in restricted rats compared with C animals, which was far more reduced in PER than in ER groups. Circulating IGF-1 levels were lowered by dietary restrictions. In conclusion, both energy and protein deficiencies may contribute to impairment in peak bone mass acquisition, which may affect skeleton strength and potentially render individuals more susceptible to osteoporosis. In particular, alterations in energy intake have been demonstrated to impair bone quality and strength in rodent models (1-5). Lamothe et al. (1) and Mardon et al. (2) reported that energy restriction adversely affected bone mineral content (BMC), bone mineral density (BMD), and mechanical properties in old rats, despite a micronutrient compensation. Nevertheless, the impact of energy restriction on bone was suggested to be modulated by the age at onset of restriction (5,6). To date, no clear consensus regarding the effects of energy restriction on peak bone mass acquisition has been established.Protein intake is widely linked to bone growth, hence to bone strength (7). Indeed, collagen is the major constituent of bone organic matrix, and noncollagenic proteins are involved in the regulation of the mineralization process. Dietary proteins provide the essential amino acids necessary for new matrix synthesis and may modulate circulating IGF-1 levels as well, an osteotrophic growth factor (8). In growing animals, protein deficiency was demonstrated to lead to decreased bone status (9). Ammann et al. (10) also reported that a 2.5% casein diet during 16 wk in 5-mo-old rats was associated with bone loss.Consequently, one would expect high-protein intake to promote bone health. However, other reports suggest that such a diet may alter calcium homeostasis in ways that could lead to bone loss (11,12). The metabolic acidosis, derived from sulfur amino acids catabolism, would also exert a direct stimulatory effect on bone resorption and an inhibitory action on matrix mineralization (13,14). Actually, the role of dietary protein on bone remains controversial.In the current context of rising incidence of obesity...

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 61%

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Dietary Protein Supplementation Increases Peak Bone Mass Acquisition in Energy-Restricted Growing Rats

et al. 2009

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“…Nevertheless, because the protein intake was sufficient in all groups and within the normal range of intake (15-22%) [50, 51], we would expect no differential effect on bone. For example, a previous study found that even at 40% (vs. 17%) protein intake had no effect on bone parameters in older mice [52]. Similarly, the vitamin/mineral content differed slightly between groups since intake was lower in the HFD compared to the NFD group.…”

Section: Discussionmentioning

confidence: 97%

High fat diet enriched with saturated, but not monounsaturated fatty acids adversely affects femur, and both diets increase calcium absorption in older female mice

et al. 2016

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Diet induced obesity has been shown to reduce bone mineral density (BMD) and Ca absorption. However, previous experiments have not examined the effect of high fat diet (HFD) in the absence of obesity or addressed the type of dietary fatty acids. The primary objective of this study was to determine the effects of different types of high fat feeding, without obesity, on fractional calcium absorption (FCA) and bone health. It was hypothesized that dietary fat would increase FCA and reduce BMD. Mature 8-month-old female C57BL/6J mice were fed one of three diets: a HFD (45% fat) enriched either with monounsaturated fatty acids (MUFAs) or with saturated fatty acids (SFAs), and a normal fat diet (NFD; 10% fat). Food consumption was controlled to achieve a similar body weight gain in all groups. After 8wk, total body bone mineral content and BMD as well as femur total and cortical volumetric BMD were lower in SFA compared with NFD groups (P < 0.05). In contrast, femoral trabecular bone was not affected by the SFAs, whereas MUFAs increased trabecular volume fraction and thickness. The rise over time in FCA was greater in mice fed HFD than NFD and final FCA was higher with HFD (P < 0.05). Intestinal calbindin-D9k gene and hepatic cytochrome P450 2r1 protein levels were higher with the MUFA than the NFD diet (P < 0.05). In conclusion, HFDs elevated FCA overtime; however, an adverse effect of HFD on bone was only observed in the SFA group, while MUFAs show neutral or beneficial effects.

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“…Energy restriction is known to decrease bone mass density in adult rats (37), indicating that the decreased energy balance in pmch Ϫ/Ϫ rats could result in osteoporosis. Hypogonadism is another known inducer of osteoporosis (15,63).…”

Section: E483mentioning

confidence: 99%

Pmchexpression during early development is critical for normal energy homeostasis

Mul

Berg³

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Mul JD, Yi CX, van den Berg SAA, Ruiter M, Toonen PW, van der Elst MCJ, Voshol PJ, Ellenbroek BA, Kalsbeek A, la Fleur SE, Cuppen E. Pmch expression during early development is critical for normal energy homeostasis. Am J Physiol Endocrinol Metab 298: E477-E488, 2010. First published November 24, 2009 doi:10.1152/ajpendo.00154.2009.-Postnatal development and puberty are times of strong physical maturation and require large quantities of energy. The hypothalamic neuropeptide melanin-concentrating hormone (MCH) regulates nutrient intake and energy homeostasis, but the underlying mechanisms are not completely understood. Here we use a novel rat knockout model in which the MCH precursor Pmch has been inactivated to study the effects of loss of MCH on energy regulation in more detail. Pmch Ϫ/Ϫ rats are lean, hypophagic, osteoporotic, and although endocrine parameters were changed in pmch Ϫ/Ϫ rats, endocrine dynamics were normal, indicating an adaptation to new homeostatic levels rather than disturbed metabolic mechanisms. Detailed body weight growth and feeding behavior analysis revealed that Pmch expression is particularly important during early rat development and puberty, i.e., the first 8 postnatal weeks. Loss of Pmch resulted in a 20% lower set point for body weight that was determined solely during this period and remained unchanged during adulthood. Although the final body weight is diet dependent, the Pmch-deficiency effect was similar for all diets tested in this study. Loss of Pmch affected energy expenditure in both young and adult rats, although these effects seem secondary to the observed hypophagia. Our findings show an important role for Pmch in energy homeostasis determination during early development and indicate that the MCH receptor 1 system is a plausible target for childhood obesity treatment, currently a major health issue in first world countries. melanin-concentrating hormone; hypothalamus; childhood obesity; rat knockout model CHILDHOOD OBESITY IS NOW WIDELY recognized as a severe public health issue (43). Treatment with drugs aimed at neural systems involved in the determination of the energy balance could potentially result in a lower energy balance during puberty as well as later in adulthood. Therefore, neuropeptides involved in body weight regulation during early development and puberty are attractive targets for anti-childhood obesity drugs.The neuronal metabolic systems in humans and primates develop prenatally, while in rodents these systems develop during the first 3 postnatal weeks (5, 21). This results in the activation and optimization of neuronal systems during early rodent development. A second important metabolic period is puberty, a period of major growth, hormonal changes, and sexual maturation. In the rat, puberty is characterized by different responses of young-adolescent [postnatal day (PND) 40] and young-adult (PND 60) male rats to environmental cues like stress and cold (17,18). In addition to these age-dependent behavioral differences, the amount of food consumed durin...

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Impact of energy and casein or whey protein intake on bone status in a rat model of age-related bone loss

Cited by 17 publications

References 52 publications

Dietary Protein Supplementation Increases Peak Bone Mass Acquisition in Energy-Restricted Growing Rats

Dietary Protein Supplementation Increases Peak Bone Mass Acquisition in Energy-Restricted Growing Rats

High fat diet enriched with saturated, but not monounsaturated fatty acids adversely affects femur, and both diets increase calcium absorption in older female mice

Pmchexpression during early development is critical for normal energy homeostasis

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