Hydrolyzed collagen improves bone status and prevents bone loss in ovariectomized C3H/HeN mice

Guillerminet, Fanny; Fabien-Soulé, Véronique; Even, Patrick C.; Tomé, Daniel; Benhamou, Claude-Laurent; Roux, Clément; Blais, Anne

doi:10.1007/s00198-011-1788-6

Cited by 53 publications

(40 citation statements)

References 36 publications

(46 reference statements)

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“…4,[7][8][9][10][11] The effect of CHs on osteoblasts is likely due to its anabolic action, including proliferation and promotion of osteoblastic differentiation. 4,10 The signaling mechanisms of CHs action remain elusive.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 Oral administration of CHs in ovariectomized rats or mice was also demonstrated to reduce bone loss, 9 and increase bone strength 10 and diameter of the cortical areas of femurs. 11 In a previous study, we have demonstrated that CHs (<3 kDa) have growth promoting effects on the longitudinal bone in adolescent rats. 4 However, an in-depth study on the action mechanisms of CHs has not been carried out.…”

Section: Introductionmentioning

confidence: 98%

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Collagen hydrolysates increased osteogenic gene expressions via a MAPK signaling pathway in MG-63 human osteoblasts

Kim

Leem

2014

Food Funct.

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The present study investigated the effects of CHs on osteogenic activities and MAPK-regulation on bone matrix gene expressions. The effects of CHs on cell proliferation, alkaline phosphatase (ALP) activity, collagen synthesis, and mineralization were measured in human osteoblastic MG-63 cells. Activation of MAPKs and downstream transcription factors such as extracellular-signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase 1/2 (JNK1/2), p38, ELK1, and cJUN was examined using Western blot analysis. The expressions of osteogenic genes were measured by quantitative real-time PCR. CHs dose-dependently increased MG-63 cell proliferation, ALP activity, collagen synthesis, and calcium deposition. CHs activated ERK1/2, JNK1/2, p38, and ELK1 phosphorylation except cJUN. The COL1A1 (collagen, type I, alpha 1), ALPL (alkaline phosphatase), BGLAP (osteocalcin), and SPP1 (secreted phosphoprotein 1, osteopontin) gene expressions were increased by CH treatment. The ERK1/2 inhibitor (PD98509) blocked the CH-induced COL1A1 and ALPL gene expression, as well as ELK1 phosphorylation. The JNK1/2 inhibitor (SP600125) abolished CH-induced COL1A1 expression. The p38 inhibitor (SB203580) blocked CH-induced COL1A1 and SPP1 gene expression. In conclusion, CH treatment stimulates the osteogenic activities and increases bone matrix gene expressions via the MAPK/ELK1 signaling pathway. These results could provide a mechanistic explanation for the bone-strengthening effects of CHs.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Collagen hydrolysates increased osteogenic gene expressions via a MAPK signaling pathway in MG-63 human osteoblasts

Kim

Leem

2014

Food Funct.

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“…A second study by the same group showed that the HC administration for 3 or 6 months significantly prevented bone loss in OVX mice (Guillerminet et al, 2012). The authors further demonstrated that HC ingestion for 3 months is as efficient as raloxifene to protect 3-month-old OVX mice from bone loss.…”

Section: Evidence From Animal Modelsmentioning

confidence: 91%

Biological Effect of Hydrolyzed Collagen on Bone Metabolism

Daneault

Coxam

Wittrant

2015

Critical Reviews in Food Science and Nutrition

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Osteoporosis is a chronic and asymptomatic disease characterized by low bone mass and skeletal microarchitectural deterioration, increased risk of fracture, and associated comorbidities most prevalent in the elderly. Due to an increasingly aging population, osteoporosis has become a major health issue requiring innovative disease management. Proteins are important for bone by providing building blocks and by exerting specific regulatory function. This is why adequate protein intake plays a considerable role in both bone development and bone maintenance. More specifically, since an increase in the overall metabolism of collagen can lead to severe dysfunctions and a more fragile bone matrix and because orally administered collagen can be digested in the gut, cross the intestinal barrier, enter the circulation, and become available for metabolic processes in the target tissues, one may speculate that a collagen-enriched diet provides benefits for the skeleton. Collagen-derived products such as gelatin or hydrolyzed collagen (HC) are well acknowledged for their safety from a nutritional point of view; however, what is their impact on bone biology? In this manuscript, we critically review the evidence from literature for an effect of HC on bone tissues in order to determine whether HC may represent a relevant alternative in the design of future nutritional approaches to manage osteoporosis prevention.

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“…The observed effects on body composition and blood plasma parameters could be partly related to a difference in AA profile, as casein is richer than soy primarily in methionine, and also in proline, serine, threonine, glutamine, valine, tyrosine, isoleucine, and leucine (87–89). Previous studies suggested that reduction of particular AAs in the diet can extend lifespan in mice and rats.…”

Section: Protein Quantity/qualitymentioning

confidence: 99%

“…Incidentally, those models have been setup to study not only consequences of estrogen deficiency on obesity but also on various diseases including cancer, osteoporosis, cardiovascular diseases, and inflammation. Using the OVX C3H/Hen mice model to induce bone loss, studies (88, 89) have shown that even when the surgery was performed at 3 or 6 months, the procedure induced an increase in body weight related to an increase in the visceral and subcutaneous fat mass. However, when the OVX procedure was performed at 6 months, reduction of uterus weight was not observed compared to Sham mice.…”

Section: Impact Of Estrogen Deficiency On Body Weight and Physiologicmentioning

confidence: 99%

Animal Models for the Study of the Relationships between Diet and Obesity: A Focus on Dietary Protein and Estrogen Deficiency

et al. 2017

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Obesity is an increasing major public health concern asking for dietary strategies to limit weight gain and associated comorbidities. In this review, we present animal models, particularly rats and mice, which have been extensively used by scientists to understand the consequences of diet quality on weight gain and health. Notably, modulation of dietary protein quantity and/or quality has been shown to exert huge effects on body composition homeostasis through the modulation of food intake, energy expenditure, and metabolic pathways. Interestingly, the perinatal window appears to represent a critical period during which the protein intake of the dam can impact the offspring’s weight gain and feeding behavior. Animal models are also widely used to understand the processes and mechanisms that contribute to obesity at different physiological and pathophysiological stages. An interesting example of such aspect is the situation of decreased estrogen level occurring at menopause, which is linked to weight gain and decreased energy expenditure. To study metabolic disorders associated with such situation, estrogen withdrawal in ovariectomized animal models to mimic menopause are frequently used. According to many studies, clear species-specific differences exist between rats and mice that need to be taken into account when results are extrapolated to humans.

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Hydrolyzed collagen improves bone status and prevents bone loss in ovariectomized C3H/HeN mice

Abstract: This study confirms that dietary collagen reduces bone loss in OVX mice by increasing the diameter of the cortical areas of femurs and can have a preventive effect.

Cited by 53 publications

References 36 publications

Collagen hydrolysates increased osteogenic gene expressions via a MAPK signaling pathway in MG-63 human osteoblasts

Collagen hydrolysates increased osteogenic gene expressions via a MAPK signaling pathway in MG-63 human osteoblasts

Biological Effect of Hydrolyzed Collagen on Bone Metabolism

Animal Models for the Study of the Relationships between Diet and Obesity: A Focus on Dietary Protein and Estrogen Deficiency

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