PMID- 22009371
OWN - NLM
STAT- MEDLINE
DCOM- 20120229
LR  - 20181217
IS  - 1439-4286 (Electronic)
IS  - 0018-5043 (Linking)
VI  - 43
IP  - 11
DP  - 2011 Oct
TI  - Mechanisms of p-methoxycinnamic acid-induced increase in insulin secretion.
PG  - 766-73
LID - 10.1055/s-0031-1287793 [doi]
AB  - p-Methoxycinnamic acid (p-MCA) is a cinnamic acid derivative that shows various 
      pharmacologic actions such as hepatoprotective and antihyperglycemic activities. 
      The present study was to elucidate the mechanisms by which p-MCA increases 
      [Ca(2)(+)]i and insulin secretion in INS-1 cells. p-MCA (100 muM) increased [Ca(2)(+)]i in 
      INS-1 cells. The p-MCA-induced insulin secretion and rise in [Ca(2)(+)]i were 
      markedly inhibited in the absence of extracellular Ca(2)(+) or in the presence of an 
      L-type Ca(2)(+) channel blocker nimodipine. These results suggested that p-MCA 
      increased Ca(2)(+) influx via the L-type Ca(2)(+) channels. Diazoxide, an ATP-sensitive 
      K(+) channel opener, did not alter p-MCA-induced insulin secretion, nor [Ca(2)(+)]i 
      response. In addition, p-MCA enhanced glucose-, glibenclamide-induced insulin 
      secretion whereas it also potentiated the increase in insulin secretion induced 
      by arginine, and Bay K 8644, an L-type Ca(2)(+) channel agonist. Taken together, our 
      results suggest that p-MCA stimulated insulin secretion from pancreatic beta-cells 
      by increasing Ca(2)(+) influx via the L-type Ca(2)(+) channels, but not through the 
      closure of ATP-sensitive K(+) channels.
CI  - (c) Georg Thieme Verlag KG Stuttgart . New York.
FAU - Adisakwattana, S
AU  - Adisakwattana S
AD  - Department of Pharmacology, Faculty of Veterinary Science, Chulalongkorn 
      University, Bangkok, Thailand.
FAU - Hsu, W H
AU  - Hsu WH
FAU - Yibchok-anun, S
AU  - Yibchok-anun S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111018
PL  - Germany
TA  - Horm Metab Res
JT  - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et 
      metabolisme
JID - 0177722
RN  - 0 (Calcium Channel Agonists)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels, L-Type)
RN  - 0 (Cinnamates)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 0 (KATP Channels)
RN  - 0 (Membrane Transport Modulators)
RN  - 6G4ML8401A (4-methoxycinnamic acid)
RN  - 94ZLA3W45F (Arginine)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Arginine/metabolism
MH  - Calcium Channel Agonists/pharmacology
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels, L-Type/chemistry
MH  - Calcium Signaling/drug effects
MH  - Cell Line
MH  - Cinnamates/*pharmacology
MH  - Glucose/metabolism
MH  - Hypoglycemic Agents/*pharmacology
MH  - Insulin/*metabolism
MH  - Insulin Secretion
MH  - Insulin-Secreting Cells/*drug effects/*metabolism
MH  - KATP Channels/antagonists & inhibitors
MH  - Kinetics
MH  - Male
MH  - Membrane Transport Modulators/pharmacology
MH  - Perfusion
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Secretory Pathway/drug effects
EDAT- 2011/10/20 06:00
MHDA- 2012/03/01 06:00
CRDT- 2011/10/20 06:00
PHST- 2011/10/20 06:00 [entrez]
PHST- 2011/10/20 06:00 [pubmed]
PHST- 2012/03/01 06:00 [medline]
AID - 10.1055/s-0031-1287793 [doi]
PST - ppublish
SO  - Horm Metab Res. 2011 Oct;43(11):766-73. doi: 10.1055/s-0031-1287793. Epub 2011 
      Oct 18.