Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis

Ungerleider, Nathan A

Publication:
Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis

dc.contributor.advisor	Alan L Schneyer
dc.contributor.author	Ungerleider, Nathan A
dc.contributor.department	University of Massachusetts Amherst
dc.contributor.department	Molecular & Cellular Biology
dc.date	2023-09-22T21:24:09.000
dc.date.accessioned	2024-04-26T21:10:29Z
dc.date.available	2011-02-27T00:00:00Z
dc.date.issued	2010-01-01
dc.date.submitted	September
dc.description.abstract	TGFβ ligands, activin and myostatin have been shown to stimulate insulin production and secretion. Antagonists, Follistatin (FST) and Follistatin like 3 (FSTL3) were partially and fully ablated, respectively, creating hyperinsulinemic mice with fatty liver. Much research has surfaced on the connection between hepatic steatosis and hepatic insulin resistance. We present two different models, each with a different mechanism behind the development of fatty liver. FST288-only mice have increased synthesis of mRNA and proteins responsible for hepatic triglyceride (TG) uptake, while our double mutants have increased synthesis of mRNA and proteins responsible for TG synthesis. This alteration was likely independent of hepatic insulin resistance as livers from both mouse lines were insulin sensitive. Experiments conducted in this study to realize the causal factor of hepatic steatosis can be performed on adipose and muscle tissues in the future to better characterize the phenotype.
dc.description.degree	Master of Science (M.S.)
dc.identifier.doi	https://doi.org/10.7275/1500310
dc.identifier.uri	https://hdl.handle.net/20.500.14394/47365
dc.relation.url	https://scholarworks.umass.edu/cgi/viewcontent.cgi?article=1625&context=theses&unstamped=1
dc.source.status	published
dc.subject	hepatic steatosis
dc.subject	insulin resistance
dc.subject	srebp1
dc.subject	lipid uptake
dc.title	Deletions of Fstl3 and/or Fst Isoforms 303 and 315 Results in Hepatic Steatosis
dc.type	open
dc.type	article
dc.type	thesis
digcom.contributor.author	isAuthorOfPublication\|email:n.ungerleider@gmail.com\|institution:University of Massachusetts Amherst\|Ungerleider, Nathan A
digcom.date.embargo	2011-02-27T00:00:00-08:00
digcom.identifier	theses/478
digcom.identifier.contextkey	1500310
digcom.identifier.submissionpath	theses/478
dspace.entity.type	Publication