PMID- 23342086
OWN - NLM
STAT- MEDLINE
DCOM- 20130802
LR  - 20220616
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 1
DP  - 2013
TI  - The adipocytokine Nampt and its product NMN have no effect on beta-cell survival 
      but potentiate glucose stimulated insulin secretion.
PG  - e54106
LID - 10.1371/journal.pone.0054106 [doi]
LID - e54106
AB  - 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.
FAU - Spinnler, Robert
AU  - Spinnler R
AD  - Center for Pediatric Research Leipzig-CPL, Department for Women and Child Health, 
      University of Leipzig, Leipzig, Germany.
FAU - Gorski, Theresa
AU  - Gorski T
FAU - Stolz, Katharina
AU  - Stolz K
FAU - Schuster, Susanne
AU  - Schuster S
FAU - Garten, Antje
AU  - Garten A
FAU - Beck-Sickinger, Annette G
AU  - Beck-Sickinger AG
FAU - Engelse, Marten A
AU  - Engelse MA
FAU - de Koning, Eelco J P
AU  - de Koning EJ
FAU - Korner, Antje
AU  - Korner A
FAU - Kiess, Wieland
AU  - Kiess W
FAU - Maedler, Kathrin
AU  - Maedler K
LA  - eng
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130116
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Adiponectin)
RN  - 0 (Insulin)
RN  - 0 (Leptin)
RN  - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
EIN - PLoS One. 2022 Jun 16;17(6):e0270243. PMID: 35709079
MH  - Adiponectin/metabolism
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Blotting, Western
MH  - Cell Survival/drug effects
MH  - Glucose/pharmacology
MH  - Humans
MH  - Insulin/metabolism
MH  - Insulin Secretion
MH  - Insulin-Secreting Cells/*drug effects/*metabolism
MH  - Leptin/metabolism
MH  - Nicotinamide Phosphoribosyltransferase/*pharmacology
MH  - Rats
PMC - PMC3546920
COIS- Competing Interests: The authors would also like to confirm that Kathrin Madler 
      is co-author of this manuscript and a PLOS ONE Editorial Board member. This does 
      not alter the authors' adherence to all the PLOS ONE policies on sharing data and 
      materials.
EDAT- 2013/01/24 06:00
MHDA- 2013/08/03 06:00
PMCR- 2013/01/16
CRDT- 2013/01/24 06:00
PHST- 2012/06/28 00:00 [received]
PHST- 2012/12/10 00:00 [accepted]
PHST- 2013/01/24 06:00 [entrez]
PHST- 2013/01/24 06:00 [pubmed]
PHST- 2013/08/03 06:00 [medline]
PHST- 2013/01/16 00:00 [pmc-release]
AID - PONE-D-12-20262 [pii]
AID - 10.1371/journal.pone.0054106 [doi]
PST - ppublish
SO  - PLoS One. 2013;8(1):e54106. doi: 10.1371/journal.pone.0054106. Epub 2013 Jan 16.