Evidence of a link between resting energy expenditure and bone remodelling, glucose homeostasis and adipokine variations in adolescent girls with anorexia nervosa
UNLABELLED: Low bone mass is a consequence of anorexia nervosa (AN). This study assessed the effects of energy deficiency on various bone and hormonal parameters. The interrelationships between energy deficiency and bone remodelling, glucose homeostasis and adipokines underscore the importance of preventing energy deficiency to limit demineralisation and hormonal alterations in AN patients.
INTRODUCTION: Low areal bone mineral density (aBMD) is a well-known consequence of AN. However, the impact of reduced energy expenditure on bone metabolism is unknown. This study assessed the effects of energy deficiency on bone remodelling and its potential interactions with glucose homeostasis and adipose tissue-derived hormones in AN, a clinical model for reduced energy expenditure.
METHODS: Fifty women with AN and 50 age-matched controls (mean age 18.1 ± 2.7 and 18.0 ± 2.1 years, respectively) were enrolled. aBMD was determined with DXA. Resting energy expenditure (REEm), a marker of energy status, was indirectly assessed by calorimetry. Bone turnover markers, undercarboxylated osteocalcin (ucOC), parameters of glucose homeostasis, adipokines and growth factors were concomitantly evaluated.
RESULTS: AN patients presented low aBMD at all bone sites. REEm, bone formation markers, ucOC, glucose, insulin, HOMA-IR, leptin and IGF-1 were significantly reduced, whereas the bone resorption marker, leptin receptor (sOB-R) and adiponectin were elevated in AN compared with CON. In AN patients, REEm was positively correlated with weight, BMI, whole body (WB) fat mass, WB fat-free soft tissue, markers of bone formation, glucose, insulin, HOMA-IR, leptin and IGF-1 and negatively correlated with the bone resorption marker and sOB-R. Biological parameters, aBMD excepted, appeared more affected by the weight variation in the last 6 months than by the disease duration.
CONCLUSIONS: The strong interrelationships between REEm and bone remodelling, glucose homeostasis and adipokines underscore the importance of preventing energy deficiency to limit short- and long-term bone demineralisation and hormonal alterations in AN patients.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2016 |
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Erschienen: |
2016 |
Enthalten in: |
Zur Gesamtaufnahme - volume:27 |
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Enthalten in: |
Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA - 27(2016), 1 vom: 06. Jan., Seite 135-46 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Maïmoun, L [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 24.10.2016 Date Revised 13.11.2018 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1007/s00198-015-3223-x |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM25156648X |
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245 | 1 | 0 | |a Evidence of a link between resting energy expenditure and bone remodelling, glucose homeostasis and adipokine variations in adolescent girls with anorexia nervosa |
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500 | |a Date Revised 13.11.2018 | ||
500 | |a published: Print-Electronic | ||
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520 | |a UNLABELLED: Low bone mass is a consequence of anorexia nervosa (AN). This study assessed the effects of energy deficiency on various bone and hormonal parameters. The interrelationships between energy deficiency and bone remodelling, glucose homeostasis and adipokines underscore the importance of preventing energy deficiency to limit demineralisation and hormonal alterations in AN patients | ||
520 | |a INTRODUCTION: Low areal bone mineral density (aBMD) is a well-known consequence of AN. However, the impact of reduced energy expenditure on bone metabolism is unknown. This study assessed the effects of energy deficiency on bone remodelling and its potential interactions with glucose homeostasis and adipose tissue-derived hormones in AN, a clinical model for reduced energy expenditure | ||
520 | |a METHODS: Fifty women with AN and 50 age-matched controls (mean age 18.1 ± 2.7 and 18.0 ± 2.1 years, respectively) were enrolled. aBMD was determined with DXA. Resting energy expenditure (REEm), a marker of energy status, was indirectly assessed by calorimetry. Bone turnover markers, undercarboxylated osteocalcin (ucOC), parameters of glucose homeostasis, adipokines and growth factors were concomitantly evaluated | ||
520 | |a RESULTS: AN patients presented low aBMD at all bone sites. REEm, bone formation markers, ucOC, glucose, insulin, HOMA-IR, leptin and IGF-1 were significantly reduced, whereas the bone resorption marker, leptin receptor (sOB-R) and adiponectin were elevated in AN compared with CON. In AN patients, REEm was positively correlated with weight, BMI, whole body (WB) fat mass, WB fat-free soft tissue, markers of bone formation, glucose, insulin, HOMA-IR, leptin and IGF-1 and negatively correlated with the bone resorption marker and sOB-R. Biological parameters, aBMD excepted, appeared more affected by the weight variation in the last 6 months than by the disease duration | ||
520 | |a CONCLUSIONS: The strong interrelationships between REEm and bone remodelling, glucose homeostasis and adipokines underscore the importance of preventing energy deficiency to limit short- and long-term bone demineralisation and hormonal alterations in AN patients | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a Anorexia nervosa | |
650 | 4 | |a Bone remodelling | |
650 | 4 | |a Insulin | |
650 | 4 | |a Leptin | |
650 | 4 | |a Resting energy expenditure | |
650 | 4 | |a Undercarboxylated osteocalcin | |
650 | 7 | |a Adipokines |2 NLM | |
650 | 7 | |a Biomarkers |2 NLM | |
650 | 7 | |a Blood Glucose |2 NLM | |
650 | 7 | |a Intercellular Signaling Peptides and Proteins |2 NLM | |
700 | 1 | |a Guillaume, S |e verfasserin |4 aut | |
700 | 1 | |a Lefebvre, P |e verfasserin |4 aut | |
700 | 1 | |a Philibert, P |e verfasserin |4 aut | |
700 | 1 | |a Bertet, H |e verfasserin |4 aut | |
700 | 1 | |a Picot, M-C |e verfasserin |4 aut | |
700 | 1 | |a Gaspari, L |e verfasserin |4 aut | |
700 | 1 | |a Paris, F |e verfasserin |4 aut | |
700 | 1 | |a Seneque, M |e verfasserin |4 aut | |
700 | 1 | |a Dupuys, A-M |e verfasserin |4 aut | |
700 | 1 | |a Courtet, P |e verfasserin |4 aut | |
700 | 1 | |a Thomas, E |e verfasserin |4 aut | |
700 | 1 | |a Mariano-Goulart, D |e verfasserin |4 aut | |
700 | 1 | |a Bringer, J |e verfasserin |4 aut | |
700 | 1 | |a Renard, E |e verfasserin |4 aut | |
700 | 1 | |a Sultan, C |e verfasserin |4 aut | |
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