Burmese pythons exhibit a transient adaptation to nutrient overload that prevents liver damage

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dc.article.numbere202113008
dc.catalogadorgrr
dc.contributor.authorMagida, Jason A.
dc.contributor.authorTan, Yuxiao
dc.contributor.authorWall, Christopher E.
dc.contributor.authorHarrison, Brooke C.
dc.contributor.authorMarr, Thomas G.
dc.contributor.authorPeter, Angela K.
dc.contributor.authorRiquelme Illanes, Cecilia Angélica
dc.contributor.authorLeinwand, Leslie A.
dc.date.accessioned2024-09-27T13:12:49Z
dc.date.available2024-09-27T13:12:49Z
dc.date.issued2022
dc.description.abstractAs an opportunistic predator, the Burmese python (Python molurus bivittatus) consumes large and infrequent meals, fasting for up to a year. Upon consuming a large meal, the Burmese python exhibits extreme metabolic responses. To define the pathways that regulate these postprandial metabolic responses, we performed a comprehensive profile of plasma metabolites throughout the digestive process. Following ingestion of a meal equivalent to 25% of its body mass, plasma lipoproteins and metabolites, such as chylomicra and bile acids, reach levels observed only in mammalian models of extreme dyslipidemia. Here, we provide evidence for an adaptive response to postprandial nutrient overload by the python liver, a critical site of metabolic homeostasis. The python liver undergoes a substantial increase in mass through proliferative processes, exhibits hepatic steatosis, hyperlipidemia-induced insulin resistance indicated by PEPCK activation and pAKT deactivation, and de novo fatty acid synthesis via FASN activation. This postprandial state is completely reversible. We posit that Burmese pythons evade the permanent hepatic damage associated with these metabolic states in mammals using evolved protective measures to inactivate these pathways. These include a transient activation of hepatic nuclear receptors induced by fatty acids and bile acids, including PPAR and FXR, respectively. The stress-induced p38 MAPK pathway is also transiently activated during the early stages of digestion. Taken together, these data identify a reversible metabolic response to hyperlipidemia by the python liver, only achieved in mammals by pharmacologic intervention. The factors involved in these processes may be relevant to or leveraged for remediating human hepatic pathology.
dc.description.funderHiberna Corporation
dc.description.funderNational Institutes of Health
dc.description.funderUniversity of Alabama
dc.description.funderLeducq Foundation
dc.fuente.origenScopus
dc.identifier.doi10.1085/jgp.202113008
dc.identifier.eissn15407748
dc.identifier.issn221295
dc.identifier.pubmedid35323838
dc.identifier.scopusidSCOPUS_ID:85129278028
dc.identifier.urihttps://doi.org/10.1085/jgp.202113008
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/87992
dc.identifier.wosidWOS:000868296200001
dc.information.autorucFacultad de Ciencias Biológicas; Riquelme Illanes, Cecilia Angélica; S/I; 3268
dc.issue.numero4
dc.language.isoen
dc.nota.accesocontenido parcial
dc.revistaJournal of General Physiology
dc.rightsacceso restringido
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleBurmese pythons exhibit a transient adaptation to nutrient overload that prevents liver damage
dc.typeartículo
dc.volumen154
sipa.codpersvinculados3268
sipa.trazabilidadSCOPUS;2022-07-08
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