PMID- 10414928
OWN - NLM
STAT- MEDLINE
DCOM- 19990908
LR  - 20190910
IS  - 0168-8227 (Print)
IS  - 0168-8227 (Linking)
VI  - 44
IP  - 2
DP  - 1999 May
TI  - W-5 and quin 2-AM reverse the inhibitory effect of insulin on lipolysis due to 
      dibutyryl cAMP.
PG  - 101-6
AB  - The effects of W-5, a weak calmodulin antagonist, and quin 2-AM, a cell permeant 
      calcium chelator, on lipolysis and antilipolytic activity of insulin were studied 
      in isolated rat adipocytes. We have previously shown that W-7, a strong 
      calmodulin antagonist, suppresses the inhibitory effect of insulin on lipolysis 
      due to dibutyryl cAMP (Bt2cAMP) in a dose-dependent manner [H. Goko, A. Matsuoka, 
      Diabetes Res. Clin. Prac. 19 (1993) 177-181] and verapamil, a calcium antagonist, 
      potentiates lipolysis due to Bt2cAMP. Like W-7, W-5 suppressed the antilipolytic 
      action of insulin on lipolysis due to Bt2cAMP in a dose-dependent manner. 
      However, when lipolysis was potentiated with 3-isobutyryl-1-methylxanthine 
      (IBMX), W-5 did not suppress the antilipolytic action of insulin. At the same 
      time, like verapamil, W-5 also potentiated lipolysis due to Bt2cAMP in a 
      dose-dependent manner. Thus W-5 has the pharmaceutical effects of both W-7 and 
      verapamil. The chelation of intracellular Ca2+ in adipocytes with quin 2-AM also 
      produced a dose-dependent potentiation of lipolysis due to Bt2cAMP and 
      suppression of the antilipolytic action of insulin on lipolysis due to Bt2cAMP. 
      These effects of quin 2-AM are the same as those of W-5. Therefore, our results 
      suggest that the cytoplasmic Ca2+ plays a pivotal role in mediating the 
      potentiation of lipolysis and antilipolytic action of insulin when lipolysis is 
      induced by Bt2cAMP in rat adipocytes and that W-5 appears to exert its 
      pharmaceutical effects through the inhibition of intracellular calcium-dependent 
      steps other than calmodulin.
FAU - Goko, H
AU  - Goko H
AD  - Department of Medical Technology, Kobe University School of Medicine, Japan.
FAU - Matsuoka, A
AU  - Matsuoka A
LA  - eng
PT  - Journal Article
PL  - Ireland
TA  - Diabetes Res Clin Pract
JT  - Diabetes research and clinical practice
JID - 8508335
RN  - 0 (Aminoquinolines)
RN  - 0 (Chelating Agents)
RN  - 0 (Insulin)
RN  - 0 (Sulfonamides)
RN  - 63X7MBT2LQ (Bucladesine)
RN  - 7B979CWO03 (N-(6-aminohexyl)-1-naphthalenesulfonamide)
RN  - 83104-85-2 (Quin2-acetoxymethyl ester)
SB  - IM
MH  - Adipocytes/drug effects/*physiology
MH  - Aminoquinolines/*pharmacology
MH  - Animals
MH  - Bucladesine/antagonists & inhibitors/*pharmacology
MH  - Cells, Cultured
MH  - Chelating Agents/pharmacology
MH  - Epididymis
MH  - Insulin/*pharmacology
MH  - Kinetics
MH  - Lipolysis/*drug effects/physiology
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sulfonamides/*pharmacology
EDAT- 1999/07/22 00:00
MHDA- 1999/07/22 00:01
CRDT- 1999/07/22 00:00
PHST- 1999/07/22 00:00 [pubmed]
PHST- 1999/07/22 00:01 [medline]
PHST- 1999/07/22 00:00 [entrez]
AID - S0168-8227(99)00029-7 [pii]
AID - 10.1016/s0168-8227(99)00029-7 [doi]
PST - ppublish
SO  - Diabetes Res Clin Pract. 1999 May;44(2):101-6. doi: 
      10.1016/s0168-8227(99)00029-7.