Search Results
Search for other papers by Katherine Van Loon in
Google Scholar
PubMed
Search for other papers by Li Zhang in
Google Scholar
PubMed
Search for other papers by Jennifer Keiser in
Google Scholar
PubMed
Search for other papers by Cendy Carrasco in
Google Scholar
PubMed
Search for other papers by Katherine Glass in
Google Scholar
PubMed
Search for other papers by Maria-Teresa Ramirez in
Google Scholar
PubMed
Search for other papers by Sarah Bobiak in
Google Scholar
PubMed
Search for other papers by Eric K Nakakura in
Google Scholar
PubMed
Search for other papers by Alan P Venook in
Google Scholar
PubMed
Search for other papers by Manisha H Shah in
Google Scholar
PubMed
Search for other papers by Emily K Bergsland in
Google Scholar
PubMed
Neuroendocrine tumors (NETs) metastasize to bone; however, a multi-institution evaluation of the natural history and complications of bone metastases across multiple NET subtypes has not, to our knowledge, previously been conducted. At two tertiary academic centers, we identified patients with bone metastases from databases of patients with a diagnosis of NET between 2004 and 2008. Detection of bone metastases, occurrence of skeletal-related events (SREs), and interventions were analyzed using summary statistics and categorical methods. Time-to-event data were assessed using Kaplan–Meier estimates and log-rank tests. Between 2004 and 2008, 82 out of 691 NET patients (12%) were reported to have bone metastases. Of the 82 patients with bone metastases, 55% were men and their median age was 49. Bone metastases occurred in 25% of pheochromocytomas and paragangliomas, 20% of high-grade neuroendocrine carcinomas, 9% of carcinoid tumors, and 8% of pancreatic NETs. At time of detection of bone metastases, 60% reported symptoms, including pain; 10% developed cord compression, 9% suffered a pathological fracture, and 4% developed hypercalcemia. Occurrence of SREs did not differ significantly with regard to tumor histology. Of patients with bone metastases, 67 (82%) received at least one form of bone-directed treatment, 50% received radiation, 45% received a bisphosphonate, 18% underwent surgery, 11% received 131I-MIBG, 5% received denosumab, and 46% were treated with more than one treatment modality. Bone metastases occur in a substantial number of patients diagnosed with NETs. Patients are often symptomatic and many develop SREs. Given the recent therapeutic advances and increasing life expectancy of patients with NETs, development of guidelines for surveillance and clinical care of bone metastases from NETs is needed.
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Marie Reeberg Sass in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Search for other papers by Nicolai Jacob Wewer Albrechtsen in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Endocrinology and Nephrology, Nordsjællands University Hospital, Hillerød, Denmark
Search for other papers by Jens Pedersen in
Google Scholar
PubMed
Search for other papers by Kristine Juul Hare in
Google Scholar
PubMed
Center for Neonatal Screening, Department of Congenital Disorders, Statens Serum Institute, Copenhagen, Denmark
Search for other papers by Nis Borbye-Lorenzen in
Google Scholar
PubMed
Search for other papers by Katalin Kiss in
Google Scholar
PubMed
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Search for other papers by Tina Vilsbøll in
Google Scholar
PubMed
Steno Diabetes Center Copenhagen, Gentofte, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
Search for other papers by Filip Krag Knop in
Google Scholar
PubMed
Search for other papers by Steen Seier Poulsen in
Google Scholar
PubMed
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Niklas Rye Jørgensen in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Jens Juul Holst in
Google Scholar
PubMed
Search for other papers by Cathrine Ørskov in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Bolette Hartmann in
Google Scholar
PubMed
Objective:
Parathyroid hormone (PTH) is a key hormone in regulation of calcium homeostasis and its secretion is regulated by calcium. Secretion of PTH is attenuated during intake of nutrients, but the underlying mechanism(s) are unknown. We hypothesized that insulin acts as an acute regulator of PTH secretion.
Methods:
Intact PTH was measured in plasma from patients with T1D and matched healthy individuals during 4-h oral glucose tolerance tests (OGTT) and isoglycemic i.v. glucose infusions on 2 separate days. In addition, expression of insulin receptors on surgical specimens of parathyroid glands was assessed by immunochemistry (IHC) and quantitative PCR (qPCR).
Results:
The inhibition of PTH secretion was more pronounced in healthy individuals compared to patients with T1D during an OGTT (decrementalAUC0–240min: −5256 ± 3954 min × ng/L and −2408 ± 1435 min × ng/L, P = 0.030). Insulin levels correlated significantly and inversely with PTH levels, also after adjusting for levels of several gut hormones and BMI (P = 0.002). Expression of insulin receptors in human parathyroid glands was detected by both IHC and qPCR.
Conclusion:
Our study suggests that insulin may act as an acute regulator of PTH secretion in humans.
Search for other papers by Maryam Iravani in
Google Scholar
PubMed
Search for other papers by Marie K Lagerquist in
Google Scholar
PubMed
Search for other papers by Elham Karimian in
Google Scholar
PubMed
Institute for Regenerative Medicine, Sechenov University, Moscow, Russian Federation
Search for other papers by Andrei S Chagin in
Google Scholar
PubMed
Search for other papers by Claes Ohlsson in
Google Scholar
PubMed
Search for other papers by Lars Sävendahl in
Google Scholar
PubMed
Estrogens may affect bone growth locally or systemically via the known estrogen receptors ESR1, ESR2 and G protein-coupled estrogen receptor 1 (GPER1). Mouse and human growth plate chondrocytes have been demonstrated to express GPER1 and ablation of this receptor increased bone length in mice. Therefore, GPER1 is an attractive target for therapeutic modulation of bone growth, which has never been explored. To investigate the effects of activated GPER1 on the growth plate, we locally exposed mouse metatarsal bones to different concentrations of the selective GPER1 agonist G1 for 14 days ex vivo. The results showed that none of the concentrations of G1 had any direct effect on metatarsal bone growth when compared to control. To evaluate if GPER1 stimulation may systemically modulate bone growth, ovariectomized C57BL/6 mice were treated with G1 or β-estradiol (E2). Similarly, G1 did not influence tibia and femur growth in treated mice. As expected, E2 treatment suppressed bone growth in vivo. We conclude that ligand stimulation of GPER1 does not influence bone growth in mice.
Search for other papers by Haojie Zhang in
Google Scholar
PubMed
Search for other papers by Yuke Cui in
Google Scholar
PubMed
Search for other papers by Ruihua Dong in
Google Scholar
PubMed
Search for other papers by Wen Zhang in
Google Scholar
PubMed
Search for other papers by Shihan Chen in
Google Scholar
PubMed
Search for other papers by Heng Wan in
Google Scholar
PubMed
Search for other papers by Chi Chen in
Google Scholar
PubMed
Search for other papers by Yi Chen in
Google Scholar
PubMed
Search for other papers by Yuying Wang in
Google Scholar
PubMed
Search for other papers by Chunfang Zhu in
Google Scholar
PubMed
Search for other papers by Bo Chen in
Google Scholar
PubMed
Search for other papers by Ningjian Wang in
Google Scholar
PubMed
Search for other papers by Yingli Lu in
Google Scholar
PubMed
Background
Bone is thought to be the reservoir of the human lead burden, and vitamin D is associated with bone turnover. We aimed to explore whether exposure to lower 25-hydroxy vitamin D (25(OH)D) levels was associated with higher blood lead levels (BLLs) by increasing the bone turnover rate in individuals with type 2 diabetes.
Methods
A total of 4103 type 2 diabetic men and postmenopausal women in Shanghai, China, were enrolled in 2018. Their 25(OH)D, β-C-terminal telopeptide (β-CTX), N-MID osteocalcin and procollagen type 1 N-peptide (P1NP) levels were detected. Their BLLs were determined by atomic absorption spectrometry. Mediation analyses were performed to identify the possible role that bone turnover played in the underlying mechanisms.
Results
In both the men and postmenopausal women, all three bone turnover markers were inversely associated with 25(OH)D and positively associated with the BLL (all P < 0.01) after adjusting for age, current smoking habits, metabolic parameters, duration of diabetes, vitamin D intake, and use of anti-osteoporosis medication. In the mediation analyses, none of the direct associations between 25(OH)D and BLL was significant for the three bone turnover markers, but all three bone turnover markers were found to be significant mediators of the indirect associations between 25(OH)D and BLL.
Conclusion
The association between vitamin D and BLL was fully mediated by bone turnover markers in type 2 diabetic patients (mediation effect). This finding suggested that vitamin D may protect against blood lead exposure from the bone reservoir by decreasing bone turnover in individuals with type 2 diabetes.
Search for other papers by Stephen A Martin in
Google Scholar
PubMed
Search for other papers by Kenneth A Philbrick in
Google Scholar
PubMed
Search for other papers by Carmen P Wong in
Google Scholar
PubMed
Search for other papers by Dawn A Olson in
Google Scholar
PubMed
Search for other papers by Adam J Branscum in
Google Scholar
PubMed
Search for other papers by Donald B Jump in
Google Scholar
PubMed
Search for other papers by Charles K Marik in
Google Scholar
PubMed
Search for other papers by Jonathan M DenHerder in
Google Scholar
PubMed
Search for other papers by Jennifer L Sargent in
Google Scholar
PubMed
Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA
Search for other papers by Russell T Turner in
Google Scholar
PubMed
Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA
Search for other papers by Urszula T Iwaniec in
Google Scholar
PubMed
Mice are a commonly used model to investigate aging-related bone loss but, in contrast to humans, mice exhibit cancellous bone loss prior to skeletal maturity. The mechanisms mediating premature bone loss are not well established. However, our previous work in female mice suggests housing temperature is a critical factor. Premature cancellous bone loss was prevented in female C57BL/6J mice by housing the animals at thermoneutral temperature (where basal rate of energy production is at equilibrium with heat loss). In the present study, we determined if the protective effects of thermoneutral housing extend to males. Male C57BL/6J mice were housed at standard room temperature (22°C) or thermoneutral (32°C) conditions from 5 (rapidly growing) to 16 (slowly growing) weeks of age. Mice housed at room temperature exhibited reductions in cancellous bone volume fraction in distal femur metaphysis and fifth lumbar vertebra; these effects were abolished at thermoneutral conditions. Mice housed at thermoneutral temperature had higher levels of bone formation in distal femur (based on histomorphometry) and globally (serum osteocalcin), and lower global levels of bone resorption (serum C-terminal telopeptide of type I collagen) compared to mice housed at room temperature. Thermoneutral housing had no impact on bone marrow adiposity but resulted in higher abdominal white adipose tissue and serum leptin. The overall magnitude of room temperature housing-induced cancellous bone loss did not differ between male (current study) and female (published data) mice. These findings highlight housing temperature as a critical experimental variable in studies using mice of either sex to investigate aging-related changes in bone metabolism.
Search for other papers by Herjan J T Coelingh Bennink in
Google Scholar
PubMed
Search for other papers by Jan Krijgh in
Google Scholar
PubMed
Search for other papers by Jan F M Egberts in
Google Scholar
PubMed
Search for other papers by Maria Slootweg in
Google Scholar
PubMed
Search for other papers by Harm H E van Melick in
Google Scholar
PubMed
Search for other papers by Erik P M Roos in
Google Scholar
PubMed
Search for other papers by Diederik M Somford in
Google Scholar
PubMed
Search for other papers by Yvette Zimmerman in
Google Scholar
PubMed
Search for other papers by Iman J Schultz in
Google Scholar
PubMed
Search for other papers by Noel W Clarke in
Google Scholar
PubMed
Search for other papers by R Jeroen A van Moorselaar in
Google Scholar
PubMed
Search for other papers by Frans M J Debruyne in
Google Scholar
PubMed
The purpose of androgen deprivation therapy (ADT) in prostate cancer (PCa), using luteinizing hormone-releasing hormone agonists (LHRHa) or gonadotrophin-releasing hormone antagonists, is to suppress the levels of testosterone. Since testosterone is the precursor of estradiol (E2), one of the major undesired effects of ADT is the concomitant loss of E2, causing among others an increased bone turnover and bone loss and an increased risk of osteoporosis and fractures. Therefore, the guidelines for ADT indicate to combine ADT routinely with bone-sparing agents such as bisphosphonates, denosumab or selective estrogen receptor modulators. However, these compounds may have side effects and some require inconvenient parenteral administration. Co-treatment with estrogens is an alternative approach to prevent bone loss and at the same time, to avoid other side effects caused by the loss of estrogens, which is the topic explored in the present narrative review. Estrogens investigated in PCa patients include parenteral or transdermal E2, diethylstilbestrol (DES), and ethinylestradiol (EE) as monotherapy, or high-dose estetrol (HDE4) combined with ADT. Cardiovascular adverse events have been reported with parenteral E2, DES and EE. Encouraging effects on bone parameters have been obtained with transdermal E2 (tE2) and HDE4, in the tE2 development program (PATCH study), and in the LHRHa/HDE4 co-treatment study (PCombi), respectively. Confirmation of the beneficial effects of estrogen therapy with tE2 or HDE4 on bone health in patients with advanced PCa is needed, with special emphasis on bone mass and fracture rate.
Search for other papers by Qian Wang in
Google Scholar
PubMed
Search for other papers by Jiacheng Wang in
Google Scholar
PubMed
Search for other papers by Yunhui Xin in
Google Scholar
PubMed
Search for other papers by Ziyang He in
Google Scholar
PubMed
Search for other papers by Xiang Zhou in
Google Scholar
PubMed
Search for other papers by Xing Liu in
Google Scholar
PubMed
Search for other papers by Teng Zhao in
Google Scholar
PubMed
Search for other papers by Lihan He in
Google Scholar
PubMed
Search for other papers by Hong Shen in
Google Scholar
PubMed
Search for other papers by Mulan Jin in
Google Scholar
PubMed
Search for other papers by Bojun Wei in
Google Scholar
PubMed
Background
Parathyroid carcinoma (PC), often misdiagnosed as a parathyroid adenoma (PA), is prone to local relapse due to the initial surgery being restricted to parathyroid lesions instead of en bloc resection of parathyroid lesions with negative incision margins. However, it is very challenging to distinguish PC from PA preoperatively; hence, this study investigated an effective biomarker for increasing accuracy in PC diagnosis.
Method
First, the differentially expressed circular RNAs between three PC tissues and three PA tissues were screened by high-throughput circular RNA sequencing, and the expression of hsa_circ_0005729 was verified by qRT-PCR in 14 patients with PC and 40 patients with PA. Secondly, the receiver operating characteristic curve and the area under the curve (AUC) were used to analyze the diagnostic efficiency of hsa_circ_0005729 in PC by combining with laboratory data. Thirdly, RNF138mRNA, the corresponding linear transcript of hsa_circ_0005729, was measured, and the relationship between hsa_circ_0005729 and RNF138 mRNA was analyzed in patients with PA and patients with PC.
Results
Hsa_circ_0005729 expression was significantly higher in patients with PC than in patients with PA. Serum calcium (P = 0.045), alkaline phosphatase (ALP) (P = 0.048), and creatinine levels (P = 0.036) were significantly higher in patients with PC than in patients with PA. The AUC increased to 0.86 when hsa_circ_0005729 combined with serum calcium, creatinine, and ALP. In addition, hsa_circ_0005729 was positively correlated with RNF138 mRNA in patients with PA but not in patients with PC.
Conclusion
The novel circular RNA hsa_circ_0005729 was found to have a higher expression in patients with PC, indicating its usefulness for distinguishing PC from PA.
Search for other papers by Kaisa K Ivaska in
Google Scholar
PubMed
Search for other papers by Maikki K Heliövaara in
Google Scholar
PubMed
Search for other papers by Pertti Ebeling in
Google Scholar
PubMed
Search for other papers by Marco Bucci in
Google Scholar
PubMed
Department of Cell Biology and Anatomy, Department of Medicine, Turku PET Centre, Department of Radiology, Medical Imaging Centre of Southwest Finland, Department of Endocrinology, Abdominal Center: Endocrinology, Minerva Foundation Institute for Medical Research, Institute of Biomedicine, University of Turku, FI-20520 Turku, Finland
Department of Cell Biology and Anatomy, Department of Medicine, Turku PET Centre, Department of Radiology, Medical Imaging Centre of Southwest Finland, Department of Endocrinology, Abdominal Center: Endocrinology, Minerva Foundation Institute for Medical Research, Institute of Biomedicine, University of Turku, FI-20520 Turku, Finland
Search for other papers by Ville Huovinen in
Google Scholar
PubMed
Search for other papers by H Kalervo Väänänen in
Google Scholar
PubMed
Department of Cell Biology and Anatomy, Department of Medicine, Turku PET Centre, Department of Radiology, Medical Imaging Centre of Southwest Finland, Department of Endocrinology, Abdominal Center: Endocrinology, Minerva Foundation Institute for Medical Research, Institute of Biomedicine, University of Turku, FI-20520 Turku, Finland
Search for other papers by Pirjo Nuutila in
Google Scholar
PubMed
Department of Cell Biology and Anatomy, Department of Medicine, Turku PET Centre, Department of Radiology, Medical Imaging Centre of Southwest Finland, Department of Endocrinology, Abdominal Center: Endocrinology, Minerva Foundation Institute for Medical Research, Institute of Biomedicine, University of Turku, FI-20520 Turku, Finland
Search for other papers by Heikki A Koistinen in
Google Scholar
PubMed
Insulin signaling in bone-forming osteoblasts stimulates bone formation and promotes the release of osteocalcin (OC) in mice. Only a few studies have assessed the direct effect of insulin on bone metabolism in humans. Here, we studied markers of bone metabolism in response to acute hyperinsulinemia in men and women. Thirty-three subjects from three separate cohorts (n=8, n=12 and n=13) participated in a euglycaemic hyperinsulinemic clamp study. Blood samples were collected before and at the end of infusions to determine the markers of bone formation (PINP, total OC, uncarboxylated form of OC (ucOC)) and resorption (CTX, TRAcP5b). During 4 h insulin infusion (40 mU/m2 per min, low insulin), CTX level decreased by 11% (P<0.05). High insulin infusion rate (72 mU/m2 per min) for 4 h resulted in more pronounced decrease (−32%, P<0.01) whereas shorter insulin exposure (40 mU/m2 per min for 2 h) had no effect (P=0.61). Markers of osteoblast activity remained unchanged during 4 h insulin, but the ratio of uncarboxylated-to-total OC decreased in response to insulin (P<0.05 and P<0.01 for low and high insulin for 4 h respectively). During 2 h low insulin infusion, both total OC and ucOC decreased significantly (P<0.01 for both). In conclusion, insulin decreases bone resorption and circulating levels of total OC and ucOC. Insulin has direct effects on bone metabolism in humans and changes in the circulating levels of bone markers can be seen within a few hours after administration of insulin.
Search for other papers by Jiaxin Luo in
Google Scholar
PubMed
Search for other papers by Weili Yin in
Google Scholar
PubMed
Search for other papers by Qiuxia Lin in
Google Scholar
PubMed
Search for other papers by Juqing Wu in
Google Scholar
PubMed
Search for other papers by Pan Chen in
Google Scholar
PubMed
Search for other papers by Yuanna Ling in
Google Scholar
PubMed
Search for other papers by Jing Wang in
Google Scholar
PubMed
Search for other papers by Zhen Li in
Google Scholar
PubMed
Search for other papers by Liqin Pan in
Google Scholar
PubMed
Search for other papers by Yanying Chen in
Google Scholar
PubMed
Search for other papers by Wei Ouyang in
Google Scholar
PubMed
Search for other papers by Huijuan Feng in
Google Scholar
PubMed
To evaluate the locoregional progression-free survival (LPFS) of bone metastatic lesions from differentiated thyroid cancer (DTC) after radioiodine therapy (RAIT) and to define its influencing factors, we performed a retrospective cohort analysis of 89 patients with bone metastases from DTC who received RAIT in our department over a 17-year period. The median follow-up time was calculated using the reverse Kaplan–Meier method. The log-rank test and a multivariate Cox proportional hazards regression model were performed in the analysis of prognostic indicators for LPFS. In this research, the median follow-up time for all patients was 47 (95% CI, 35.752–58.248) months, and that for patients with no progression was 42 months. The longest follow-up time was 109 months. The median LPFS time was 58 (95% CI, 32.602–83.398) months, and the 3- and 5-year LPFS probabilities were 57.8 and 45.1%, respectively. Multivariate analysis revealed bone structural changes as an independent risk factor for LPFS (P= 0.004; hazard ratio, 49.216; 95% CI, 3.558–680.704). Furthermore, the non–total-lesion uptake subgroup presented a worse LPFS than the total-lesion uptake subgroup in patients with structural bone lesions (P = 0.027). RAIT can improve the LPFS of radioiodine-avid bone metastases from DTC, especially those without bone structural changes.
PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France
Search for other papers by Laurent Maïmoun in
Google Scholar
PubMed
PhyMedExp, Université de Montpellier, INSERM, CNRS, Montpellier, France
Search for other papers by Denis Mariano-Goulart in
Google Scholar
PubMed
Search for other papers by Helena Huguet in
Google Scholar
PubMed
CIC INSERM 1411, Hôpital Gui de Chauliac, CHU Montpellier, Montpellier Cedex 5, France
Institut de Génomique Fonctionnelle, CNRS UMR 5203/INSERM U661/Université Montpellier, Montpellier, France
Search for other papers by Eric Renard in
Google Scholar
PubMed
Search for other papers by Patrick Lefebvre in
Google Scholar
PubMed
CIC INSERM 1411, Hôpital Gui de Chauliac, CHU Montpellier, Montpellier Cedex 5, France
Search for other papers by Marie-Christine Picot in
Google Scholar
PubMed
Search for other papers by Anne-Marie Dupuy in
Google Scholar
PubMed
Département de Biochimie, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France
Search for other papers by Jean-Paul Cristol in
Google Scholar
PubMed
Département d’Urgence et Post-Urgence Psychiatrique, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France
Search for other papers by Philippe Courtet in
Google Scholar
PubMed
Search for other papers by Vincent Boudousq in
Google Scholar
PubMed
Search for other papers by Antoine Avignon in
Google Scholar
PubMed
Département d’Urgence et Post-Urgence Psychiatrique, Hôpital Lapeyronie, CHU Montpellier, Montpellier, France
Search for other papers by Sébastien Guillaume in
Google Scholar
PubMed
Département Endocrinologie, Nutrition, Diabète, Equipe Nutrition, Diabète, CHU Montpellier, Montpellier, France
Search for other papers by Ariane Sultan in
Google Scholar
PubMed
Objectives
The two-fold aim of this study was: (i) to determine the effects of undernutrition on the myokines in patients with restrictive anorexia nervosa (AN) and (ii) to examine the potential link between myokines and bone parameters.
Methods
In this study, 42 young women with restrictive AN and 42 age-matched controls (CON) (mean age, 18.5 ± 4.2 years and 18.6 ± 4.2 years, respectively) were enrolled. aBMD and body composition were determined with DXA. Resting energy expenditure (REEm), a marker of energy status, was indirectly assessed by calorimetry. Bone turnover markers and myokines (follistatin, myostatin and irisin) were concomitantly evaluated.
Results
AN patients presented low aBMD at all bone sites. REEm, bone formation markers, myostatin and IGF-1 were significantly lower, whereas the bone resorption marker and follistatin were higher in AN compared with controls. No difference was observed between groups for irisin levels. When the whole population was studied, among myokines, only myostatin was positively correlated with aBMD at all bone sites. However, multiple regression analyses showed that in the AN group, the independent variables for aBMD were principally amenorrhoea duration, lean tissue mass (LTM) and procollagen type I N-terminal propeptide (PINP). For CON, the independent variables for aBMD were principally LTM, age and PINP. Whatever the group analysed, none of the myokines appeared as explicative independent variables of aBMD.
Conclusion
This study demonstrated that despite the altered myokine levels in patients with AN, their direct effect on aBMD loss and bone turnover alteration seems limited in comparison with other well-known disease-related factors such as oestrogen deprivation.
