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dc.contributor.authorMcDermott, Lindsay C.en
dc.contributor.authorJadoon, Ayeshaen
dc.contributor.authorCunningham, Philen
dc.date.accessioned2018-04-27T10:42:08Z
dc.date.available2018-04-27T10:42:08Z
dc.date.issued2012-08-31
dc.identifier.citationMcDermott L, Jadoon A, Cunningham P (2012) 'ZAG and a potential role in systemic lipid homeostastis: examining the evidence from in vitro human studies and patients with chronic illness', Clinical Lipidology, 7 (4), pp.409-417.en
dc.identifier.issn1758-4299
dc.identifier.doi10.2217/clp.12.45
dc.identifier.urihttp://hdl.handle.net/10547/622690
dc.description.abstractZAG, a 42 kDa ubiquitously expressed soluble and secreted protein, consists of an MHC-like fold and binds fatty acids with an affinity similar to that of albumin. In human adipocytes, cytoplasmic and secreted ZAG appear inversely related to fat mass. Immunoblotting and biochemical measurements of human cachectic adipocytes and plasma suggest that ZAG’s lipolytic function may be mediated by βIAR. Plasma ZAG correlates with cholesterol in human populations, as does its single nucleotide polymorphism rs4215, which also associates with obesity. Biochemical and human genetic data, in vitro experiments and theoretical data imply that adipocyte ZAG’s expression is regulated by PPAR-γ and glucocorticoids. Cell biological experiments and data from human tissue indicate that ZAG may induce fatty-acid oxidation in skeletal muscle. Overall, these findings suggest ZAG’s participation in systemic lipid homeostasis. Understanding the molecular mechanisms behind ZAG’s in vivo behavior potentially allows for rational drug design to control body fat mass.
dc.language.isoenen
dc.publisherFuture Medicineen
dc.relation.urlhttps://www.tandfonline.com/doi/10.2217/clp.12.45en
dc.rightsYellow - can archive pre-print (ie pre-refereeing)
dc.subjectn-3 polyunsaturated fatty acidsen
dc.subjectC700 Molecular Biology, Biophysics and Biochemistryen
dc.titleZAG and a potential role in systemic lipid homeostastis: examining the evidence from in vitro human studies and patients with chronic illnessen
dc.typeArticleen
dc.identifier.journalClinical Lipidologyen
dc.date.updated2018-04-27T09:56:46Z
html.description.abstractZAG, a 42 kDa ubiquitously expressed soluble and secreted protein, consists of an MHC-like fold and binds fatty acids with an affinity similar to that of albumin. In human adipocytes, cytoplasmic and secreted ZAG appear inversely related to fat mass. Immunoblotting and biochemical measurements of human cachectic adipocytes and plasma suggest that ZAG’s lipolytic function may be mediated by βIAR. Plasma ZAG correlates with cholesterol in human populations, as does its single nucleotide polymorphism rs4215, which also associates with obesity. Biochemical and human genetic data, in vitro experiments and theoretical data imply that adipocyte ZAG’s expression is regulated by PPAR-γ and glucocorticoids. Cell biological experiments and data from human tissue indicate that ZAG may induce fatty-acid oxidation in skeletal muscle. Overall, these findings suggest ZAG’s participation in systemic lipid homeostasis. Understanding the molecular mechanisms behind ZAG’s in vivo behavior potentially allows for rational drug design to control body fat mass.


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