[New pathophysiological mechanisms of metabolic syndrome: implication of orphan nuclear receptors?]. / Nouveaux mécanismes physiopathologiques du Syndrome Métabolique: implication des récepteurs nucléaires orphelins?
Ann Endocrinol (Paris)
; 73 Suppl 1: S9-16, 2012 Oct.
Article
en Fr
| MEDLINE
| ID: mdl-23089382
ABSTRACT
This review focuses on a number of new data on biology and pathophysiology of the metabolic syndrome (MetS) and the involvement of nuclear receptors that have been presented during the last Endocrine Society meeting, held in Houston in June 2012. Several studies have reported beneficial effects of various orphan nuclear receptors, including SHP (Small Heterodimeric Partner, NR0B2) and LXR (Liver X Receptor, NR1H3 and NR1H2), on various components of MetS. By using an inactivation model of SHP, David Moore has shown that SHP exerts "antidiabetic" effects but associated with hepatic steatosis development. He also showed that DLPC (dilauroyl phosphatidylcholine), an unconventional phospholipid, exhibited anti-diabetic properties through its binding to LRH-1 (Liver Receptor Homolog-1, NR5A2), a molecular partner of SHP. Interestingly, Carolyn Cummins investigated LXR α and ß isoforms knock-out mice and provided experimental evidence for the detailed mechanisms involved in the deleterious metabolic effects of glucocorticoids, pointing out to the functional interaction between LXRß, and the glucocorticoid receptor. These new and original studies open new therapeutic opportunities for the management of metabolic disorders in humans by selective modulators of these receptors.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Síndrome Metabólico
/
Receptores Nucleares Huérfanos
Límite:
Animals
/
Humans
Idioma:
Fr
Revista:
Ann Endocrinol (Paris)
Año:
2012
Tipo del documento:
Article
País de afiliación:
Francia