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- 저자 : Philipson, Louis H (검색결과 2 건)
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Partial rescue of the Na+-Ca2+ exchanger (NCX1) knock-out mouse by transgenic expression of NCX1
Chung-HyunCho,So-YoungLee,Hee-SupShin,KennethD.Philipson,ChinO.Lee 생화학분자생물학회 2003 Experimental and molecular medicine Vol.35 No.2
The nul mutation of cardiac Na+-Ca2+ exchanger (NCX1) gene in mice caused death of embryo in utero at embryonic day (ED) 9.0-9.5 and this em-bryonic lethality appears resulted from abnormal heart development. In the present study, we in-vestigated whether transgenic re-expression of these lethal defects. Transgenic mice expresing the canine NCX1 in a cardiac specific maner were bred into the NCX1 knock-out background but did not prevent the fetal lethality asociated with the NCX1 nul alele. However, the NCX1 knock-out embryos with an NCX1 transgene sur-vived with heart beatings until ED 10.5 which was one day longer than the survival of the NCX1 knock-out embryos (ED 9.5). At ED 10.5, however, the partialy rescued NCX1 embryos might have succumbed to the lack of an organized vascula-ture in the yolk sacs. The placental labyrinth la-The transgenic re-expression of NCX1 rescued heart beatings and survived longer, but was stil insuficient for the mice to be completely rescued. Importantly, NCX1 was observed to expres in the yolk sac and the placenta of wild type mice. The results sugest that defects in extra-embryo-nic compartments are causal to the lethality, and that NCX1 may play an important role in es-tablishing vascularization in extra-embryonic tis-sues.
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Functional role of serotonin in insulin secretion in a diet-induced insulin-resistant state.
Kim, Kyuho,Oh, Chang-Myung,Ohara-Imaizumi, Mica,Park, Sangkyu,Namkung, Jun,Yadav, Vijay K,Tamarina, Natalia A,Roe, Michael W,Philipson, Louis H,Karsenty, Gerard,Nagamatsu, Shinya,German, Michael S,Kim The Endocrine Society 2015 Endocrinology Vol.156 No.2
<P>The physiological role of serotonin, or 5-hydroxytryptamine (5-HT), in pancreatic β-cell function was previously elucidated using a pregnant mouse model. During pregnancy, 5-HT increases β-cell proliferation and glucose-stimulated insulin secretion (GSIS) through the Gαq-coupled 5-HT2b receptor (Htr2b) and the 5-HT3 receptor (Htr3), a ligand-gated cation channel, respectively. However, the role of 5-HT in β-cell function in an insulin-resistant state has yet to be elucidated. Here, we characterized the metabolic phenotypes of β-cell-specific Htr2b(-/-) (Htr2b βKO), Htr3a(-/-) (Htr3a knock-out [KO]), and β-cell-specific tryptophan hydroxylase 1 (Tph1)(-/-) (Tph1 βKO) mice on a high-fat diet (HFD). Htr2b βKO, Htr3a KO, and Tph1 βKO mice exhibited normal glucose tolerance on a standard chow diet. After 6 weeks on an HFD, beginning at 4 weeks of age, both Htr3a KO and Tph1 βKO mice developed glucose intolerance, but Htr2b βKO mice remained normoglycemic. Pancreas perfusion assays revealed defective first-phase insulin secretion in Htr3a KO mice. GSIS was impaired in islets isolated from HFD-fed Htr3a KO and Tph1 βKO mice, and 5-HT treatment improved insulin secretion from Tph1 βKO islets but not from Htr3a KO islets. Tph1 and Htr3a gene expression in pancreatic islets was not affected by an HFD, and immunostaining could not detect 5-HT in pancreatic islets from mice fed an HFD. Taken together, these results demonstrate that basal 5-HT levels in β-cells play a role in GSIS through Htr3, which becomes more evident in a diet-induced insulin-resistant state.</P>
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