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  • Choi, Young Hun (author)

Alterations in regulation of energy homeostasis in cyclic nucleotide phosphodiesterase 3B-null mice

  • Article/chapterEnglish2006

Publisher, publication year, extent ...

  • 2006

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  • LIBRIS-ID:oai:lup.lub.lu.se:c33cfbd3-0a56-4a90-a485-5091051caa1c
  • https://lup.lub.lu.se/record/683632URI
  • https://doi.org/10.1172/JCI24867DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • Cyclic nucleotide phosphodiesterase 3B (PDE3B) has been suggested to be critical for mediating insulin/IGF-1 inhibition of cAMP signaling in adipocytes, liver, and pancreatic beta cells. In Pde3b-KO adipocytes we found decreased adipocyte size, unchanged insulin-stimulated phosphorylation of protein kinase B and activation of glucose uptake, enhanced catecholamine-stimulated lipolysis and insulin-stimulated hpogenesis, and blocked insulin inhibition of catecholamine-stimulated lipolysis. Glucose, alone or in combination with glucagon-like peptide-1, increased insulin secretion more in isolated pancreatic KO islets, although islet size and morphology and immunoreactive insulin and glucagon levels were unchanged. The beta(3)-adrenergic agonist CL 316,243 (CL) increased lipolysis and serum insulin more in KO mice, but blood glucose reduction was less in CL-treated KO mice. Insulin resistance was observed in KO mice, with liver an important site of alterations in insulin-sensitive glucose production. In KO mice, liver triglyceride and cAMP contents were increased, and the liver content and phosphorylation states of several insulin signaling, gluconeogenic, and inflammation- and stress-related components were altered. Thus, PDE3B may be important in regulating certain cAMP signaling pathways, including lipolysis, insulin-induced antilipolysis, and cAMP-mediated insulin secretion. Altered expression and/or regulation of PDE3B may contribute to metabolic dysregulation, including systemic insulin resistance.

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  • Park, Sunhee (author)
  • Hockman, Steven (author)
  • Zmuda-Trzebiatowska, Emilia (author)
  • Svennelid, FredrikLund University,Lunds universitet,Biokemi och Strukturbiologi,Centrum för Molekylär Proteinvetenskap,Kemiska institutionen,Institutioner vid LTH,Lunds Tekniska Högskola,Biochemistry and Structural Biology,Center for Molecular Protein Science,Department of Chemistry,Departments at LTH,Faculty of Engineering, LTH(Swepub:lu)pbio-fsv (author)
  • Haluzik, Martin (author)
  • Gavrilova, Oksana (author)
  • Ahmad, Faiyaz (author)
  • Pepin, Laurent (author)
  • Napolitano, Maria (author)
  • Taira, Masato (author)
  • Sundler, FrankLund University,Lunds universitet,Institutionen för experimentell medicinsk vetenskap,Medicinska fakulteten,Department of Experimental Medical Science,Faculty of Medicine(Swepub:lu)mphy-fsu (author)
  • Stenson, LenaLund University,Lunds universitet,Signaltransduktionsforskning,Forskargrupper vid Lunds universitet,Insulin Signal Transduction,Lund University Research Groups(Swepub:lu)medk-lsh (author)
  • Degerman, EvaLund University,Lunds universitet,Signaltransduktionsforskning,Forskargrupper vid Lunds universitet,Insulin Signal Transduction,Lund University Research Groups(Swepub:lu)medk-ede (author)
  • Manganiello, Vincent C. (author)
  • Biokemi och StrukturbiologiCentrum för Molekylär Proteinvetenskap (creator_code:org_t)

Related titles

  • In:Journal of Clinical Investigation116:12, s. 3240-32510021-9738

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