Protein Intake and Bone Growth

2001 ◽  
Vol 26 (S1) ◽  
pp. S153-S166 ◽  
Author(s):  
Jean-Philippe Bonjour ◽  
Patrick Ammann ◽  
Thierry Chevalley ◽  
René Rizzoli
Keyword(s):  
Bone Mass ◽  
Protein Intake ◽  
Bone Growth ◽  
Bone Mineralization ◽  
Weight Bearing ◽  
Positive Association ◽  
Healthy Children ◽  
Low Protein ◽  
Bone Response ◽  
Igf I

Among osteotrophic nutrients, proteins play an important role in bone development, thereby influencing peak bone mass. Consequently, protein malnutrition during development can increase the risk of osteoporosis and of fragility fracture later in life. Both animal and human studies indicate that low protein intake can be detrimental for both the acquisition of bone mass during growth and its conservation during adulthood. Low protein intake impairs both the production and action of IGF-I (Insulin-like growthfactor-I). IGF-I is an essential factorf or bone longitudinal growth, as it stimulates proliferation and difef rentiation of chondrocytes in the epiphyseal plate, and also for bone formation. It can be considered as a key factor in the adjustments of calcium-phosphate metabolism required for normal skeletal development and bone mineralization during growth. In healthy children and adolescents, a positive association between the amount of ingested proteins and bone mass gain was observed in both sexes at the level of the lumbar spine, the proximal femur and the midfemoral shaft. This association appears to be particularly significant in prepubertal children. This suggests that, like for the bone response to either the intake of calcium or weight-bearing exercise, the skeleton would be particularly responsive to the protein intake during the years preceding the onset of pubertal maturation.

Influence of protein nutrition on the response of growing lambs to exogenous bovine growth hormone

1991 ◽  
Vol 130 (1) ◽  
pp. 53-61 ◽  
Author(s):  
J. C. MacRae ◽  
L. A. Bruce ◽  
F. D. DeB. Hovell ◽  
I. C. Hart ◽  
J. Inkster ◽  
...  
Keyword(s):  
Protein Intake ◽  
Volatile Fatty Acids ◽  
High Protein ◽  
Anabolic Response ◽  
Indwelling Catheters ◽  
Factor I ◽  
Low Protein ◽  
Igf I ◽  
Plasma Gh ◽  
Protein Supply

ABSTRACT Interactions between protein supply and the anabolic response to exogenous bovine (b) GH have been examined in two experiments using 28–35 kg lambs sustained entirely by intragastric infusion of volatile fatty acids (700 kJ/kg W0·75 per day) into the rumen and the casein (600 mg (low protein; LP) or 1200 mg (high protein; HP)/kg W0·75 per day) into the abomasum. Sheep received continuous i.v. infusions of bGH for 6 days in experiment 1 and for 18 days in experiment 2. Nitrogen balances were determined daily throughout both experiments and blood samples, from indwelling catheters, were assayed for GH, insulin-like growth factor-I (IGF-I), insulin and glucose. Infusion of bGH increased plasma GH concentration by five- to sixfold in all animals. There was an increase in N retention in both HP and LP animals over the first 2–3 days of GH administration. HP animals sustained higher N retentions (31%; P < 0·05) throughout the GH administration but LP animals did not. In contrast, plasma IGF-I concentrations increased progressively over the first 72 to 96 h of GH administration in all sheep and thereafter remained significantly (P < 0·05) elevated until termination of the GH infusion. In lambs which received both HP and LP infusions in experiment 1 the increase in IGF-I concentration by day 6 of GH administration was significantly (P < 0·05) greater when they received the higher protein intake. Plasma insulin concentrations increased rapidly (P < 0·05) with the onset of GH administration to levels which were 2·5 (LP)- and 4·8 (HP)-fold greater than those observed in the pre-and post-GH periods. Glucose concentration also increased during GH administration (P < 0·05), by 35% in LP animals and by 58% in HP animals. High protein availability appeared necessary to sustain a protein anabolic response where lambs received exogenous GH infusions, even though plasma IGF-I concentrations were elevated on both high and low protein treatments. Journal of Endocrinology (1991) 130, 53–61

scholarly journals Dietary protein and bone health

2003 ◽  
Vol 62 (4) ◽  
pp. 867-876 ◽  
Author(s):  
Fiona Ginty
Keyword(s):  
Bone Health ◽  
Dietary Protein ◽  
Protein Intake ◽  
Protein Quality ◽  
Skeletal Development ◽  
Positive Association ◽  
The Elderly ◽  
Dietary Factors ◽  
Low Protein ◽  
The Usa

The effects of dietary protein on bone health are paradoxical and need to be considered in context of the age, health status and usual diet of the population. Over the last 80 years numerous studies have demonstrated that a high protein intake increases urinary Ca excretion and that on average 1 mg Ca is lost in urine for every 1 g rise in dietary protein. This relationship is primarily attributable to metabolism of S amino acids present in animal and some vegetable proteins, resulting in a greater acid load and buffering response by the skeleton. However, many of these early studies that demonstrated the calciuric effects of protein were limited by low subject numbers, methodological errors and the use of high doses of purified forms of protein. Furthermore, the cross-cultural and population studies that showed a positive association between animal-protein intake and hip fracture risk did not consider other lifestyle or dietary factors that may protect or increase the risk of fracture. The effects of protein on bone appear to be biphasic and may also depend on intake of Ca- and alkali-rich foods, such as fruit and vegetables. At low protein intakes insulin-like growth factor production is reduced, which in turn has a negative effect on Ca and phosphate metabolism, bone formation and muscle cell synthesis. Although growth and skeletal development is impaired at very low protein intakes, it is not known whether variations in protein quality affect the achievement of optimal peak bone mass in adolescents and young adults. Prospective studies in the elderly in the USA have shown that the greatest bone losses occur in elderly men and women with an average protein intake of 16–50 g/d. Although a low protein intake may be indicative of a generally poorer diet and state of health, there is a need to evaluate whether there is a lower threshold for protein intake in the elderly in Europe that may result in increased bone loss and risk of osteoporotic fracture.

scholarly journals Effect of Soluble Corn Fiber Supplementation for 1 Year on Bone Metabolism in Children: MetA-Bone Trial Study Protocol-Rationale and Design

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1845-1845
Author(s):  
Maria Trak-Fellermeier ◽  
Cristina Palacios ◽  
Cynthia Pérez ◽  
Fatma Huffman ◽  
Yolangel Hernandez Suarez ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Health ◽  
Calcium Intake ◽  
Calcium Absorption ◽  
Bone Mineralization ◽  
Adult Life ◽  
Corn Fiber ◽  
Major Constituent ◽  
Healthy Children ◽  
Bone Biomarkers

Abstract Objectives The adolescent period is crucial for optimizing future bone health because during these years bone accumulates rapidly accounting for up to half of adult peak bone mass (PBM). Calcium intake during this stage is critical for adequate bone mineralization but this essential nutrient, the major constituent of hydroxyapatite, is usually inadequate in the diets of US adolescents. A strategy to maximize bone mineralization is to increase calcium absorption. This could be achieved by soluble corn fiber (SCF) supplementation, which fermentation through bacteria in the lower intestine produces short-chain fatty acids and increase calcium absorption. However, there are no studies determining the long-term effects of SCF on bone mass in children. The main aim of the MetA-Bone Trial is to determine the effect of one-year SCF supplementation compared to placebo on bone mass in children with low habitual calcium intake. We hypothesize that SCF supplementation will result in a higher Bone Mineral Content. We will also determine the effects of SCF supplementation on bone biomarkers; we hypothesize that supplementation with SCF will result in higher levels of bone formation and lower bone resorption biomarkers. Methods A total of 240 healthy children (10–13 years), with usual low dietary calcium, will be randomized to four experimental groups for 1 year: (1) SCF (12 g/d); (2) SCF (12 g/d) + 600 mg/d of calcium; (3) Placebo (maltodextrin); and (4) Placebo + 600 mg/d of calcium. The supplements will be mixed with a flavored powder beverage to dilute in water and participants will be instructed to drink this twice per day. Bone mass will be measured using dual energy x-ray absorptiometry (DXA) at baseline, 6 and 12 months. Serum bone biomarkers will be measured at baseline and at 12 months. Results NA Conclusions If supplementing diets with SCF lead to higher bone mass during adolescence, this could help achieve the genetic potential for PBM and to start adult life with stronger bones. Incorporating SCF into diets may be a cost-effective intervention for bone health than increasing dairy products consumption, particularly in adolescents. Funding Sources Eunice Kennedy Shriver National Institute of Child Health & Human Development of the National Institutes of Health.

scholarly journals Prepubertal Impact of Protein Intake and Physical Activity on Weight Bearing Peak Bone Mass and Strength in Males

2016 ◽  
pp. jc.2016-2449 ◽  
Author(s):  
Chevalley Thierry ◽  
Jean-Philippe Bonjour ◽  
Marie-Claude Audet ◽  
Fanny Merminod ◽  
Bert van Rietbergen ◽  
...  
Keyword(s):  
Physical Activity ◽  
Bone Mass ◽  
Protein Intake ◽  
Peak Bone Mass ◽  
Weight Bearing

scholarly journals Nutritional Support and Physical Modalities for People with Osteoporosis: Current Opinion

Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2848 ◽  
Author(s):  
Li-Ru Chen ◽  
Peng-Hsuan Hou ◽  
Kuo-Hu Chen
Keyword(s):  
Bone Mass ◽  
Nutritional Support ◽  
Bone Mineralization ◽  
Weight Bearing ◽  
Effective Prevention ◽  
Gradual Loss ◽  
Modifiable Factors ◽  
Hormonal Milieu ◽  
Pharmacologic Agents ◽  
Physical Modalities

Osteoporosis is a vital healthcare issue among elderly people. During the aging process, a gradual loss of bone mass results in osteopenia and osteoporosis. Heritable factors account for 60–80% of optimal bone mineralization, whereas modifiable factors such as nutrition, weight-bearing exercise, body mass, and hormonal milieu affect the development of osteopenia and osteoporosis in adulthood. Osteoporosis substantially increases the risk of skeletal fractures and further morbidity and mortality. The effective prevention of fractures by reducing the loss of bone mass is the primary goal for physicians treating people with osteoporosis. Other than pharmacologic agents, lifestyle adjustment, nutritional support, fall prevention strategies, exercise, and physical modalities can be used to treat osteoporosis or prevent further osteoporotic fracture. Each of these factors, alone or in combination, can be of benefit to people with osteoporosis and should be implemented following a detailed discussion with patients. This review comprises a systematic survey of the current literature on osteoporosis and its nonpharmacologic and nonsurgical treatment. It provides clinicians and healthcare workers with evidence-based information on the assessment and management of osteoporosis. However, numerous issues regarding osteoporosis and its treatment remain unexplored and warrant future investigation.

scholarly journals The dietary protein, IGF-I, skeletal health axis

2016 ◽  
Vol 28 (1) ◽  
Author(s):  
Jean-Philippe Bonjour
Keyword(s):  
Serum Level ◽  
Bone Loss ◽  
Bone Health ◽  
Dietary Protein ◽  
Protein Intake ◽  
Bone Growth ◽  
Height Velocity ◽  
Igf I ◽  
The Impact ◽  
Positive Effect

AbstractDietary protein represents an important nutrient for bone health and thereby for the prevention of osteoporosis. Besides its role as a brick provider for building the organic matrix of skeletal tissues, dietary protein stimulates the production of the anabolic bone trophic factor IGF-I (insulin-like growth factor I). The liver is the main source of circulating IGF-I. During growth, protein undernutrition results in reduced bone mass and strength. Genetic defect impairing the production of IGF-I markedly reduces bone development in both length and width. The serum level of IGF-I markedly increases and then decreases during pubertal maturation in parallel with the change in bone growth and standing height velocity. The impact of physical activity on bone structure and strength is enhanced by increased dietary protein consumption. This synergism between these two important environmental factors can be observed in prepubertal boys, thus modifying the genetically determined bone growth trajectory. In anorexia nervosa, IGF-I is low as well as bone mineral mass. In selective protein undernutrition, there is a resistance to the exogenous bone anabolic effect of IGF-I. A series of animal experiments and human clinical trials underscore the positive effect of increased dietary intake of protein on calcium-phosphate economy and bone balance. On the contrary, the dietary protein-induced acidosis hypothesis of osteoporosis is not supported by several experimental and clinical studies. There is a direct effect of amino acids on the local production of IGF-I by osteoblastic cells. IGF-I is likely the main mediator of the positive effect of parathyroid hormone (PTH) on bone formation, thus explaining the reduction in fragility fractures as observed in PTH-treated postmenopausal women. In elderly women and men, relatively high protein intake protects against spinal and femoral bone loss. In hip fracture patients, isocaloric correction of the relatively low protein intake results in: increased IGF-I serum level, significant attenuation of postsurgical bone loss, improved muscle strength, better recovery, and shortened hospital stay. Thus, dietary protein contributes to bone health from early childhood to old age. An adequate intake of protein should be recommended in the prevention and treatment of osteoporosis.

scholarly journals Combined Treatment With GH and IGF-I: Additive Effect on Cortical Bone Mass But Not on Linear Bone Growth in Female Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (12) ◽  
pp. 4798-4807 ◽  
Author(s):  
Katja Sundström ◽  
Therese Cedervall ◽  
Claes Ohlsson ◽  
Cecilia Camacho-Hübner ◽  
Lars Sävendahl
Keyword(s):  
Bone Mass ◽  
Cortical Bone ◽  
Growth Plate ◽  
Bone Growth ◽  
Combined Therapy ◽  
Combined Treatment ◽  
Female Rats ◽  
Longitudinal Bone Growth ◽  
Igf I ◽  
Cortical Bone Mass

The growth-promoting effect of combined therapy with GH and IGF-I in normal rats is not known. We therefore investigated the efficacy of treatment with recombinant human (rh)GH and/or rhIGF-I on longitudinal bone growth and bone mass in intact, prepubertal, female Sprague-Dawley rats. rhGH was injected twice daily sc (5 mg/kg·d) and rhIGF-I continuously infused sc (2.2 or 4.4 mg/kg·d) for 28 days. Longitudinal bone growth was monitored by weekly x-rays of tibiae and nose-anus length measurements, and tibial growth plate histomorphology was analyzed. Bone mass was evaluated by peripheral quantitative computed tomography. In addition, serum levels of IGF-I, rat GH, acid labile subunit, IGF binding protein-3, 150-kDa ternary complex formation, and markers of bone formation and degradation were measured. Monotherapy with rhGH was more effective than rhIGF-I (4.4 mg/kg·d) to increase tibia and nose-anus length, whereas combined therapy did not further increase tibia, or nose-anus, lengths or growth plate height. In contrast, combined rhGH and rhIGF-I (4.4 mg/kg·d) therapy had an additive stimulatory effect on cortical bone mass vs rhGH alone. Combined treatment with rhGH and rhIGF-I resulted in markedly higher serum IGF-I concentrations vs rhGH alone but did not compromise the endogenous secretion of GH. We conclude that rhIGF-I treatment augments cortical bone mass but does not further improve bone growth in rhGH-treated young, intact, female rats.

scholarly journals SAT0450 GLUCOCORTICOID-INDUCED OSTEOPOROSIS IN PATIENTS WITH CHRONIC INFLAMMATORY RHEUMATIC DISEASES: A MULTIVARIATE LINEAR REGRESSION ANALYSIS IDENTIFYING PREDICTIVE FACTORS FOR LOW BONE MASS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1182.2-1182
Author(s):  
E. Wiebe ◽  
D. Freier ◽  
D. Huscher ◽  
R. Biesen ◽  
S. Hermann ◽  
...  
Keyword(s):  
Bone Mass ◽  
Rheumatic Diseases ◽  
Positive Association ◽  
Fragility Fractures ◽  
Life Time ◽  
Inflammatory Rheumatic Diseases ◽  
Low Bone Mass ◽  
Cross Sectional ◽  
Chronic Inflammatory Rheumatic Diseases ◽  
Prevalence Of Osteoporosis

Background:Rheumatic diseases are associated with increased systemic bone loss and fracture risk related to chronic inflammation, disease-specific, general and demographic risk factors as well as treatment with glucocorticoids (GC). Yet, there is evidence that GCs may, by adequately suppressing systemic inflammation, also have a positive effect on bone mineral density (BMD) and fracture risk1.Objectives:The purpose of this study was to investigate the prevalence of osteoporosis and fragility fractures in patients with inflammatory rheumatic diseases and to analyze the impact that treatment with GCs, other known risk factors and preventive measures have on bone health in these patients.Methods:Rh-GIOP is an ongoing prospective observational study collecting and analyzing disease- and bone-related data from patients with chronic inflammatory rheumatic diseases and psoriasis treated with GCs. In this cross-sectional analysis, we evaluated the initial visit of 1091 patients. A multivariate linear regression model with known or potentially influential factors adjusted for age and sex was used to identify predictors of BMD as measured by dual-energy X-ray absorptiometry (DXA). Multiple imputation was applied for missing baseline covariate data.Results:In the total cohort of 1091 patients (75% female of which 87.5% were postmenopausal) with a mean age of 62.1 (±13.2) years, the prevalence of osteoporosis by DXA was 21.7%, while fragility fractures have occurred in 31.2% of the study population (6.7% vertebral, 27.7% non-vertebral). Current GC therapy was common (64.9%), with a median daily dose of 5.0mg [0.0;7.5], a mean life-time total GC dose of 17.7g (±24.6), and a mean GC therapy duration of 7.8 years (±8.5). Bisphosphonates were the most commonly used anti-osteoporotic drug (12.6%).Multivariate analysis showed that BMD as expressed by the minimum T-Score at all measured sites was negatively associated with higher age, female sex and menopause as well as Denosumab and Bisphosphonate treatment. A positive association with BMD was found for body mass index as well as current and life-time (cumulative) GC dose. While comedication with proton-pump-inhibitors significantly predicted low bone mass, concomitant use of non-steroidal anti-inflammatory drugs showed a positive association with BMD. Of the measured bone-specific laboratory parameters, higher alkaline phosphatase levels were determinants of low DXA-values, while the association was positive for gamma-glutamyltransferase.BMD was neither predicted by duration of GC treatment nor by treatment with disease modifying anti-rheumatic drugs.Predictive variables for BMD differed at the respective anatomical site. While treatment with Denosumab predicted low bone mass at the lumbar spine and not at the femoral neck, the opposite was true for health assessment questionnaire (HAQ) score. Current and life-time GC-dose as well as direct sun-exposure of more than 30 minutes daily were positively associated with bone mass at the femoral sites only.Conclusion:This cross-sectional analysis of a prospective cohort study quantified the prevalence of osteoporosis and identified predictive variables of BMD in patients with rheumatic diseases.Multivariate analyses corroborated low BMD to be predicted by traditional factors like age, female sex and menopause but showed current and well as life-time GC dose to be positively associated with BMD in our cohort of patients with chronic inflammatory rheumatic diseases. This suggests that optimal management of disease activity with GCs might be beneficial in order to avoid bone loss due to inflammation.References:[1]Güler-Yüksel et al. “Glucocorticoids, Inflammation and Bone.” Calcified Tissue International (January 08 2018).Disclosure of Interests:Edgar Wiebe: None declared, Desiree Freier: None declared, Dörte Huscher: None declared, Robert Biesen: None declared, Sandra Hermann: None declared, Frank Buttgereit Grant/research support from: Amgen, BMS, Celgene, Generic Assays, GSK, Hexal, Horizon, Lilly, medac, Mundipharma, Novartis, Pfizer, Roche, and Sanofi.

scholarly journals Differential Diagnosis of the Short IGF-I-Deficient Child with Apparently Normal Growth Hormone Secretion

2021 ◽  
pp. 1-24
Author(s):  
Jan M. Wit ◽  
Sjoerd D. Joustra ◽  
Monique Losekoot ◽  
Hermine A. van Duyvenvoorde ◽  
Christiaan de Bruin
Keyword(s):  
Growth Hormone ◽  
Differential Diagnosis ◽  
Growth Hormone Secretion ◽  
Normal Growth ◽  
Stimulation Test ◽  
Healthy Children ◽  
Genetic Causes ◽  
Gh Secretion ◽  
Igf I

The current differential diagnosis for a short child with low insulin-like growth factor I (IGF-I) and a normal growth hormone (GH) peak in a GH stimulation test (GHST), after exclusion of acquired causes, includes the following disorders: (1) a decreased spontaneous GH secretion in contrast to a normal stimulated GH peak (“GH neurosecretory dysfunction,” GHND) and (2) genetic conditions with a normal GH sensitivity (e.g., pathogenic variants of <i>GH1</i> or <i>GHSR</i>) and (3) GH insensitivity (GHI). We present a critical appraisal of the concept of GHND and the role of 12- or 24-h GH profiles in the selection of children for GH treatment. The mean 24-h GH concentration in healthy children overlaps with that in those with GH deficiency, indicating that the previously proposed cutoff limit (3.0–3.2 μg/L) is too high. The main advantage of performing a GH profile is that it prevents about 20% of false-positive test results of the GHST, while it also detects a low spontaneous GH secretion in children who would be considered GH sufficient based on a stimulation test. However, due to a considerable burden for patients and the health budget, GH profiles are only used in few centres. Regarding genetic causes, there is good evidence of the existence of Kowarski syndrome (due to <i>GH1</i> variants) but less on the role of <i>GHSR</i> variants. Several genetic causes of (partial) GHI are known (<i>GHR</i>, <i>STAT5B</i>, <i>STAT3</i>, <i>IGF1</i>, <i>IGFALS</i> defects, and Noonan and 3M syndromes), some responding positively to GH therapy. In the final section, we speculate on hypothetical causes.

Sign in / Sign up

Export Citation Format

Share Document