详细记录  
题名:The adipocytokine Nampt and its product NMN have no effect on beta-cell survival but potentiate glucose stimulated insulin secretion.
作者:SPINNLER R; GORSKI T; STOLZ K; SCHUSTER S; GARTEN A; BECK-SICKINGER AG; ENGELSE MA; DE KONING EJ; KORNER A; KIESS W; MAEDLER K;
来源:PLoS One. 2013;8(1):e54106. doi: 10.1371/journal.pone.0054106. Epub 2013 Jan 16. [ IF= 4.09 ] ]
URL :10.1371/journal.pone.0054106
日期:20130131
摘要:AIMS/HYPOTHESIS: Obesity is associated with a dysregulation of beta-cell and
adipocyte function. The molecular interactions between adipose tissue and
beta-cells are not yet fully elucidated. We investigated, whether or not the
adipocytokine Nicotinamide phosphoribosyltransferase (Nampt) and its enzymatic
product Nicotinamide mononucleotide (NMN), which has been associated with obesity
and type 2 diabetes mellitus (T2DM) directly influence beta-cell survival and
function. METHODS: The effect of Nampt and NMN on viability of INS-1E cells was
assessed by WST-1 assay. Apoptosis was measured by Annexin V/PI and TUNEL assay.
Activation of apoptosis signaling pathways was evaluated. Adenylate kinase
release was determined to assess cytotoxicity. Chronic and acute effects of the
adipocytokine Nampt and its enzymatic product NMN on insulin secretion were
assessed by glucose stimulated insulin secretion in human islets. RESULTS: While
stimulation of beta-cells with the cytokines IL-1beta, TNFalpha and IFN-gamma or
palmitate significantly decreased viability, Nampt and NMN showed no direct
effect on viability in INS-1E cells or in human islets, neither alone nor in the
presence of pro-diabetic conditions (elevated glucose concentrations and
palmitate or cytokines). At chronic conditions over 3 days of culture, Nampt and
its product NMN had no effects on insulin secretion. In contrast, both Nampt and
NMN potentiated glucose stimulated insulin secretion acutely during 1 h
incubation of human islets. CONCLUSION/INTERPRETATION: Nampt and NMN neither
influenced beta-cell viability nor apoptosis but acutely potentiated glucose
stimulated insulin secretion.

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