Alström syndrome: an ultra-rare monogenic disorder as a model for insulin resistance, type 2 diabetes mellitus and obesity.


Journal

Endocrine
ISSN: 1559-0100
Titre abrégé: Endocrine
Pays: United States
ID NLM: 9434444

Informations de publication

Date de publication:
03 2021
Historique:
received: 02 11 2020
accepted: 19 01 2021
pubmed: 11 2 2021
medline: 9 7 2021
entrez: 10 2 2021
Statut: ppublish

Résumé

Alström syndrome (ALMS) is a monogenic ultra-rare disorder with a prevalence of one per million inhabitants caused by pathogenic variants of ALMS1 gene. ALMS1 is located on chromosome 2p13, spans 23 exons and encodes a predicted 461.2-kDa protein of 4169 amino acids. The infantile cone-rod dystrophy with nystagmus and severe visual impairment is the earliest and most consistent clinical manifestation of ALMS. In addition, infantile transient cardiomyopathy, early childhood obesity with hyperphagia, deafness, insulin resistance (IR), type 2 diabetes mellitus (T2DM), systemic fibrosis and progressive renal or liver dysfunction are common findings. ALMS1 encodes a large ubiquitously expressed protein that is associated with the centrosome and the basal body of primary cilium. The localisation of ALMS1 to the ciliary basal body suggests its contribution to ciliogenesis and/or normal ciliary function, or centriolar stability. ALMS1 regulate glucose transport through the actin cytoskeleton, which plays an important role in insulin-stimulated GLUT4 transport. Both extreme IR and β-cell failure are the two determinant factors responsible for the development of glucose metabolism alterations in ALMS. Currently, there is no known cure for ALMS other than managing the underlying systemic diseases. When possible, individuals with ALMS and families should be referred to a centre of expertise and followed by a multidisciplinary team. Lifestyle modification, aerobic exercise and dietary induced weight loss are highly recommended as primary treatment for ALMS patients with T2DM and obesity. Managing a rare disease requires not only medical care but also a support network including patient associations.

Sections du résumé

BACKGROUND
Alström syndrome (ALMS) is a monogenic ultra-rare disorder with a prevalence of one per million inhabitants caused by pathogenic variants of ALMS1 gene. ALMS1 is located on chromosome 2p13, spans 23 exons and encodes a predicted 461.2-kDa protein of 4169 amino acids. The infantile cone-rod dystrophy with nystagmus and severe visual impairment is the earliest and most consistent clinical manifestation of ALMS. In addition, infantile transient cardiomyopathy, early childhood obesity with hyperphagia, deafness, insulin resistance (IR), type 2 diabetes mellitus (T2DM), systemic fibrosis and progressive renal or liver dysfunction are common findings. ALMS1 encodes a large ubiquitously expressed protein that is associated with the centrosome and the basal body of primary cilium.
CURRENT RESEARCH
The localisation of ALMS1 to the ciliary basal body suggests its contribution to ciliogenesis and/or normal ciliary function, or centriolar stability. ALMS1 regulate glucose transport through the actin cytoskeleton, which plays an important role in insulin-stimulated GLUT4 transport. Both extreme IR and β-cell failure are the two determinant factors responsible for the development of glucose metabolism alterations in ALMS.
TREATMENT
Currently, there is no known cure for ALMS other than managing the underlying systemic diseases. When possible, individuals with ALMS and families should be referred to a centre of expertise and followed by a multidisciplinary team. Lifestyle modification, aerobic exercise and dietary induced weight loss are highly recommended as primary treatment for ALMS patients with T2DM and obesity.
CONCLUSION
Managing a rare disease requires not only medical care but also a support network including patient associations.

Identifiants

pubmed: 33566311
doi: 10.1007/s12020-021-02643-y
pii: 10.1007/s12020-021-02643-y
doi:

Substances chimiques

Cell Cycle Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

618-625

Références

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Auteurs

Francesca Dassie (F)

Department of Medicine (DIMED), Clinica Medica 3, Padua University Hospital, Padua, Italy.

Francesca Favaretto (F)

Department of Medicine (DIMED), Clinica Medica 3, Padua University Hospital, Padua, Italy.

Silvia Bettini (S)

Department of Medicine (DIMED), Clinica Medica 3, Padua University Hospital, Padua, Italy.

Matteo Parolin (M)

Department of Medicine (DIMED), Clinica Medica 3, Padua University Hospital, Padua, Italy.

Marina Valenti (M)

Italian Association of Alström Syndrome Patients-ASS.A.I., Endo-ERN ePAG, Padua, Italy.

Felix Reschke (F)

Department of General Pediatrics, Endocrinology/Diabetology and Clinical Research, Children's Hospital Auf der Bult, Hannover, Germany.

Thomas Danne (T)

Department of General Pediatrics, Endocrinology/Diabetology and Clinical Research, Children's Hospital Auf der Bult, Hannover, Germany.

Roberto Vettor (R)

Department of Medicine (DIMED), Clinica Medica 3, Padua University Hospital, Padua, Italy.

Gabriella Milan (G)

Department of Medicine (DIMED), Clinica Medica 3, Padua University Hospital, Padua, Italy.

Pietro Maffei (P)

Department of Medicine (DIMED), Clinica Medica 3, Padua University Hospital, Padua, Italy. pietro.maffei@aopd.veneto.it.

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