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Article: Hypophosphatasia: Biological and Clinical Aspects, Avenues for Therapy.

Salles, Jean Pierre

2019 Volume 41, Issue 1, Page(s) 13–27

Abstract: Hypophosphatasia (HPP) is a rare inherited systemic metabolic disease caused by mutations in the tissue-nonspecific alkaline phosphatase ( ...

Abstract	Hypophosphatasia (HPP) is a rare inherited systemic metabolic disease caused by mutations in the tissue-nonspecific alkaline phosphatase (
Language	English
Publishing date	2019-12-10
Publishing country	Australia
Document type	Journal Article ; Review
ZDB-ID	1018054-0
ISSN	1838-0212 ; 0159-8090
ISSN (online)	1838-0212
ISSN	0159-8090
DOI	10.33176/AACB-19-00031
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Article ; Online: Biochemical assessment of phosphate homeostasis.

Houillier, Pascal / Salles, Jean-Pierre

Archives de pediatrie : organe officiel de la Societe francaise de pediatrie

2021 Volume 28, Issue 7, Page(s) 588–593

Abstract: Phosphate homeostasis is a requirement for normal life. Phosphate is involved in the synthesis of membrane lipids, DNA, RNA, and energy-rich molecules (ATP and GTP), and the regulation of protein activity by phosphorylation/dephosphorylation. Moreover, ... ...

Abstract	Phosphate homeostasis is a requirement for normal life. Phosphate is involved in the synthesis of membrane lipids, DNA, RNA, and energy-rich molecules (ATP and GTP), and the regulation of protein activity by phosphorylation/dephosphorylation. Moreover, phosphate is a component of apatite crystals, which provide stability to the bone, and is essential for normal growth. Phosphate balance in the body is the difference between net phosphate absorption through the intestine and phosphate excretion through the kidney. Numerous disorders, both genetic and acquired, may alter phosphate homeostasis. In affected individuals, it is crucial to identify the underlying mechanism(s) to provide adequate treatment; however, phosphate homeostasis assessment remains challenging. Besides the measurement of key hormones involved in the control of phosphate homeostasis (parathyroid hormone, vitamin D and metabolites, fibroblast growth factor 23), assessing the magnitude of phosphate reabsorption by the kidney is a crucial step. It makes it possible to distinguish between a primary disorder of renal phosphate reabsorption, associated with an intrinsic defect or endocrine disturbance, and a nutritional cause of phosphate deficiency. This strategy is described, and the potential consequences for therapeutic decisions are discussed.
MeSH term(s)	Biochemical Phenomena/physiology ; Fibroblast Growth Factors/pharmacokinetics ; Fibroblast Growth Factors/pharmacology ; Homeostasis/drug effects ; Homeostasis/physiology ; Humans ; Phosphates/metabolism
Chemical Substances	Phosphates ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
Language	English
Publishing date	2021-09-28
Publishing country	France
Document type	Journal Article
ZDB-ID	1181947-9
ISSN	1769-664X ; 0929-693X
ISSN (online)	1769-664X
ISSN	0929-693X
DOI	10.1016/j.arcped.2021.09.001
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Article ; Online: Growth Hormone Dose Modulation and Final Height in Short Children Born Small for Gestational Age: French Real-Life Data.

Coutant, Régis / Leheup, Bruno / Nicolino, Marc / Salles, Jean-Pierre

Hormone research in paediatrics

2023 Volume 96, Issue 5, Page(s) 495–508

Abstract: Introduction: Growth hormone (GH) therapy improves height outcomes in short children born small for gestational age (SGA); however, real-world data on long-term GH exposure are few.: Methods: We report results from an observational study (NCT01578135) ...

Abstract	Introduction: Growth hormone (GH) therapy improves height outcomes in short children born small for gestational age (SGA); however, real-world data on long-term GH exposure are few. Methods: We report results from an observational study (NCT01578135) including children born SGA, treated with GH at 126 sites in France, and followed up for >5 years until achieving final adult height (FAH) or until study termination. Primary endpoints were the proportion of patients with normal (>-2) height standard deviation score (SDS) at the last visit and with normal FAH SDS. Post hoc analyses were performed by multivariate logistic regression analysis with stepwise elimination to identify factors associated with GH dose modulation and normal height SDS achievement. Results: Of 1,408 registered patients, a representative sample (n = 291) was selected for long-term follow-up. At the last visit, 193/291 (66.3%) children achieved normal height SDS and 72/291 (24.7%) reached FAH. FAH SDS was >-2 for chronological age in 48 (66.7%) children and >-2 for adult age in 40 (55.6%) children. In the post hoc analyses, height SDS at the last visit was a significant determinant of whether GH dose had been modulated. Factors significantly associated with reaching normal height SDS were baseline height SDS (taller, better), age at treatment start (younger, better), treatment duration excluding discontinuation periods (longer, better), and absence of a chronic disease. Most (70%) adverse events were non-serious, with 39% considered possibly/probably related to GH treatment. Conclusions: GH therapy was fairly effective in most short children born SGA. No new safety concerns were identified.
MeSH term(s)	Adult ; Child ; Humans ; Infant, Newborn ; Body Height ; Gestational Age ; Human Growth Hormone/therapeutic use ; Infant, Small for Gestational Age
Chemical Substances	Human Growth Hormone (12629-01-5)
Language	English
Publishing date	2023-04-11
Publishing country	Switzerland
Document type	Observational Study ; Journal Article
ZDB-ID	2537278-6
ISSN	1663-2826 ; 1663-2818
ISSN (online)	1663-2826
ISSN	1663-2818
DOI	10.1159/000530572
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Article ; Online: Bone metabolism during pregnancy.

Salles, Jean Pierre

Annales d'endocrinologie

2016 Volume 77, Issue 2, Page(s) 163–168

Abstract: During pregnancy, mineral concentrations, of calcium and phosphorus in particular, are maintained at a high level in fetal blood so that the developing skeleton may accrete adequate mineral content. The placenta actively transports minerals for this ... ...

Abstract	During pregnancy, mineral concentrations, of calcium and phosphorus in particular, are maintained at a high level in fetal blood so that the developing skeleton may accrete adequate mineral content. The placenta actively transports minerals for this purpose. Maternal intestinal absorption increases in order to meet the fetal demand for calcium, which is only partly dependent on calcitriol. Mineral regulation is essentially dependent on parathyroid hormone (PTH) and PTH-related protein (PTHrP). The calcium-sensing receptor (CaSR) regulates PTH and PTHrP production. If calcium intake is insufficient, the maternal skeleton will undergo resorption due to PTHrP. After birth, a switch from fetal to neonatal homeostasis occurs through increase in PTH and calcitriol, and developmental adaptation of the kidneys and intestines with bone turnover contributing additional mineral to the circulation. Calcium absorption becomes progressively active and dependent on calcitriol. The postnatal skeleton can transiently present with osteoposis but adequate mineral diet usually allows full restoration. Cases of primary osteoporosis must be identified. Loss of trabecular mineral content occurs during lactation in order to provide calcium to the newborn. This programmed bone loss is dependent on a "brain-breast-bone" circuit. The physiological bone resorption during reproduction does not normally cause fractures or persistent osteoporosis. Women who experience fracture are likely to have other causes of bone loss.
MeSH term(s)	Animals ; Bone Remodeling/physiology ; Bone and Bones/metabolism ; Female ; Humans ; Infant, Newborn ; Osteoporosis/diagnosis ; Osteoporosis/therapy ; Parathyroid Hormone/physiology ; Pregnancy/metabolism ; Pregnancy/physiology ; Receptors, Calcium-Sensing/physiology
Chemical Substances	Parathyroid Hormone ; Receptors, Calcium-Sensing
Language	English
Publishing date	2016-06
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	299-9
ISSN	2213-3941 ; 0003-4266
ISSN (online)	2213-3941
ISSN	0003-4266
DOI	10.1016/j.ando.2016.04.004
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Article: Clinical Forms and Animal Models of Hypophosphatasia.

Salles, Jean Pierre

Sub-cellular biochemistry

2015 Volume 76, Page(s) 3–24

Abstract: Hypophosphatasia (HPP) is due to mutations of the tissue non-specific alkaline phosphatase (TNAP) gene expressed in the liver, kidney, and bone. TNAP substrates include inorganic pyrophosphate cleaved into inorganic phosphate (Pi) in bone, pyridoxal-5'- ... ...

Abstract	Hypophosphatasia (HPP) is due to mutations of the tissue non-specific alkaline phosphatase (TNAP) gene expressed in the liver, kidney, and bone. TNAP substrates include inorganic pyrophosphate cleaved into inorganic phosphate (Pi) in bone, pyridoxal-5'-phosphate (PLP), the circulating form of vitamin B6, and phosphoethanolamine (PEA). As an autosomal recessive or dominant disease, HPP results in a range of clinical forms. Its hallmarks are low alkaline phosphatase (AP) and elevated PLP and PEA levels. Perinatal HPP may cause early death with respiratory insufficiency and hypomineralization resulting in deformed limbs and sometimes near-absence of bones and skull. Infantile HPP is diagnosed before 6 months of life. Respiratory failure, rib fractures and seizures due to vitamin B6 deficiency in the brain indicate poor prognosis. Craniosynostosis is frequent. Unlike in other forms of rickets, calcium and phosphorus are not decreased, resulting in hypercalciuria and nephrocalcinosis. Hypercalcemic crisis may occur. Failure to thrive and growth retardation are concerns. In infantile and adult forms of HPP, non-traumatic fractures may be the prominent manifestation, with otherwise unexplained chronic pain. Progressive myopathy has been described. Dental manifestations with early loss of teeth are usual in HPP and in a specific form, odontohypophosphatasia. HPP has been studied in knock-out mice models which mimic its severe form. Animal models have made a major contribution to the development of an original enzyme therapy for human infantile HPP, which is however essentially targeted at mineralized tissues. Better knowledge of its extraskeletal manifestations, including pain and neurological symptoms, is therefore required.
MeSH term(s)	Adult ; Animals ; Child ; Disease Models, Animal ; Humans ; Hypophosphatasia/classification ; Hypophosphatasia/diagnosis ; Hypophosphatasia/genetics ; Hypophosphatasia/pathology ; Infant ; Mice ; Mice, Knockout ; Pain/diagnosis ; Pain/etiology ; Pain/pathology
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Review
ISSN	0306-0225 ; 0096-8757
ISSN	0306-0225 ; 0096-8757
DOI	10.1007/978-94-017-7197-9_1
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Article ; Online: Differential DNA methylation in iPSC-derived dopaminergic neurons: a step forward on the role of SNORD116 microdeletion in the pathophysiology of addictive behavior in Prader-Willi syndrome.

Salles, Juliette / Eddiry, Sanaa / Amri, Saber / Galindo, Mélissa / Lacassagne, Emmanuelle / George, Simon / Mialhe, Xavier / Lhuillier, Émeline / Franchitto, Nicolas / Jeanneteau, Freddy / Gennero, Isabelle / Salles, Jean-Pierre / Tauber, Maithé

Molecular psychiatry

2024

Abstract: Introduction: A microdeletion including the SNORD116 gene (SNORD116 MD) has been shown to drive the Prader-Willi syndrome (PWS) features. PWS is a neurodevelopmental disorder clinically characterized by endocrine impairment, intellectual disability and ... ...

Abstract	Introduction: A microdeletion including the SNORD116 gene (SNORD116 MD) has been shown to drive the Prader-Willi syndrome (PWS) features. PWS is a neurodevelopmental disorder clinically characterized by endocrine impairment, intellectual disability and psychiatric symptoms such as a lack of emotional regulation, impulsivity, and intense temper tantrums with outbursts. In addition, this syndrome is associated with a nutritional trajectory characterized by addiction-like behavior around food in adulthood. PWS is related to the genetic loss of expression of a minimal region that plays a potential role in epigenetic regulation. Nevertheless, the role of the SNORD116 MD in DNA methylation, as well as the impact of the oxytocin (OXT) on it, have never been investigated in human neurons. Methods: We studied the methylation marks in induced pluripotent stem-derived dopaminergic neurons carrying a SNORD116 MD in comparison with those from an age-matched adult healthy control. We also performed identical neuron differentiation in the presence of OXT. We performed a genome-wide DNA methylation analysis from the iPSC-derived dopaminergic neurons by reduced-representation bisulfite sequencing. In addition, we performed RNA sequencing analysis in these iPSC-derived dopaminergic neurons differentiated with or without OXT. Results: The analysis revealed that 153,826 cytosines were differentially methylated between SNORD116 MD neurons and control neurons. Among the differentially methylated genes, we determined a list of genes also differentially expressed. Enrichment analysis of this list encompassed the dopaminergic system with COMT and SLC6A3. COMT displayed hypermethylation and under-expression in SNORD116 MD, and SLC6A3 displayed hypomethylation and over-expression in SNORD116 MD. RT-qPCR confirmed significant over-expression of SLC6A3 in SNORD116 MD neurons. Moreover, the expression of this gene was significantly decreased in the case of OXT adjunction during the differentiation. Conclusion: SNORD116 MD dopaminergic neurons displayed differential methylation and expression in the COMT and SLC6A3 genes, which are related to dopaminergic clearance.
Language	English
Publishing date	2024-04-02
Publishing country	England
Document type	Journal Article
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-024-02542-4
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Article ; Online: Can antidepressants unlock prescription of rimonabant in the fight against COVID-19?

Salles, Juliette / Briand-Mésange, Fabienne / Trudel, Stéphanie / Ausseil, Jérôme / Salles, Jean-Pierre / Chap, Hugues

Molecular psychiatry

2021 Volume 26, Issue 12, Page(s) 7091–7092

MeSH term(s)	Antidepressive Agents/therapeutic use ; COVID-19 ; Humans ; Prescriptions ; Rimonabant/therapeutic use ; SARS-CoV-2
Chemical Substances	Antidepressive Agents ; Rimonabant (RML78EN3XE)
Language	English
Publishing date	2021-07-19
Publishing country	England
Document type	Letter ; Comment
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-021-01221-y
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Article ; Online: Growth hormone treatment improves final height in children with X-linked hypophosphatemia.

André, Julia / Zhukouskaya, Volha V / Lambert, Anne-Sophie / Salles, Jean-Pierre / Mignot, Brigitte / Bardet, Claire / Chaussain, Catherine / Rothenbuhler, Anya / Linglart, Agnès

Orphanet journal of rare diseases

2022 Volume 17, Issue 1, Page(s) 444

Abstract: Background/aim: Despite optimal conventional treatment (oral phosphate supplements and active vitamin D analogs), about 40-50% of children with well-controlled X-linked hypophosphatemia (XLH) show linear growth failure, making them less likely to ... ...

Abstract	Background/aim: Despite optimal conventional treatment (oral phosphate supplements and active vitamin D analogs), about 40-50% of children with well-controlled X-linked hypophosphatemia (XLH) show linear growth failure, making them less likely to achieve an acceptable final height. Here, we studied the hypothesis that rhGH treatment improves final height in children with XLH and growth failure. Methods: Two cohorts of children with XLH were included in this retrospective longitudinal analysis: (1) a cohort treated with rhGH for short stature (n = 34) and (2) a cohort not treated with rhGH (n = 29). The mean duration of rhGH treatment was 4.4 ± 2.9 years. We collected the auxological parameters at various time points during follow-up until final height. Results: In rhGH-treated children, 2 years of rhGH therapy was associated with a significant increase in height from - 2.4 ± 0.9 to - 1.5 ± 0.7 SDS (p < 0.001). Their mean height at rhGH discontinuation was - 1.2 ± 0.9 SDS and at final height was - 1.3 ± 0.9 SDS corresponding to 165.5 ± 6.4 cm in boys and 155.5 ± 6.3 cm in girls. Notably, the two groups had similar final heights; i.e., the final height in children not treated with rhGH being - 1.2 ± 1.1 SDS (165.4 ± 6.8 cm in boys and 153.7 ± 7.8 cm in girls), p = 0.7. Conclusion: Treatment with rhGH permits to improve final height in children with XLH and growth failure, despite optimal conventional treatment. We propose therefore that rhGH therapy could be considered as an option for short stature in the context of XLH.
MeSH term(s)	Child ; Female ; Humans ; Male ; Body Height ; Dwarfism/drug therapy ; Familial Hypophosphatemic Rickets/drug therapy ; Growth Disorders/drug therapy ; Growth Hormone/therapeutic use ; Human Growth Hormone/therapeutic use ; Retrospective Studies
Chemical Substances	Growth Hormone (9002-72-6) ; Human Growth Hormone (12629-01-5)
Language	English
Publishing date	2022-12-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2225857-7
ISSN	1750-1172 ; 1750-1172
ISSN (online)	1750-1172
ISSN	1750-1172
DOI	10.1186/s13023-022-02590-5
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Article ; Online: Possible Role of Adipose Tissue and the Endocannabinoid System in Coronavirus Disease 2019 Pathogenesis: Can Rimonabant Return?

Briand-Mésange, Fabienne / Trudel, Stéphanie / Salles, Juliette / Ausseil, Jérôme / Salles, Jean-Pierre / Chap, Hugues

Obesity (Silver Spring, Md.)

2020 Volume 28, Issue 9, Page(s) 1580–1581

MeSH term(s)	Adipose Tissue ; Betacoronavirus ; COVID-19 ; Coronavirus ; Coronavirus Infections ; Endocannabinoids ; Humans ; Obesity ; Pandemics ; Pneumonia, Viral ; Prevalence ; Respiration, Artificial ; Rimonabant ; SARS-CoV-2 ; Severe Acute Respiratory Syndrome
Chemical Substances	Endocannabinoids ; Rimonabant (RML78EN3XE)
Keywords	covid19
Language	English
Publishing date	2020-08-06
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.22916
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Article ; Online: What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?

Salles, Juliette / Lacassagne, Emmanuelle / Eddiry, Sanaa / Franchitto, Nicolas / Salles, Jean-Pierre / Tauber, Maithé

Molecular psychiatry

2020 Volume 26, Issue 1, Page(s) 51–59

Abstract: Addictive disorders have been much investigated and many studies have underlined the role of environmental factors such as social interaction in the vulnerability to and maintenance of addictive behaviors. Research on addiction pathophysiology now ... ...

Abstract	Addictive disorders have been much investigated and many studies have underlined the role of environmental factors such as social interaction in the vulnerability to and maintenance of addictive behaviors. Research on addiction pathophysiology now suggests that certain behavioral disorders are addictive, one example being food addiction. Yet, despite the growing body of knowledge on addiction, it is still unknown why only some of the individuals exposed to a drug become addicted to it. This observation has prompted the consideration of genetic heritage, neurodevelopmental trajectories, and gene-environment interactions in addiction vulnerability. Prader-Willi syndrome (PWS) is a rare neurodevelopmental disorder in which children become addicted to food and show early social impairment. PWS is caused by the deficiency of imprinted genes located on the 15q11-q13 chromosome. Among them, the SNORD116 gene was identified as the minimal gene responsible for the PWS phenotype. Several studies have also indicated the role of the Snord116 gene in animal and cellular models to explain PWS pathophysiology and phenotype (including social impairment and food addiction). We thus present here the evidence suggesting the potential involvement of the SNORD116 gene in addictive disorders.
MeSH term(s)	Animals ; Behavior, Addictive/genetics ; Behavior, Addictive/physiopathology ; Food Addiction/genetics ; Humans ; Phenotype ; Prader-Willi Syndrome/genetics ; RNA, Small Nucleolar/genetics
Chemical Substances	RNA, Small Nucleolar ; SNORD116 RNA, human
Language	English
Publishing date	2020-10-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-020-00917-x
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