File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Essential role of Pten in body size determination and pancreatic β-cell homeostasis in vivo

TitleEssential role of Pten in body size determination and pancreatic β-cell homeostasis in vivo
Authors
Issue Date2006
Citation
Molecular and Cellular Biology, 2006, v. 26, n. 12, p. 4511-4518 How to Cite?
AbstractPTEN (phosphatase with tensin homology) is a potent negative regulator of phosphoinositide 3-kinase (PI3K)/Akt signaling, an evolutionarily conserved pathway that signals downstream of growth factors, including insulin and insulin-like growth factor 1. In lower organisms, this pathway participates in fuel metabolism and body size regulation and insulin-like proteins are produced primarily by neuronal structures, whereas in mammals, the major source of insulin is the pancreatic β cells. Recently, rodent insulin transcription was also shown in the brain, particularly the hypothalamus. The specific regulatory elements of the PI3K pathway in these insulin-expressing tissues that contribute to growth and metabolism in higher organisms are unknown. Here, we report PTEN as a critical determinant of body size and glucose metabolism when targeting is driven by the rat insulin promoter in mice. The partial deletion of PTEN in the hypothalamus resulted in significant whole-body growth restriction and increased insulin sensitivity. Efficient PTEN deletion in β cells led to increased islet mass without compromise of β-cell function. Parallel enhancement in PI3K signaling was found in PTEN-deficient hypothalamus and β cells. Together, we have shown that PTEN in insulin-transcribing cells may play an integrative role in regulating growth and metabolism in vivo. Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/291758
ISSN
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 1.452
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNguyen, Kinh Tung T.-
dc.contributor.authorTajmir, Panteha-
dc.contributor.authorLin, Chia Hung-
dc.contributor.authorLiadis, Nicole-
dc.contributor.authorZhu, Xu Dong-
dc.contributor.authorEweida, Mohammed-
dc.contributor.authorTolasa-Karaman, Gunce-
dc.contributor.authorCai, Fang-
dc.contributor.authorWang, Rennian-
dc.contributor.authorKitamura, Tadahiro-
dc.contributor.authorBelsham, Denise D.-
dc.contributor.authorWheeler, Michael B.-
dc.contributor.authorSuzuki, Akira-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorWoo, Minna-
dc.date.accessioned2020-11-17T14:55:03Z-
dc.date.available2020-11-17T14:55:03Z-
dc.date.issued2006-
dc.identifier.citationMolecular and Cellular Biology, 2006, v. 26, n. 12, p. 4511-4518-
dc.identifier.issn0270-7306-
dc.identifier.urihttp://hdl.handle.net/10722/291758-
dc.description.abstractPTEN (phosphatase with tensin homology) is a potent negative regulator of phosphoinositide 3-kinase (PI3K)/Akt signaling, an evolutionarily conserved pathway that signals downstream of growth factors, including insulin and insulin-like growth factor 1. In lower organisms, this pathway participates in fuel metabolism and body size regulation and insulin-like proteins are produced primarily by neuronal structures, whereas in mammals, the major source of insulin is the pancreatic β cells. Recently, rodent insulin transcription was also shown in the brain, particularly the hypothalamus. The specific regulatory elements of the PI3K pathway in these insulin-expressing tissues that contribute to growth and metabolism in higher organisms are unknown. Here, we report PTEN as a critical determinant of body size and glucose metabolism when targeting is driven by the rat insulin promoter in mice. The partial deletion of PTEN in the hypothalamus resulted in significant whole-body growth restriction and increased insulin sensitivity. Efficient PTEN deletion in β cells led to increased islet mass without compromise of β-cell function. Parallel enhancement in PI3K signaling was found in PTEN-deficient hypothalamus and β cells. Together, we have shown that PTEN in insulin-transcribing cells may play an integrative role in regulating growth and metabolism in vivo. Copyright © 2006, American Society for Microbiology. All Rights Reserved.-
dc.languageeng-
dc.relation.ispartofMolecular and Cellular Biology-
dc.titleEssential role of Pten in body size determination and pancreatic β-cell homeostasis in vivo-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/MCB.00238-06-
dc.identifier.pmid16738317-
dc.identifier.pmcidPMC1489140-
dc.identifier.scopuseid_2-s2.0-33745030531-
dc.identifier.volume26-
dc.identifier.issue12-
dc.identifier.spage4511-
dc.identifier.epage4518-
dc.identifier.isiWOS:000238143100011-
dc.identifier.issnl0270-7306-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats