Nicotinic acid inhibits glucose-stimulated insulin secretion via the G protein-coupled receptor PUMA-G in murine islet β cells

Hong Ming Li, Mei Zhang, Sheng Tao Xu, Di Zheng Li, Lin Yun Zhu, Si Wu Peng, Guo Qiang Chen, Pamela Moore Martin, Vadivel Ganapathy, Chi Ju Wei

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Objectives: Chronic administration of nicotinic acid (NA), a potent antilipidemic compound, aggravates glycemic control in diabetic patients. It is not known if NA has direct effects on islet β cells. Methods: Real-time reverse transcriptase-polymerase chain reaction, in situ hybridization, and immunofluorescence techniques were used to examine the expression of NA receptor PUMA-G, a member of the G protein-coupled receptor (G-PCR) family, in murine islet β cells. Calcium transient was measured using confocal microscopy, whereas the intracellular cyclic adenosine monophosphate and glucose-stimulated insulin secretion (GSIS) from isolated islets were determined by the enzyme-linked immunosorbent assay. Results: High levels of PUMA-G transcripts and protein were detected in all β cells, and about 40% of α cells. PUMA-G transcripts increased more than 3-fold in islets incubated with interferon γ. Cyclic adenosine monophosphate accumulation, induced by IBMX/forskolin, was inhibited by NA; however, the inhibition was completely abolished by pretreatment of the culture with pertussis toxin. No calcium transient was detected in islet cells in the presence of NA. Static incubation of islets with NA led to an approximately 30% reduction of GSIS. Conclusions: The results indicated that PUMA-G stimulation by NA in islet β cells inhibited GSIS likely via activation of the Gi signaling pathway.

Original languageEnglish (US)
Pages (from-to)615-621
Number of pages7
JournalPancreas
Volume40
Issue number4
DOIs
StatePublished - May 1 2011

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Niacin
G-Protein-Coupled Receptors
Islets of Langerhans
Insulin
Glucose
Cyclic AMP
Calcium
1-Methyl-3-isobutylxanthine
Pertussis Toxin
Colforsin
Reverse Transcriptase Polymerase Chain Reaction
Confocal Microscopy
Interferons
In Situ Hybridization
Fluorescent Antibody Technique
Real-Time Polymerase Chain Reaction
Enzyme-Linked Immunosorbent Assay
Proteins

Keywords

  • cAMP
  • diabetes
  • insulin secretion
  • Nicotinic acid
  • PUMA-G

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology

Cite this

Nicotinic acid inhibits glucose-stimulated insulin secretion via the G protein-coupled receptor PUMA-G in murine islet β cells. / Li, Hong Ming; Zhang, Mei; Xu, Sheng Tao; Li, Di Zheng; Zhu, Lin Yun; Peng, Si Wu; Chen, Guo Qiang; Martin, Pamela Moore; Ganapathy, Vadivel; Wei, Chi Ju.

In: Pancreas, Vol. 40, No. 4, 01.05.2011, p. 615-621.

Research output: Contribution to journalArticle

Li, Hong Ming ; Zhang, Mei ; Xu, Sheng Tao ; Li, Di Zheng ; Zhu, Lin Yun ; Peng, Si Wu ; Chen, Guo Qiang ; Martin, Pamela Moore ; Ganapathy, Vadivel ; Wei, Chi Ju. / Nicotinic acid inhibits glucose-stimulated insulin secretion via the G protein-coupled receptor PUMA-G in murine islet β cells. In: Pancreas. 2011 ; Vol. 40, No. 4. pp. 615-621.
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AU - Li, Di Zheng

AU - Zhu, Lin Yun

AU - Peng, Si Wu

AU - Chen, Guo Qiang

AU - Martin, Pamela Moore

AU - Ganapathy, Vadivel

AU - Wei, Chi Ju

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